🔗 Causal Assertions
15202615: However, the functional significance of changes in the formation of 20-hydroxyeicosatetraenoic acid and epoxyeicosatrienoic acids in the pathogenesis of hypertension are just being uncovered. 17462541: Increased oxidative stress and 20-HETE production may be linked, at least in part, to the pathogenesis of alcohol-related hypertension. 18067589: The vasoconstrictor 20-HETE may play a role in the genesis of ACTH-induced hypertension. Arachidonic acid metabolism in glucocorticoid-induced hypertension. 19458537: The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension. HET0016 also prevented the development of hypertension induced by ACTH (P < 0.01). In the present study, we investigated the effect of a specific enzyme inhibitor of 20-HETE production, N-hydroxy-N'-(4-butyl-2-methylphenyl) formamidine (HET0016), on glucocorticoid-induced hypertension in rats, a sodium-independent model. These results suggest that 20-HETE may play a role in the genesis of ACTH-induced hypertension but not in dexamethasone-induced hypertension. 19675180: We have previously reported that adenoviral-mediated delivery of cytochrome P-450 (CYP) 4A2, which catalyzes the synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE), results in endothelial dysfunction and hypertension in Sprague-Dawley (SD) rats (Wang JS, Singh H, Zhang F, Ishizuka T, Deng H, Kemp R, Wolin MS, Hintze TH, Abraham NG, Nasjletti A, Laniado-Schwartzman M. 22723444: CONCLUSIONS: These results indicate that ACE and angiotensin II type 1 receptor activation contribute to 20-HETE-mediated endothelial cell and vascular dysfunction and further enforce the notion that excessive production of 20-HETE within the vasculature leads to hypertension via mechanisms that include the induction of endothelial ACE, thus, perpetuating an increase in vascular angiotensin which, together with 20-HETE, promotes vascular dysfunction. 23641057: To examine whether androgen-independent increases in 20-HETE are sufficient to cause hypertension, we studied Cyp4a12-transgenic mice, which express the CYP4A12-20-HETE synthase under the control of a doxycycline-sensitive promoter. Although the mechanism underlying the effect of androgen on BP and cardiovascular disease is not well understood, recent studies suggest that 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE), a primary cytochrome P450 4 (Cyp4)-derived eicosanoid, may mediate androgen-induced hypertension. 25071086: In the kidney, 20-hydroxyeicosatetraenoic acid (20-HETE) is a primary cytochrome P450 4 (Cyp4)-derived eicosanoid that enhances vasoconstriction of renal vessels and induces hypertension, renal tubular cell hypertrophy, and podocyte apoptosis. 9039121: Inhibition of renal outer medullary 20-HETE production produces hypertension in Lewis rats. 9160783: Finally, induction of renal production of 20-HETE with clofibrate prevents the development of hypertension in Dahl S rats and inhibition of renal 20-HETE formation produces hypertension in Lewis rats fed a high salt diet. 16369530: APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy. 20955934: Positional cloning led to the identification of rare, disease-causing mutations in APP, PSEN1, and PSEN2 causing early-onset familial AD, followed by the discovery of APOE as the single most important risk factor for late-onset AD. 25018108: Together, our data suggest that APP K724M gene mutation may contribute to the cause of this Chinese early-onset familial AD. 25220527: Alzheimer's disease (AD) is the most common form of dementia characterized by deterioration of memory and other cognitive domains which leads to death in 3-9years after diagnosis. In addition to mutations in APP, PSEN1 and PSEN2 genes, that cause early onset autosomal dominant AD, several genetic risk factors for late onset AD are now known. 26225732: Although genetic Abeta variants cause early-onset Alzheimer's disease, literature reports on Abeta properties are heterogeneous, obscuring molecular mechanisms, as illustrated by recent failures of Abeta-level targeting trials. 27274215: Linkage analysis was the first milestone in unraveling the mutations in APP, PSEN1, and PSEN2 that cause early-onset AD, followed by the discovery of apolipoprotein E-epsilon4 allele as the only one genetic risk factor for late-onset AD. 29478590: Genetically, the first clues were provided by genetic linkage studies that led to the identification of APP, PSEN1, and PSEN2 mutations as the main causes of autosomal-dominant early-onset AD. 30168435: PSEN1, APP and PSEN2 are the major causes of monogenic EOAD while GRN, MAPT and C9ORF72 are the most frequently mutated genes in familial FTLD. 30851551: Generation of two iPSC lines (ICGi008-A and ICGi008-B) from skin fibroblasts of a patient with early-onset Alzheimer's disease caused by London familial APP mutation (V717I). 30909216: With the exception of rare mutations in APP, PSEN1, and PSEN2 genes causing autosomal dominant EOAD, little is known about the genetic factors underlying most of the EOAD cases. 31446431: Abeta bearing the familial English H6R mutation, known to cause early-onset AD, had an even greater inhibitory effect on protein degradation through the Arg/N-end rule pathway than intact Abeta. 33519353: With the exception or rare mutations in PSEN and APP genes causing early-onset autosomal dominant AD (EOADAD), little is known about the genetic factors that underlie the vast majority (>95%) of early onset AD (EOAD) cases. 10212241: Polymerization of the amyloid beta (Abeta) peptide into protease-resistant fibrils is a significant step in the pathogenesis of Alzheimer's disease. 10729621: A small fraction of AD and CAA cases are caused by gene mutations leading to increased production and deposition of Abeta, but for the majority, there is no known direct genetic cause. Brain deposition of the amyloid beta-peptide (Abeta) is a critical step in the pathogenesis of Alzheimer's disease (AD) and human cerebral amyloid angiopathy (CAA). 10880853: The amyloid beta-peptide (A beta), a hallmark in the pathogenesis of AD and the main component of senile plaques, generates free radicals in a metal-catalyzed reaction inducing neuronal cell death by a reactive oxygen species mediated process which damage neuronal membrane lipids, proteins and nucleic acids. 10899433: Polymerization of the amyloid beta-peptide (Abeta) has been identified as a major feature of the pathogenesis of Alzheimer's disease (AD). 10949910: BACKGROUND: The amyloid beta (Abeta) peptide is a key molecule in the pathogenesis of Alzheimer's disease. 11483961: The former process (termed gamma-secretase cleavage) generates amyloid beta-peptide (Abeta), which is involved in the pathogenesis of Alzheimer's disease. 11588612: The formation, aggregation and deposition of amyloid beta peptide (Abeta) is implicated in the aetiology of Alzheimer's disease. 11786314: The amyloid beta peptide as the major culprit of Alzheimer's disease pathogenesis entered the research arena about a decade ago. 11815632: Extracellular amyloid beta peptides (Abetas) have long been thought to be a primary cause of Alzheimer's disease (AD). 11912198: Amyloid plaques formed by aggregation of the amyloid beta-peptide (Abeta) are an intrinsic component of Alzheimer disease pathogenesis. 12025816: Increased production of neurotoxic forms of amyloid beta-peptide (Abeta) and abnormalities in neuronal calcium homeostasis play central roles in the pathogenesis of Alzheimer's disease (AD). 12025858: Our data show that Abeta can impair cortical neurogenesis, and suggest that this adverse effect of Abeta contributes to the depletion of neurons and the resulting olfactory and cognitive deficits in AD. We now report that amyloid beta-peptide (Abeta), a self-aggregating neurotoxic protein thought to cause AD, can impair neurogenesis in the SVZ/cerebral cortex of adult mice and in human cortical NPC in culture. 12063304: The amyloid-beta (A beta) peptide, which is derived from the amyloid precursor protein (APP), is involved in the pathogenesis of Alzheimer's dementia and impairs endothelium-dependent vasodilation in cerebral vessels. 12074840: Metabolism of amyloid-beta peptide (Abeta) is closely associated with the pathology and etiology of Alzheimer's disease (AD). 12176077: Over the past several years, experiments with synthetic amyloid-beta peptide (Abeta) and animal models have strongly suggested that pathogenesis of Alzheimer's disease (AD) involves soluble assemblies of Abeta peptides (Trends Neurosci. 24 (2001) 219). 12359256: Polymerization of the amyloid beta-peptide (Abeta) has been identified as a major feature of the pathogenesis of Alzheimer's disease (AD). 12391610: Metabolism of amyloid-beta peptide (A beta) is closely associated with the pathology and etiology of Alzheimer's disease (AD). 12392766: Amyloid beta-peptide [Abeta(1-42)] is central to the pathogenesis of Alzheimer's disease (AD), and the AD brain is under intense oxidative stress, including membrane lipid peroxidation. 12446966: It is generally accepted that amyloid beta peptides (Abeta) play a significant role in the etiology of Alzheimer's disease. 12446972: Over-production and/or altered metabolism of AbetaPP, resulting in increased amyloid beta-peptide (Abeta), appear pivotal in the pathogenesis of AD. 12493601: The amyloid precursor protein (APP) and its proteolytic cleavage products, the amyloid beta peptides, have been implicated as a cause of Alzheimer's disease. 12607822: Amyloid beta-peptide (1-42) [Abeta(1-42)] may be central to the pathogenesis of AD. 12846562: Cellular release and subsequent aggregation of the amyloid-beta peptide is thought to be causative for the pathogenesis of Alzheimer's disease. 14646594: Amyloid beta-peptide (Abeta), a causative molecule in the pathogenesis of Alzheimer's disease and the main component of senile plaques, is known to be neurotoxic in vitro and in vivo. 14698294: Extensive data suggest that the conversion of the amyloid-beta (Abeta) peptide from soluble to insoluble forms is a key factor in the pathogenesis of Alzheimer's disease (AD). 14732699: Amyloid-beta peptide (Abeta) is central to the pathogenesis of Alzheimer's disease, and the low-density lipoprotein receptor-related protein (LRP) has been shown to alter Abeta metabolism in vitro. 15065253: The cerebral deposition of amyloid beta-peptide, a central event in Alzheimer's disease (AD) pathogenesis, begins several years before the onset of clinical symptoms. 15267231: Gamma-secretase is the second of two proteolytic enzymes responsible for the release of the amyloid beta-peptide implicated in the etiology of Alzheimer's disease. 15304503: Because Abeta peptides are thought to be causative for Alzheimer's disease, inhibiting gamma-secretase represents a potential treatment for this neurodegenerative condition. 15341515: Gamma-secretase performs the final processing step in the generation of amyloid-beta (Abeta) peptides, which are believed to be causative for Alzheimer's disease. 15347683: The deposition of the amyloid beta (Abeta) peptide in neuritic plaques plays a critical role in the pathogenesis of Alzheimer's disease (AD). 15502844: The Arctic mutation within the amyloid-beta (Abeta) peptide causes Alzheimer disease. 15633014: A second example is the cleavage of amyloid beta-peptide by IgM and IgG from aged humans, a phenomenon that may represent a specific proteolytic response to a neurotoxic endogenous peptide implicated in the pathogenesis of Alzheimer's disease. 15880461: The potential neurotoxicity of soluble forms of amyloid beta peptide (Abeta) as a key factor in early pathogenesis of Alzheimer's disease is being recognized. 15882358: In this review, the case is made that amyloid-beta peptide in the brain of patients with Alzheimer's disease is a primary cause of the disease and that immunotherapy directed against this peptide has the potential to halt and/or reverse disease progression. 15955457: Protection against amyloid beta-peptide (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes by tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester: implications for Alzheimer's disease. 15959937: LRP also binds the amyloid precursor protein (APP) and its proteolytic fragment, the amyloid-beta peptide (Abeta), which are major players in the pathogenesis of AD. 15975052: The amyloid beta-peptide (Abeta) plays an early and critical role in the pathogenic cascade leading to Alzheimer's disease (AD). 16255678: Aberrant production or decreased clearance of amyloid-beta peptides is widely accepted to be causative for AD. 16364896: Aggregation of the amyloid-beta (Abeta) peptide in the extracellular space of the brain is central to Alzheimer's disease pathogenesis. 16446073: Ectodomain shedding of the amyloid precursor protein (APP) is a key regulatory step in the generation of the amyloid beta peptide (Abeta), which is thought to provoke the pathogenesis of Alzheimer's disease. 16595673: Amyloid-beta peptide (Abeta) is pivotal to the pathogenesis of Alzheimer disease. 16696577: Genetic and experimental evidence points to amyloid-beta (Abeta) peptide as the culprit in Alzheimer's disease pathogenesis. 16781151: The interaction of amyloid beta peptide (Abeta) and Abeta-binding alcohol dehydrogenase (ABAD) was recently implicated in the pathogenesis of Alzheimer's disease (AD). 16817891: The amyloid beta peptide (A beta) is crucial for the pathogenesis of Alzheimer's disease. 16893185: Aggregation of the 40-42 residue amyloid beta-peptide (Abeta) into amyloid plaques is a central event in Alzheimer's disease (AD) pathogenesis. 16897184: Deposition of amyloid beta-peptide (Abeta) and neurofibrillary tangles in the brain are hallmarks of Alzheimer's disease (AD) pathogenesis. 16946102: Accumulation of amyloid beta-peptide (Abeta) is considered a key step in the etiology of Alzheimer's disease. 17035538: Aberrant processing of the amyloid precursor protein (APP) and the subsequent accumulation of amyloid beta (Abeta) peptide has been widely established as a central event in Alzheimer's disease (AD) pathogenesis. 17054909: Amyloid beta-peptide (Abeta) and glutamate are generally believed to be closely related to the pathogenesis of Alzheimer's disease and cerebrovascular disease, respectively. 17169612: Data accumulated during the past two decades place amyloid beta-peptide (Abeta) at center stage as the main perpetrator in initiating the pathological cascade that eventually leads to Alzheimer's disease. 17177887: We have found that a quartz-crystal microbalance is a facile and useful tool for detecting the specific aggregation of the amyloid-beta peptides responsible for Alzheimer's disease. 17382287: The aggregation and deposition onto neuronal cells of amyloid beta-peptide (Abeta) is central to the pathogenesis of Alzheimer's disease. 17404210: The conformational change in amyloid beta (Abeta) peptide from its monomeric form to aggregates is crucial in the pathogenesis of Alzheimer's disease (AD). 17428603: Alternative proteolytic processing of APP releases potentially neurotoxic species, including the amyloid-beta (Abeta) peptide that is centrally implicated in the pathogenesis of Alzheimer's disease (AD). 17471072: Accumulating evidence suggests that amyloid beta-peptide (1-42) plays an important role in the etiology of Alzheimer's disease. 17495608: Intracellular cholesterol levels influence the generation of amyloid-beta peptides, the toxic species thought to be a primary cause of Alzheimer's disease. 17511455: Dysfunctional interactions of metal ions, especially Cu, Zn, and Fe, with the amyloid-beta (A beta) peptide are hypothesized to play an important role in the etiology of Alzheimer's disease (AD). 17551018: Aggregation of the amyloid-beta (Abeta) peptide in the extracellular space of the brain is critical in the pathogenesis of Alzheimer's disease. 17606418: The amyloid cascade hypothesis assigns the amyloid-beta peptide (Abeta) a central role in the pathogenesis of Alzheimer's disease (AD). 17876751: Amyloid beta peptide (Abeta) fibril formation is widely believed to be the causative event of Alzheimer's disease pathogenesis. 17897958: BACE1 (beta-site amyloid precursor protein-cleaving enzyme-1) is a membrane-bound aspartic protease that cleaves amyloid precursor protein to produce a neurotoxic peptide, amyloid beta-peptide, and has been implicated in triggering the pathogenesis of Alzheimer disease. 17997700: Amyloid-beta peptide (Abeta), a major peptide deposited in neuritic plaques, has been considered as an important initiating molecule in the pathogenesis of AD. 18063474: Alzheimer's disease (AD) is a neurodegenerative disorder, due to excess amyloid-beta peptide (Abeta). 18252750: Although it is not yet established, whether the resulting Abeta aggregates are the causative agent or just a result of the disease progression, polymerization of Abeta has been identified as a major feature during AD pathogenesis. The 'amyloid cascade hypothesis' assigns the amyloid-beta-peptide (Abeta) a central role in the pathogenesis of AD. 18258258: Aggregation of the amyloid beta (A beta) peptide plays a key role in the molecular etiology of Alzheimer's disease. 18385378: beta-Site APP-cleaving enzyme 1 (BACE1) is required for the penultimate cleavage of the amyloid-beta precursor protein (APP) leading to the generation of amyloid-beta peptides that is central to the pathogenesis of Alzheimer's disease. 18387708: Amyloid-beta peptide (Abeta) has been proposed to be the primary cause of AD. 18400162: Aggregation of amyloid-beta (Abeta) peptide into soluble and insoluble forms within the brain extracellular space is central to the pathogenesis of Alzheimer's disease. 18411275: The catalytic domain of insulin-degrading enzyme forms a denaturant-resistant complex with amyloid beta peptide: implications for Alzheimer disease pathogenesis. 18471993: The aggregation of amyloid beta-peptide (Abeta) into beta-sheet-rich aggregates is a crucial step in the etiology of Alzheimer's disease. 18625450: The 4-kDa amyloid beta-peptide (Abeta) is strongly implicated the pathogenesis of Alzheimer's disease (AD), and this peptide is cut out of the amyloid beta-protein precursor (APP) by the sequential action of beta- and gamma-secretases. gamma-Secretase is a membrane-embedded protease complex that cleaves the transmembrane region of APP to produce Abeta, and this protease is a top target for developing AD therapeutics. 18930548: Neurotoxic oligomers of amyloid beta (Abeta) peptide have been incriminated in the pathogenesis of Alzheimer's disease. 18957217: Impaired degradation of amyloid beta (Abeta) peptides could lead to Abeta accumulation, an early trigger of Alzheimer's disease (AD). 19057576: Amyloid beta-peptide (Abeta) accumulation leads to neurodegeneration and Alzheimer disease; however, amyloid metabolism is a dynamic process and enzymic mechanisms exist for Abeta removal. 19075706: Extracellular deposition of amyloid beta-peptide (Abeta) has been implicated as a critical step in the pathogenesis of AD. 19122666: Amyloid-beta (Abeta) peptides, widely presumed to cause Alzheimer's disease, increased mouse neuronal expression of collagen VI through a mechanism involving transforming growth factor signaling. 19198114: Genetic and biological studies provide evidence that the production and deposition of amyloid-beta peptides (Abeta) contribute to the etiology of Alzheimer's disease. 19277012: Accumulation of aggregated amyloid-beta (Abeta) peptide was studied as an initial step for Alzheimer's disease (AD) pathogenesis. 19352532: Dysfunctional interactions of metal ions, especially those of Cu, Zn, and Fe, with the amyloid-beta (Abeta) peptide are hypothesised to play an important role in the aetiology of AD, and disruption of these aberrant metal-peptide interactions via chelation therapy holds considerable promise as a therapeutic strategy. 19402777: Genetic and biological studies provide strong evidence that the deposition of amyloid-beta peptide (Abeta) contributes to the etiology of Alzheimer's disease (AD). 19450545: The overproduction and extracellular buildup of amyloid-beta peptide (Abeta) is a critical step in the etiology of Alzheimer's disease. 19469700: Most disease-modifying therapeutic approaches in Alzheimer's disease (AD) aim to reduce the accumulation of neurotoxic amyloid-beta (Abeta) peptides as a hallmark of AD pathogenesis. 19558683: Extensive genetic, biochemical, and histological evidence has implicated the amyloid-beta peptide (Abeta) in Alzheimer's disease pathogenesis, and several mechanisms have been suggested, such as metal binding, reactive oxygen species production, and membrane pore formation. 19646546: The neurotoxic amyloid-beta-peptide (Abeta) is important in the pathogenesis of Alzheimer's disease (AD). 19751725: Subcellular and metabolic examination of amyloid-beta peptides in Alzheimer disease pathogenesis: evidence for Abeta(25-35). 19782682: Alzheimer's disease (AD) is the principal cause of dementia in older people, and accumulation of amyloid-beta (Abeta) peptide is a crucial event in AD pathogenesis. 19837693: The hypothesis that amyloid-beta (Abeta) peptides are the primary cause of Alzheimer's disease (AD) remains the best supported theory of AD pathogenesis. 19841277: Accumulation of amyloid beta-peptide (Abeta) and tau aggregates, possibly linked to age-associated deficiencies in protein homeostasis, appear to cause Alzheimer's disease. 19862643: Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid beta-peptide, the principal event in the pathogenesis of Alzheimer's disease. 19906677: Microglia are critical for amyloid-beta peptide (Abeta)-mediated neuronal perturbation relevant to Alzheimer's disease (AD) pathogenesis. 19926793: The amyloid-beta (Abeta) peptide, widely known as the causative molecule of Alzheimer disease (AD), is generated by the sequential cleavage of amyloid precursor protein (APP) by the aspartyl proteases BACE1/beta-secretase and presenilin/gamma-secretase. 19928820: The adsorption and aggregation of the amyloid-beta (Abeta) peptides on the cell membrane plays a causal role in the pathogenesis of Alzheimer's disease. 20008660: BACKGROUND: Supported by compelling genetic data regarding early-onset familial Alzheimer disease (AD), the amyloid beta-peptide (Abeta)-centric theory holds that Abeta is involved in the pathogenesis of sporadic AD. 20014755: Amyloid-beta (Abeta) peptides exhibit many distinct structural morphology at the early aggregate stage, some of which are biological relevant to the pathogenesis of Alzheimer's disease (AD). 20021564: The protease not only releases small peptides, such as the amyloid-beta peptide, which drives Alzheimer's disease pathogenesis, but also intracellular domains, which can have critical functions in nuclear signaling. 20026079: Aggregation of the amyloid-beta (Abeta) peptide is considered a central event in the pathogenesis of Alzheimer's disease (AD). 20030227: Several lines of evidence indicate that the production and deposition of amyloid-beta peptides (Abeta) contribute to the etiology of Alzheimer's disease. 20088802: Overwhelming evidence supports a central role for the amyloid beta-peptide (Abeta) in the pathogenesis of Alzheimer's disease (AD), and the proteases that produce Abeta from its precursor protein APP are top targets for therapeutic intervention. 20157254: Misfolding, oligomerization, and aggregation of the amyloid-beta (Abeta) peptide is widely recognized as a central event in the pathogenesis of Alzheimer's disease (AD). 20447471: We recently reported that amyloid-beta peptide, thought to be a key mediator of AD pathogenesis, engenders S-nitrosylation and thus hyperactivation of the mitochondrial fission protein Drp1. 20456731: The abnormal processing of amyloid-beta peptide (A beta) and resultant formation of fibrillar A beta (fA beta) are major events in the pathogenesis of Alzheimer disease (AD). 20483339: The amphipathicity of the natively unstructured amyloid-beta (Abeta40) peptide may play an important role in its aggregation into beta-sheet rich fibrils, which is linked to the pathogenesis of Alzheimer's disease. 20514639: At present, it is rather accepted that amyloid-beta peptide acts in parallel with other factors causing Alzheimer's disease that should be also considered at the time of designing useful therapeutic strategies. 20590832: The turn formation at positions 22 and 23 in the 42-mer amyloid beta peptide: the emerging role in the pathogenesis of Alzheimer's disease. 20596738: At relatively early ages, Down syndrome patients develop progressive formation and extracellular aggregation of amyloid-beta peptide, considered as one of the causal factors for the pathogenesis of Alzheimer's disease. 20643087: Amyloid-beta (Abeta) peptides and other amyloidogenic proteins can form a wide range of soluble oligomers of varied morphologies at the early aggregation stage, and some of these oligomers are biologically relevant to the pathogenesis of Alzheimer's disease. 20674685: The amyloid beta-peptide (Abeta), which is thought to be the major cause of Alzheimer's disease (AD), is known to be capable of aggregating in different states: soluble monomers and oligomers, and insoluble aggregates. 20691893: The axonal protein tau and amyloid beta-peptide (Abeta) are key players in the pathogenesis of Alzheimer's disease, and tau mediates Abeta toxicity, but it is not clear how. 20721410: It is well known that oligomeric/aggregated amyloid beta peptides are a key player in the pathogenesis of Alzheimer's disease and that different nanoparticles influence oligomerization/aggregation processes in experiments in vitro. 20858952: Laboratory research on anesthetic-induced structural changes of amyloid beta (Abeta) peptide, from normal monomeric alpha-helix to the micro-aggregated form, has generated much interest in the scientific community as Abeta oligomerization is considered a key step in Alzheimer disease pathogenesis. 20974113: Amyloid-beta peptide (Abeta) is shown to be toxic to the mitochondria and implicates this organelle in the pathogenesis of Alzheimer's disease. 21068297: Nonetheless, a growing body of evidence shows that Abeta peptides are unlikely to be the sole factor in AD etiology. 21091946: The identification of disease-causing mutations in Alzheimer's disease has contributed greatly to the understanding of the pathogenesis of this disease. The amyloid-beta (Abeta) peptide has come into focus and is believed to be central to the pathogenesis of Alzheimer's disease. 21223993: Among the pathological factors known to be associated with Alzheimer disease (AD), oxidative stress induced by the amyloid-beta peptide (Abeta) has been demonstrated to play a key role in human brain and animal models of AD. 21297277: Amyloid-beta peptide (Abeta) is recognized by many as the leading cause of Alzheimer's disease (AD), and Abeta oligomers play a major role in the early-onset form of AD. 21491887: The interaction of amyloid-beta (Abeta) peptide with Cu(II) appears to play an important role in the etiology of Alzheimer's disease. 21513747: Amyloid-beta peptide (Abeta) is believed to be central in the pathogenesis of Alzheimer's disease (AD) characterized by cognitive deficits. 21527912: Extracellular phosphorylation of the amyloid beta-peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's disease. However, mechanisms that increase the aggregation of wild-type Abeta and cause the much more common sporadic forms of AD are largely unknown. 21559427: Amyloid beta-peptide (Abeta) accumulation leads to neurodegeneration and Alzheimer's disease (AD). 21629967: The calcium homeostasis modulator 1 (CALHM1) gene codes for a novel cerebral calcium channel controlling intracellular calcium homeostasis and amyloid-beta (Abeta) peptide metabolism, a key event in the etiology of Alzheimer's disease (AD). 21712440: The proteolytic processing of human amyloid precursor protein (APP) into shorter aggregating amyloid beta (Abeta)-peptides, e.g., Abeta1-42, is considered a critical step in the pathogenesis of Alzheimer's disease (AD). 21858698: Substantial evidence suggests that the aggregation of amyloid-beta (Abeta) peptide into fibrillar structures that is rich in beta-sheets is implicated as the cause of Alzheimer's disease. 21958962: Extracellular deposition of amyloid beta peptide (Abeta) has been implicated as a critical step in the pathogenesis of Alzheimer's disease (AD). 22044482: Amyloid-beta peptide (Abeta), which is generated by the beta- and gamma-secretase-mediated proteolysis of beta-amyloid precursor protein (APP), plays an important role in the pathogenesis of Alzheimer's disease (AD). 22090477: According to the amyloid cascade hypothesis, cerebral deposition of amyloid-beta peptide (Abeta) is critical for Alzheimer's disease (AD) pathogenesis. 22102917: The accumulation of the amyloid-beta peptide (Abeta) into amyloid plaques, an essential event in Alzheimer's disease (AD) pathogenesis, has caused researchers to seek compounds that physiologically bind Abeta and modulate its aggregation and neurotoxicity. 22202057: RAGE is an important cellular cofactor for amyloid beta-peptide (Abeta)-mediated cellular perturbation relevant to the pathogenesis of Alzheimer's disease (AD). 22267726: Pyroglutamate-modified Abeta peptides at amino acid position three (Abeta(pE3-42)) are gaining considerable attention as potential key players in the pathogenesis of Alzheimer disease (AD). 22279212: An early role of amyloid-beta peptide (Abeta) aggregation in Alzheimer's disease pathogenesis is well established. 22332002: The 42-mer amyloid beta (Abeta42) peptide is thought to be a culprit in the pathogenesis of Alzheimer's disease (AD). 22384101: Here we report for the first time that tacrine-6-ferulic acid (T6FA), one of these compounds, can prevent amyloid-beta peptide (Abeta)-induced AD-associated pathological changes in vitro and in vivo. 22514691: Amyloid beta (Abeta) peptide is the key molecule in AD pathogenesis, and has been highlighted in the implication of mitochondrial abnormality during the disease progress. 22528098: Neurotoxicity in Alzheimer's disease (AD) is associated to dishomeostasis of intracellular Ca(2+) induced by amyloid beta peptide (Abeta) species. 22544746: Aggregates of amyloid-beta (Abeta) peptides have been implicated in the etiology of Alzheimer disease. 22551668: Cholesterol accumulation in Niemann-Pick type C disease (NPC) causes increased levels of the amyloid-precursor-protein C-terminal fragments (APP-CTFs) and intracellular amyloid-beta peptide (Abeta), the two central molecules in Alzheimer's disease (AD) pathogenesis. 22570624: The aggregation or oligomerization of amyloid-beta (Abeta) peptide is thought to be the primary causative event in the pathogenesis of Alzheimer's disease (AD). 22621900: Proteolytic processing of the amyloid-beta precursor protein (APP) and generation of amyloid-beta peptide (Abeta) are key events in Alzheimer's disease (AD) pathogenesis. 22735675: Amyloid-beta peptide (Abeta) is considered a key protein in the pathogenesis of Alzheimer's disease (AD) because of its neurotoxicity and capacity to form characteristic insoluble deposits known as senile plaques. 22834820: Amyloid beta peptides, causative factors for AD, potentiate the influx of Ca(2+) into neurons via L-VDCCs. 22879596: The amyloid beta (Abeta) peptide, which is abundantly found in the brains of patients suffering from Alzheimer disease, is central in the pathogenesis of this disease. 22886024: The Chinese hamster ovary cell line 7PA2, stably transfected with the 751 amino acid isoform of amyloid-beta protein precursor (AbetaPP) containing the Val -> Phe mutation at residue 717, is one of the most used models to study the biochemistry and toxicity of secreted amyloid-beta (Abeta) peptides, particularly Abeta oligomers, which are considered to be of relevance to the pathogenesis of Alzheimer's disease. 22988239: In this study, we investigated the effects of two different crowding polymers (dextran and Ficoll) and two different experimental conditions (with and without shaking) on the fibrilization of amyloid-beta peptide, a major player in AD pathogenesis. 23023105: beta-Site amyloid precursor protein cleaving enzyme-1 (BACE-1) is a transmembrane aspartic protease that mediates the initial cleavage of the amyloid precursor protein (APP), leading to the generation of amyloid-beta (Abeta) peptides that are thought to be causative of Alzheimer's disease (AD). 23092134: The biogenesis and clearance of the amyloid beta peptide (A beta ), the main component of the lesions, lie at the center of the pathogenesis of AD. 23196551: Genetic and biological studies provide strong evidence that the deposition of amyloid-beta peptide (Abeta) contributes to the etiology of Alzheimer's disease (AD). 23232068: In Alzheimer's disease, amyloid beta (Abeta) peptides and their aggregation are believed to be at least partially responsible for the etiology of Alzheimer's disease. 23237322: gamma-Secretase plays a central role in the generation of the Alzheimer disease-causing amyloid beta-peptide (Abeta) from the beta-amyloid precursor protein (APP) and is thus a major Alzheimer's disease drug target. 23249207: Copper(II) binding to the amyloid-beta peptide has been proposed to be a key event in the cascade leading to Alzheimer's disease. 23270374: Deposition of amyloid-beta (Abeta) peptides in the brain is a central event in the pathogenesis of Alzheimer's disease (AD), which makes Abeta peptides a crucial target for therapeutic intervention. 23387074: Tyrosinase is a key enzyme related to skin pigmentation disorders of elderly people, while self-aggregation of the amyloid-beta peptide, Abeta42, has been considered as a key event in the pathogenesis of Alzheimer's disease (AD). 23420419: The accumulation of extracellular amyloid-beta peptide (Abeta) has been considered as one of the important causes of Alzheimer's disease (AD), the most prevalent form of dementia. 23456036: The selenium-deficiency could possibly promote the onset and/or progression of Alzheimer's disease (AD) dementia, if the Abeta peptides initiate a sequence of events that lead to AD dementia. 23461850: In the present study, we investigated whether SalB has neuroprotective effects in an amyloid beta (Abeta) peptide-induced Alzheimer's disease mouse model. 23509904: The amyloid hypothesis asserts that excess production or reduced clearance of the amyloid-beta (Abeta) peptides in the brain initiates a sequence of events that ultimately lead to Alzheimer's disease and dementia. 23525279: The accumulation of amyloid-beta (Abeta) peptide is thought to be a major causative mechanism of Alzheimer's disease. 23565721: INTRODUCTION: Alzheimer's disease (AD), which is characterized by progressive intellectual deterioration, is the most common cause of dementia. beta-Secretase (or BACE1) expression is a trigger for amyloid beta peptide formation, a cause of AD, and thus is a molecular target for the development of drugs against AD. 23585568: Presenilin comprises the catalytic subunit of gamma-secretase, a protease responsible for the generation of amyloid-beta peptides causative of Alzheimer disease. 23659495: In addition to amyloid-beta (Abeta) peptide and phosphorylated tau, lipid dysregulation is suggested to participate in AD pathogenesis. 23708585: Aggregation of amyloid beta (Abeta) peptides into fibrils has been implicated in the pathogenesis of Alzheimer's disease (AD). 23714261: Abundant evidence suggests a central role for the amyloid-beta (Abeta) peptide in Alzheimer's disease (AD) pathogenesis. 23948943: Soluble oligomeric species of amyloid-beta (Abeta) peptide are presumed to be drivers of synaptic impairment, and the resulting cognitive dysfunction in Alzheimer's disease. 24008925: BACKGROUND: Generation of amyloid-beta peptide is at the beginning of a cascade that leads to Alzheimer's disease. 24081144: A common hypothesis suggests that AD is caused by aggregated Abeta peptides, but treatments with either inhibitors of Abeta production or anti-Abeta antibodies showed no therapeutic value. 24251391: Accumulation, aggregation and deposition of the amyloid-beta (Abeta) peptides in the brain are widely accepted as the central events in the pathogenesis of Alzheimer's disease (AD). 24295810: Amyloid beta (Abeta) peptides are key molecules in the pathogenesis of Alzheimer's disease (AD). 24361736: The amyloid precursor protein (APP) and amyloid-beta (Abeta) peptide play central roles in the pathology and etiology of Alzheimer's disease. 24366271: Accumulation of the amyloid-beta (Abeta) peptide in the brain seems to initiate a cascade of key events in the pathogenesis of AD. 24446231: Defective clearance of the amyloid-beta peptide (Abeta) from the brain is considered a strong promoter in Alzheimer's disease (AD) pathogenesis. 24494584: The amyloid-beta (Abeta) peptide is one key molecule in the pathogenesis of Alzheimer's disease. 24503618: Amyloid-beta peptide (Abeta), the cerebral accumulation of which is thought to cause Alzheimer's disease (AD), is produced throughout life. 24503620: Since both modifications are increased in Alzheimer's disease (AD) due to amyloid-beta peptide (Abeta) accumulation, we have studied their effect on albumin, the most abundant protein in cerebrospinal fluid and blood. 24512022: Amyloid-beta (Abeta) peptide is the original causative factor of Alzheimer's disease (AD) according to the amyloid cascade hypothesis. 24566006: Amyloid beta (Abeta) peptides, which are generated from amyloid precursor protein (APP), are thought to play a major role in the pathogenesis of Alzheimer's disease (AD). 24649396: Alzheimer's disease (AD) is widely considered to be caused by amyloid-beta peptide (Abeta) accumulation in the brain. 24815946: Neuroinflammatory responses induced by amyloid-beta peptide (Abeta) are important causes in the pathogenesis of Alzheimer's disease (AD). 24832605: Although Abeta peptides have been proposed to be the main cause of AD pathogenesis, the role of AICD has been underappreciated. 25221640: Mitochondrial functions can be negatively affected by amyloid beta peptide (Abeta), an important component in Alzheimer's disease (AD) pathogenesis, and Abeta can interact with mitochondria and cause mitochondrial dysfunction. 25456402: The cellular prion protein (PrP(C)), a cell surface glycoprotein involved in prion disorders, has been shown to mediate the toxicity of several pathological aggregates, including its own misfolded state and some oligomeric assemblies of the amyloid beta peptide, which are thought to be primarily responsible for the synaptic dysfunction characterizing Alzheimer's disease. 25505877: As amyloid-beta peptide (Abeta) is a causative factor for the cognitive impairments of AD, developing a mechanistic understanding of the contribution of Abeta to cognitive impairments may yield important insights into the pathophysiology of AD. 25533654: Amyloid-beta peptides generated by proteolysis of the beta-amyloid precursor protein (APP) play an important role in the pathogenesis of Alzheimer's disease. 25553446: Amyloid-beta peptide (Abeta) is believed to be a central player in the Alzheimer disease (AD) pathogenesis. 25650940: The aggregation of amyloid-beta (Abeta) peptides plays a crucial role in the etiology of Alzheimer's disease (AD). 25747232: The amyloid beta-peptide (Abeta) is suspected to play a central role in the cascade leading to Alzheimer's disease, but the precise mechanisms are still incompletely known. 25818846: Abeta is aggregated with Zn(2+) and the aggregation of Abeta-peptides is widely considered to be the critical step in the pathogenesis of AD. 25825723: Metal ions have emerged to play a key role in the aggregation process of amyloid beta (Abeta) peptide that is closely related to the pathogenesis of Alzheimer's disease. 25997382: In addition, phenolic compounds and hormones (cytokinins) found in coconut may assist in preventing the aggregation of amyloid-beta peptide, potentially inhibiting a key step in the pathogenesis of AD. 26023729: The aggregation of the amyloid-beta peptide, Abeta(1-42), is believed to play an important role in the pathogenesis of AD. 26024352: Alzheimer's disease (AD)-associated amyloid beta peptide (Abeta) is one of the main actors in AD pathogenesis. 26092626: Flavonoids have been found to play a neuroprotective role by inhibiting and/or modifying the self-assembly of the amyloid-beta (Abeta) peptide into oligomers and fibrils, which are linked to the pathogenesis of Alzheimer's disease. 26271894: Amyloid beta (Abeta) peptides are identified in cause of neurodegenerative diseases such as Alzheimer's disease (AD). 26359500: Thus, this study suggests that GAPDH aggregates accelerate Abeta amyloidogenesis, subsequently leading to mitochondrial dysfunction and neuronal cell death in the pathogenesis of AD. Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by loss of neurons and formation of pathological extracellular deposits induced by amyloid-beta peptide (Abeta). 26491725: Decreased brain clearance of the neurotoxic amyloid-beta (Abeta) peptide is a central event in the pathogenesis of Alzheimer's disease (AD). 26593432: In the present study, we investigated whether these compounds have neuroprotective effects in an amyloid-beta peptide-induced Alzheimer's disease mouse model. 26652010: Understanding of the mechanistic progess of amyloid-beta peptide (Abeta) aggregation is critical for elucidating the underlying pathogenesis of Alzheimer's disease (AD). 26794527: We describe a strategy for fluorescent imaging of organelle transport in primary hippocampal neurons treated with amyloid-beta (Abeta) peptides that cause Alzheimer's disease (AD). 26868929: The oligomerization of amyloid beta (Abeta) peptides into soluble non-fibrillar species plays a critical role in the pathogenesis of Alzheimer's disease. 26890786: Neurotoxic amyloid-beta (Abeta) peptide causing cognitive function disabilities is one of the most characteristic pathological features in Alzheimer's disease (AD). 26963025: IDE (insulin-degrading enzyme) is one of the major proteases of amyloid beta peptide (Abeta), a presumed causative molecule in Alzheimer disease (AD) pathogenesis. 26981406: One of the primary hallmarks of the neuropathological disease is the accretion of amyloid beta peptide in the brain that leads to Alzheimer's disease, but the mechanism is still a mystery. Alzheimer's disease is the prevalent cause of premature senility, a progressive mental disorder due to degeneration in brain and deposition of amyloid beta peptide (1-42, a misfolded protein) in the form of aggregation that prevails for a prolonged time and obstructs every aspect of life. 27030596: Accumulation of amyloid-beta (Abeta) peptide in the brain is the first critical step in the pathogenesis of Alzheimer's disease (AD). 27093940: Accumulating evidence points to the amyloid-beta (Abeta) peptide as the culprit in the pathogenesis of Alzheimer's disease (AD). 27137996: Amyloid-beta peptides form polymorphous amyloid fibrils are correlated with the pathogenesis of Alzheimer's disease. 27151330: BACKGROUND: The accumulation, aggregation and deposition of amyloid-beta (Abeta) peptides in the brain are central to the pathogenesis of Alzheimer's disease (AD). 27163800: Alzheimer's disease (AD) is thought to be caused by amyloid-beta peptide that triggers tau hyperphosphorylation, which is neurotoxic. 27392871: The involvement of Abeta peptides in the etiology of AD remains a subject of debate. 27441457: The aggregation of amyloid-beta peptides (Abeta) is considered as the main possible cause of Alzheimer's disease (AD). 27562438: Polyproline-II helices form two interaction sites in the amyloid-beta peptides, which are pivotal for pathogenesis of Alzheimer's disease (AD). 27580372: gamma-secretase is responsible for the proteolysis of amyloid precursor protein (APP) into short, aggregation-prone amyloid-beta (Abeta) peptides, which are centrally implicated in the pathogenesis of Alzheimer's disease (AD). 27660034: Accumulation of amyloid beta (Abeta) peptide and hyperphosphorylated tau protein has been proposed to play roles in neural destruction which induce Alzheimer's disease (AD) progresses, glutamate transporter type 1 (GLT-1) and Glycogen synthase kinase3beta (GSK3beta) may be the pathological links between Abeta and tau pathology. 27663971: Amyloid-beta peptide (Abeta) is considered a key protein in the pathogenesis of Alzheimer's disease because of its neurotoxicity, resulting in impaired synaptic function and memory. 27750416: Histidine state (deprotonated, neutral, and protonated) is considered an important factor influencing the structural properties and aggregation mechanisms in amyloid beta-peptides (Abeta), which are associated with the pathogenesis of Alzheimer's disease. 27769888: Aggregation of amyloid-beta peptide (Abeta) is a key event in the pathogenesis of Alzheimer's disease (AD). 27777990: Accumulation of the amyloid beta (Abeta) peptide in the brain is responsible for debilitating neurodegenerative diseases, such as Alzheimer's disease (AD). 27796749: Oxidative stress is considered a major contributor to the pathogenesis of AD, and accumulating evidence indicates that high levels of reactive oxygen species (ROS) are involved in Abeta-induced neurodegeneration. Amyloid-beta peptide (Abeta) is one of the major players in the pathogenesis of Alzheimer's disease (AD). 27884599: The hallmark characteristics of plaque formation and neuronal cell death in Alzheimer's disease (AD) are caused principally by the amyloid beta-peptide (Abeta). 28017718: The toxic amyloid beta-peptide (Abeta) is a key player in Alzheimer Disease (AD) pathogenesis and selective inhibition of the production of this peptide is sought for. 28052060: Aggregation of amyloid-beta peptides into fibrils or other self-assembled states is central to the pathogenesis of Alzheimer's disease. 28096459: For example, increased intracellular copper or zinc has been linked to a reduction in secreted levels of the AD-causing amyloid-beta peptide (Abeta). 28260388: Oligomer species of amyloid beta (Abeta) peptides are intensively investigated because of their relevance to Alzheimer's disease (AD), and a stable oligomer will be a cause of AD. 28288354: The enzyme beta-secretase-1 is responsible for the cleavage of the amyloid precursor protein, a vital step in the process of the formation of amyloid-beta peptides which are known to lead to neurodegeneration causing Alzheimer's disease. 28360830: Amyloid fibril formation by the amyloid beta-peptide (Abeta) is considered to be an underlying cause of AD, and strategies designed to reduce Abeta production and/or its toxic effects are being extensively investigated in both laboratory and clinical settings. 28400058: Amyloid-beta peptide (Abeta) is believed to be a primary cause of Alzheimer's disease. 28562008: The self-assembling of the amyloid beta (Abeta) peptide into neurotoxic aggregates is considered a central event in the pathogenesis of Alzheimer's disease (AD). 28569090: Impaired brain clearance of amyloid-beta peptides (Abeta) 40 and 42 across the blood-brain barrier (BBB) is believed to be one of the pathways responsible for Alzheimer's disease (AD) pathogenesis. 28570778: Zinc-induced oligomerization of amyloid-beta peptide (Abeta) produces potentially pathogenic agents of Alzheimer's disease. 28650319: The amyloid beta peptide (Abeta) is a key player in the etiology of Alzheimer disease (AD), yet a systematic investigation of its molecular interactions has not been reported. 28670737: Brain accumulation of soluble oligomers of the amyloid-beta peptide (AbetaOs) is increasingly considered a key early event in the pathogenesis of Alzheimer's disease (AD). 28674340: The abnormal aggregation of amyloid beta-peptide (Abeta) is central to the pathogenesis of Alzheimer's disease, the major form of dementia. 28687859: According to amyloid cascade hypothesis, the deposit of amyloid-beta (Abeta) peptide is the main cause of Alzheimer's disease (AD). 28861757: AD-like pathology was produced by administering AbetaP (1-40) intracerebroventricular (i.c.v.) in the left lateral ventricle (250 ng/10 MUl, once daily) for 4 weeks. Alzheimer's disease (AD) is one of the leading causes for disability and death affecting millions of people worldwide. 28870815: Cerebral accumulation of amyloid beta-peptide (Abeta), which is produced from amyloid precursor protein (APP), is the primary cause of Alzheimer's disease (AD). 28889204: The beta-secretase (BACE1) initiates the generation of toxic amyloid-beta peptide (Abeta) from amyloid-beta precursor protein (APP), which was widely considered to play a key role in the pathogenesis of Alzheimer's disease (AD). 28941799: Amyloid-beta peptides (Abeta) accumulate in cerebral capillaries indicating a central role of the blood-brain barrier (BBB) in the pathogenesis of Alzheimer's disease (AD). 28985224: The accumulation of amyloid beta (Abeta) peptide (Amyloid cascade hypothesis), an APP protein cleavage product, is a leading hypothesis in the etiology of Alzheimer's disease (AD). 28987946: Amyloid-beta peptide (Abeta) ranks as a pivotal cause of Alzheimer's disease (AD), a common devastating dementia form in elderly. 29118109: gamma-Secretase is an intramembrane cleaving protease that is responsible for the generation of amyloid-beta peptides, which are linked to the pathogenesis of Alzheimer disease. 29132916: While impaired clearance of amyloid beta (Abeta) peptides is considered as one of the major causes of AD, it was recently complemented by a potential role of other toxic amyloidogenic species. 29138762: The aggregation of amyloid beta (Abeta) peptides plays a crucial role in the pathology and etiology of Alzheimer's disease. 29161341: Accumulation of amyloid-beta peptides is a dominant feature in the pathogenesis of Alzheimer's disease; however, it is not clear how individual amyloid-beta species accumulate and affect other neuropathological and clinical features in the disease. 29192843: The amyloid beta (Abeta) peptide is central to the pathogenesis of Alzheimer's disease (AD). 29199321: BACKGROUND: Vanutide Cridificar (ACC-001), a novel investigational immunotherapeutic vaccine designed to elicit antibodies against the N-terminal peptide 1-7 of the amyloid-beta peptide, believed to be important in the pathogenesis of Alzheimer's disease (AD). 29210443: BACKGROUND: ACC-001 is an investigational therapeutic vaccine designed to elicit antibodies against the N-terminal peptide 1-7 of the amyloid-beta peptide, believed to be important in the pathogenesis of Alzheimer's disease. 29224965: Compelling evidence suggests a crucial role of amyloid beta peptides (Abeta(1-40/42)) in the etiology of Alzheimer's disease (AD). 29310862: AD is featured with the loss of cholinergic neurons, the amyloid-beta peptide (Abeta) plaques and the neurofibrillary tangles and several hypotheses were established to explain the pathogenesis of AD. 29315574: The production and accumulation of amyloid beta peptide (Abeta) is considered the core pathological molecular event in the pathogenesis of AD. 29440986: The so-called amyloid hypothesis, that the accumulation and deposition of oligomeric or fibrillar amyloid beta (Abeta) peptide is the primary cause of Alzheimer's disease (AD), has been the mainstream concept underlying AD research for over 20 years. 29448601: Amyloid beta (Abeta) peptide is considered to be the critical causative factor in the pathogenesis of Alzheimer's disease (AD) because the hydrophilic molecules accumulated outside of the neural cells and results in the formation of highly toxicity amyloid plaque. 29491833: Accumulation of amyloid-beta (Abeta) peptides in the brain is a critical early event in the pathogenesis of Alzheimer's disease (AD), the most common age-related neurodegenerative disorder. 29619615: Genetics strongly implicate the amyloid beta-peptide (Abeta) in the pathogenesis of Alzheimer's disease. 29648443: Senile plaques formed by aggregated amyloid beta peptides are one of the major pathological hallmarks of Alzheimer's disease (AD) which have been suggested to be the primary influence triggering the AD pathogenesis and the rest of the disease process. 29658548: The self-association of the amyloid beta (Abeta) peptide into toxic oligomers is implicated in the early events leading to Alzheimer's disease (AD). 29743204: The beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) initiates the production of amyloid-beta peptide (Abeta), which is central to the pathogenesis of Alzheimer's disease (AD). 29764453: BACKGROUND: Extracellular aggregation of the amyloid-beta (Abeta) peptide into toxic multimers is a key event in Alzheimer's disease (AD) pathogenesis. 29781021: It is believed that the self-assembly of amyloid beta (Abeta) peptides in the brain is the cause of Alzheimer's disease. 29899186: Accumulation and oligomerization of amyloid-beta (Abeta) peptides have been known to be a potent cause of neurodegenerative diseases such as Alzheimer's disease (AD). 29905953: Amyloid-beta peptide (Abeta) accumulation and aggregation have been considered for many years the main cause of Alzheimer's disease (AD), and therefore have been the principal target of investigation as well as of the proposed therapeutic approaches (Grasso [2011] Mass Spectrom Rev. In recent years, actors such as metal ions, oxidative stress, and other cofactors have been proposed as possible co-agents or, in some cases, main causative factors of AD. 29906302: Probes for monitoring aggregation of amyloid beta (Abeta) peptides are crucial to advance understanding of the molecular pathogenesis of Alzheimer's Disease (AD). 29927573: Accumulating evidence supports the abnormal deposition of amyloid beta-peptide (Abeta) as the main cause of Alzheimer's disease (AD). 29945719: Overt accumulation and aggregation of the amyloid-beta peptide (Abeta) is thought to be the initial causative factor for Alzheimer's disease. 30043821: The amyloid plaques are mainly aggregates of amyloid beta-peptide (Abeta), a primary factor contributing to the pathogenesis of AD. 30086173: Although the aggregation of amyloid-beta peptide (Abeta) clearly plays a central role in the pathogenesis of Alzheimer's disease (AD), endosomal traffic dysfunction is considered to precede Abeta aggregation and trigger AD pathogenesis. 30214656: The soluble oligomeric form of the amyloid beta (Abeta) peptide is the major causative agent in the molecular pathogenesis of Alzheimer's disease (AD). 30260016: INTRODUCTION: Aggregation of amyloid-beta (Abeta) peptides represents a crucial step in the pathogenesis of Alzheimer disease (AD). 30264333: Accumulation of amyloid-beta peptide (Abeta) and massive neuronal death due to apoptosis were the essential steps in the pathogenesis of Alzheimer's disease (AD). 30268822: Dysregulation of the Amyloid Precursor Protein (APP) processing leading to toxic species of amyloid beta peptides (Abeta) is central to Alzheimer's disease (AD) etiology. 30345755: Aggregation of amyloid beta-peptide (Abeta) plays a key role in the etiology of AD. 30362029: Growing evidence gathered from transgenic animal models of Alzheimer's disease (AD) indicates that the intraneuronal accumulation of amyloid-beta (Abeta) peptides is an early event in the AD pathogenesis, producing cognitive deficits before the deposition of insoluble plaques. 30402707: Amyloid beta (Abeta) peptide is a critical causative factor in Alzheimer's disease (AD) and of a variety of fragmented Abeta peptides Abeta1-42 thought to exhibit the most neurotoxic effect. 30426203: Brain accumulation and aggregation of amyloid-beta (Abeta) peptides is a critical step in the pathogenesis of Alzheimer's disease (AD). 30480246: Evidence suggests that fibril formation of the amyloid beta-peptide (Abeta) is a major underlying cause of AD, and treatment strategies that reduce the toxic effects of Abeta amyloid are sought for. 30486385: The amyloid beta (Abeta) peptide has been implicated in the cause of AD, where the peptides undergo a conformational change and form neurotoxic amyloid oligomers which cause neuronal cell death. 30551397: The progressive accumulation of amyloid beta (Abeta) peptide is neurotoxic and leads to Alzheimer's type dementia. 30675620: The potential therapeutic effect of puerarin against Alzheimer's disease was screened by in silico methods and confirmed by the amyloid beta-peptide-induced Alzheimer's disease (AD) rat model. 30704515: The adipocyte plasma membrane-associated protein APMAP is expressed in the brain where it associates with gamma-secretase, a protease responsible for the generation of the amyloid-beta peptides (Abeta) implicated in the pathogenesis of Alzheimer's disease (AD). 30794963: The aggregation and accumulation of amyloid beta (Abeta) peptide is believed to be the primary cause of Alzheimer's disease (AD) pathogenesis. 30830576: Human genetic and clinical studies over the past three decades have indicated that abnormal generation or accumulation of amyloid-beta (Abeta) peptides is a likely culprit in AD pathogenesis. 30900203: These pathological protein deposits, including Abeta peptides (which form senile plaques) and hyperphosphorylated tau (which aggregates into NFTs), have been assumed to be 'the cause of AD'. 30911827: SORL1 encodes SorLA, a key protein involved in the processing of the amyloid-beta (Abeta) precursor protein (APP) and the secretion of the Abeta peptide, the aggregation of which triggers AD pathophysiology. 30913789: Amyloid beta (Abeta) peptide is secreted from the outside of neural cell by a neural signal pathway and it accumulated each other results in the highly toxicity amyloid plaque which is a critical causative factor in the pathogenesis of Alzheimer's Disease (AD). 30949973: The pathological form of amyloid beta (Abeta) peptide is shown to be toxic to the mitochondria and implicates this organelle in the progression and pathogenesis of Alzheimer's disease (AD). 30964132: Aggregation of misfolded oligomeric amyloid-beta (Abeta) peptides on lipid membranes has been identified as a primary event in Alzheimer's pathogenesis. 31048748: Aggregates of amyloid-beta (Abeta) peptide are well known to be the causative substance of Alzheimer's disease (AD). 31164420: BACE1 is the rate-limiting enzyme for amyloid-beta peptides (Abeta) generation, a key event in the pathogenesis of Alzheimer's disease (AD). 31234321: Amyloid beta (Abeta) peptide is known to be a major cause of AD pathogenesis. 31247730: The variation of amyloid beta peptide (Abeta) concentration and Abeta aggregation are closely associated with the etiology of Alzheimer's diseases (AD). 31365254: Excess of amyloid beta (Abeta) peptides and their aggregation are the basis of the amyloid cascade hypothesis, which attempts to explain the causes of AD. 31367507: Amyloid beta-peptides (Abeta) play a major role in the pathogenesis of Alzheimer's disease. 31368868: BACKGROUND: Aggregation of Amyloid beta (Abeta) peptide is a crucial feature of Alzheimer disease (AD) pathogenesis. 31369984: Thus, the sialic acid-binding site on CD33 is a promising pharmacophore for developing therapeutics that promote clearance of the Abeta peptide that is thought to cause AD. 31595293: Amyloid-beta peptides (Abeta) are the major drivers of Alzheimer's disease (AD) pathogenesis, and are formed by successive cleavage of the amyloid precursor protein (APP) by the beta and gamma secretases. 31607898: Processing of amyloid beta precursor protein (APP) into amyloid-beta peptide (Abeta) by beta-secretase and gamma-secretase complex is at the heart of the pathogenesis of Alzheimer's disease (AD). 31796114: An impairment of amyloid beta-peptide (Abeta) clearance is suggested to play a key role in the pathogenesis of sporadic Alzheimer's disease (AD). 31809572: The aggregation of amyloid-beta (Abeta) peptides into senile plaques is a hallmark of Alzheimer's disease (AD) and is hypothesized to be the primary cause of AD related neurodegeneration. 31814468: Truncated or post-translationally modified Abeta peptides are becoming increasingly recognized as important players in the etiology of AD and a more thorough comprehension of their cellular origin and biochemical peculiarities might break new ground for therapeutic strategies. 7556364: There is growing evidence that the amyloid beta-peptide (beta 1-40) is involved in the aetiology of Alzheimer's disease also implicating an altered calcium homeostasis of affected cells. 7777177: Two conformational states of amyloid beta-peptide: implications for the pathogenesis of Alzheimer's disease. 11215107: [Pathophysiological roles of angiotensin in the pathogenesis of hypertension and cardiovascular remodeling]. Here, we review recent advances in the roles of AT1 and AT2 receptors in the pathogenesis of hypertension and the cardiovascular remodeling. 20431529: RESULTS: In response to TNF-alpha-induced hypertension, sFlt-1 increased from 180 +/- 5 to 2,907 +/- 412 pg/ml. Circulating sFlt-1 increased from 245 +/- 38 to 3,920 +/- 798 pg/ml in response to AT1-AA induced hypertension. 21600854: OBJECTIVES: This study was undertaken to determine if AT1-AA induced hypertension was associated with renal endothelial dysfunction. CONCLUSION: AT1-AA induced hypertension during pregnancy was associated with disparate renal endothelial responses to acetylcholine. AT1-AA induced hypertension was attenuated by the AT1 receptor and/or endothelin-1 type A receptor antagonists. 24041954: AT1-AA-induced hypertension decreased with enalapril but was not attenuated. 27903510: Therefore, we hypothesized that vitamin D would reduce PE factors during AT1-AA-induced hypertension and could lower blood pressure in a model of hypertension during pregnancy without PE features. 28404593: Whereas it has been generally assumed that the altered glomerular vascular resistances in ANG II hypertension are due to AT1 receptor-mediated vasoconstriction, these data indicate a predominant P2X1R and P2X7R control of glomerular hemodynamics in ANG II hypertension. Physiopathological implications of P2X1 and P2X7 receptors in regulation of glomerular hemodynamics in angiotensin II-induced hypertension. 30842613: Central blockade of the AT1 receptor attenuates pressor effects via reduction of glutamate release and downregulation of NMDA/AMPA receptors in the rostral ventrolateral medulla of rats with stress-induced hypertension. 30851407: The angiotensin II AT1 and the endothelin 1 ETA receptors play a crucial role in the pathogenesis of cardiovascular diseases like hypertension, heart failure, stroke, pulmonary hypertension, and cardiac hypertrophy. 8941934: These data support a critical role for AT1 receptor-mediated, angiotensin-dependent processes in the pathogenesis of hypertension in FHH, and further implicate elevated PGC as a major determinant of glomerular injury in this model. 9296928: [Significance of the angiotensin-II receptor AT1 in the pathogenesis of arterial hypertension and arteriosclerosis]. 9740621: Therefore, hypertension and myocardial fibrosis induced by NO blockade may be due in part to an elevation of PAC caused by increased AT1-R in the adrenal gland. 14616239: This action of O disturbs renal medullary adaptation to low PO2 and produces renal medullary dysfunction, resulting in sodium retention and hypertension. 16794495: BACKGROUND: Hypertension is a common disease in the Western world and approximately 5% of all cases are secondary to kidney malfunction. Hydronephrosis causes salt-sensitive hypertension in rats. 17305709: Hydronephrosis causes salt-sensitive hypertension and impaired renal concentrating ability in mice. AIM: Hypertension is a common disease in the industrialized world and approximately 5% of all cases are secondary to kidney malfunction. We have recently shown that hydronephrosis due to partial unilateral ureteral obstruction (PUUO) causes salt-sensitive hypertension in rats. 20371384: Although maternal L-Cit supplementation prevents caloric restriction-induced low nephron number and renal dysfunction, it also induces hypertension. 22991843: A 69-year-old man with a history of hypertension was admitted to our hospital because of proteinuria, renal dysfunction, and both purpura and edema in the lower extremities. 23590594: This review highlights these links between placental ischaemia, maternal endothelial activation and renal dysfunction in the pathogenesis of hypertension in pre-eclampsia. 26193676: The findings provide a new line of evidence for renal dysfunction as a primary cause of hypertension. 31045658: PURPOSE OF REVIEW: Renovascular disease (RVD) remains an important cause of hypertension and renal dysfunction. 7542491: Hypertension is common after orthotopic liver transplantation and may be due, in part, to cyclosporin A-induced renal dysfunction and/or enhanced proximal tubular sodium reabsorption. 9235547: Hypertension may to be both, cause and the results of the renal dysfunction. 9300927: Chronic occupational exposure to lead, or consumption of illicit alcohol adulterated with lead, has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes resulting in chronic renal failure, hypertension, hyperuricemia, and gout. 10362706: This study examines whether intracerebroventricular benzamil would prevent the onset of deoxycorticosterone acetate (DOCA)-salt-induced hypertension in rats and whether this effect correlates with an inhibition of ion transport through the known amiloride-sensitive cation channels at the blood-brain barrier. 10523383: These data indicate that vasopressin plays a critical role in modulating vascular structure and mechanics, as well as blood pressure, in DOCA-salt-induced hypertension. 10704274: The contributions of arterial baroreceptor and Bezold-Jarisch reflexes, and atrial natriuretic factor (ANF) to the anti-hypertensive effect of the diuretic chlorthalidone were investigated in rats with deoxycorticosterone acetate (DOCA)-salt-induced hypertension. Although it is difficult to determine the relative importance of each of the above regulatory mechanisms altered by chlorthalidone treatment, these data indicate that they may account for the prevention or decrease of DOCA-salt-induced hypertension in rats. 10725252: These evidences support strongly the view that ET(B) receptor-mediated actions are a protective factor in the pathogenesis of DOCA-salt-induced hypertension. The role of endothelin ET(B) receptor-mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)-salt-induced hypertension was evaluated using the spotting-lethal (sl) rat which carries a naturally occurring deletion in the ET(B) receptor gene. 10758056: CONCLUSIONS: These findings indicate that increased vascular superoxide production occurs not only in angiotensin II-induced hypertension but also in hypertension known to be associated with low-renin states. BACKGROUND: Angiotensin II-induced hypertension is associated with increased vascular superoxide production, which contributes to hypertension caused by the octapeptide. Vascular superoxide production and vasomotor function in hypertension induced by deoxycorticosterone acetate-salt. 10919359: Our findings indicate that SA7060 efficiently prevents DOCA-salt-induced hypertension and related tissue injury, mainly by inhibiting NEP. Daily administration of SA7060, candoxatril or enalapril significantly suppressed the development of hypertension induced by DOCA and salt, although the effect of enalapril was less potent at 4-weeks of the treatment period. Effects of SA7060, a novel dual inhibitor of neutral endopeptidase and angiotensin-converting enzyme, on deoxycorticosterone acetate-salt-induced hypertension in rats. 11078344: ET(A)-mediated actions are at least partly responsible for the increased susceptibility to DOCA-salt-induced hypertension and related tissue injuries in ET(B)-receptor-deficient rats. We evaluated the role of endothelin-B- (ET(B)) receptor-mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)-salt-induced hypertension, cardiovascular hypertrophy and renal damage, using the spotting lethal (sl) rat which carries a naturally occurring deletion in the ET(B)-receptor gene. We propose that ET(B)-receptor-mediated actions are protective factors in the pathogenesis of DOCA-salt-induced hypertension. Increased susceptibility to deoxycorticosterone acetate-salt-induced hypertension in endothelin-B-receptor-deficient rats. 11094045: CONCLUSIONS: ET(B)-mediated actions are protective in the pathogenesis of DOCA-salt-induced hypertension. Chronic treatment with ABT-627, an ET(A) receptor antagonist, completely suppressed DOCA-salt-induced hypertension in both groups. We evaluated the pathological role of ET(B) receptors in DOCA-salt-induced hypertension, cardiovascular hypertrophy, and renal damage by using the spotting-lethal (sl) rat, which carries a naturally occurring deletion in the ET(B) receptor gene. 11244026: We previously reported that inhibition of angiotensin-converting enzyme (ACE) prevented the hypertension and left ventricular hypertrophy induced by deoxycorticosterone acetate-salt (DOCA-salt) in 129/SvEvTac mice, which have 2 renin genes (Ren-1 and Ren-2). 11380524: We suggest that a proteasome-dependent proteolytic system has an important role in the development of vascular hypertrophy in cases of DOCA-salt-induced hypertension, possibly through the enhancement of ET-1 production in vascular tissues. 11642328: The DOCA-salt-induced hypertension was markedly suppressed by feeding a BEC-containing diet. Antihypertensive effects of chicken extract against deoxycorticosterone acetate-salt-induced hypertension in rats. 11834512: DOCA-salt induced significant hypertension, cardiac hypertrophy and increased NP plasma and left atrial and right and left ventricular NP gene expression. 11858800: In conclusion, these results demonstrate that in rats with hypertension induced by DOCA-salt, brain mineralocorticoid receptor blockade affects renal function and blood pressure regulation. In the present study, the coordinate cardiovascular and renal effects of brain mineralocorticoid receptor blockade were examined by intracerebroventricular (i.c.v.) administration of a selective mineralocorticoid receptor antagonist (RU28318; 3,3-oxo-7 propyl-17-hydroxy-androstan-4-en-17yl-propionic acid lactone) in rats with hypertension induced by deoxycorticosterone acetate (DOCA) and salt. 12774853: Because previous studies showed a beneficial effect of chronic exercise (swimming) on the development of arterial hypertension in spontaneously hypertensive rats (which appears similar to human essential hypertension), we decided to evaluate the effects of swimming on DOCA-salt induced hypertension and liver antioxidant status. 1281379: Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats. 1320076: These determinations were also performed in 3-week prehypertensive SHR and in adult Wistar rats submitted or not to deoxycorticosterone acetate-salt-induced hypertension. 13679473: CONCLUSIONS: 129/Sv mice are more susceptible to the development of DOCA-induced high blood pressure and renal damage than C57BL/6 mice. Strain differences in the development of hypertension and glomerular lesions induced by deoxycorticosterone acetate salt in mice. 14637180: Our data also suggest that cyclooxygenase-2 mediates free radical production, and that free radicals modulate the EDHF-mediated vascular response in DOCA-salt induced hypertension. These results show that EDHF-mediated dilation of rat mesenteric arteries is impaired in DOCA-salt induced hypertension. 14732736: Deoxycorticosterone acetate salt-induced hypertension also caused a 70% decrease in hypothalamic gamma-adducin. 1531333: Plasma concentrations of immunoreactive (ir) atrial (ANP) and brain (BNP) natriuretic peptides were measured in the prehypertensive and hypertensive phases in spontaneously hypertensive rats (SHR) and in the malignant phase of hypertension caused by deoxycorticosterone acetate (DOCA)-salt in SHR. 15830710: Progression of renal damage in the obese Zucker rat in response to deoxycorticosterone acetate-salt-induced hypertension. This study assessed the progression of renal damage in obese Zucker rats in response to deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 15834289: OBJECTIVE: To test the hypothesis that the enhanced vascular responsiveness to norepinephrine that occurs during deoxycorticosterone acetate (DOCA)-salt induced hypertension is causally related to increased expression of cyclo-oxygenase (COX)-2 and oxidative stress, which diminishes the vasomodulatory influence of endothelium-derived nitric oxide. Cyclo-oxygenase-2, endothelium and aortic reactivity during deoxycorticosterone acetate salt-induced hypertension. 1649727: Comparison of the electrical properties of arterial smooth muscle in normotensive rats and rats with deoxycorticosterone acetate-salt-induced hypertension: possible involvement of (Na(+)-K(+)-Cl-) co-transport. 16904201: Renal atrial natriuretic peptide receptors binding properties and function are resistant to DOCA-salt-induced hypertension in rats. Finally, we have found that DOCA-induced hypertension does not modify NPR-A or NPR-C expression in rat glomerular membranes. 17064681: These findings suggest that vascular O(2)(-) overproduction via gp91phox-containing NADPH oxidase is one of the crucial factors in the development of DOCA-salt-induced hypertension. We evaluated whether NADPH oxidase-dependent superoxide (O(2)(-)) production is involved in the deoxycorticosterone acetate (DOCA)-salt-induced hypertension, using mice which are genetically deficient in gp91phox, an NADPH oxidase subunit protein (gp91(-/-) mice). 17324138: Involvement of the endothelin ET(B) receptor in gender differences in deoxycorticosterone acetate-salt-induced hypertension. Thus, vascular oxidative stress is related, at least in part, to differences in the development of DOCA-salt-induced hypertension between male and female rats, but this gender difference is abolished by the genetic ET(B) receptor deficiency, suggesting that ET(B) receptor-mediated vasoprotective actions contribute to the gender differences seen. In homozygous (sl/sl) group, the SBP of male, intact female and OVX rats was markedly elevated by DOCA-salt treatment to the same extent, indicating that the gender difference in DOCA-salt-induced hypertension was abolished by the genetic ET(B) receptor deficiency. In the present study, we investigated the role of endothelin ET(B) receptors in gender differences in the development of deoxycorticosterone acetate (DOCA)-salt-induced hypertension by using the spotting-lethal (sl) rat, which carries a naturally occurring deletion in the ET(B) receptor gene. 17602962: We studied the effects of chronic treatment with RWPs and apocynin, an inhibitor of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, on blood pressure, endothelial function, and oxidative status in deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 17941888: Sesamin feeding markedly suppressed DOCA salt-induced hypertension and significantly decreased aortic O(2)(-) production. 18573249: Thus, the lack of functional SERT did not prevent development of DOCA-salt induced hypertension or modify basal blood pressure significantly. 18647880: We followed cardiac function and metabolic changes during 2 wk of angiotensin II (ANG II)-induced hypertension in control and heart-specific lipoprotein lipase knockout (hLpL0) mice. Both ANG II and deoxycorticosterone acetate-salt induced hypertension caused heart failure only in hLpL0 mice. 19145776: METHODS AND RESULTS: The development of DOCA-salt-induced hypertension during a 5-week treatment period was significantly suppressed by feeding a Flavangenol-containing diet. 19841522: CONCLUSIONS: Co-administration of vitamin C and E does not have an additive beneficial effect on reducing the kidney damage and hypertension compared to either vitamin C or E alone in DOCA-salt-induced hypertension. Unilateral nephrectomy was carried out in the study groups and hypertension was induced by deoxycorticosterone injection and 1% sodium chloride and 0.2% potassium chloride added to the drinking water. INTRODUCTION: We assessed whether co-supplementation of vitamins C and E has additive beneficial effects on reducing the kidney damage and attenuation of the arterial pressure elevation compared to administration of either vitamin C or vitamin E alone in deoxycorticosterone acetate-salt-induced hypertension. Reduction of kidney damage by supplementation of vitamins C and E in rats with deoxycorticosterone-salt-induced hypertension. 19932586: Preventive effects of low molecular mass potassium alginate extracted from brown algae on DOCA salt-induced hypertension in rats. The present study investigated the effects of L-PA on deoxycorticosterone acetate (DOCA) salt-induced hypertension in rats. 20626757: The aim of the present study was to determine the involvement of immune cells in the hypertension and renal injury produced by a non-angiotensin II-dependent form of hypertension, namely deoxycorticosterone acetate (DOCA)-salt-induced hypertension, in rats. 2065462: To clarify the role of renal thromboxane (TX)A2 in the development of deoxycorticosterone acetate (DOCA)-salt induced hypertension, relationship between systolic blood pressure and the synthesis of renal TXA2 was investigated in 18 rats without and with OKY-046 administration which suppressed the synthesis of renal TXA2. These results might suggest that the enhanced production of renomedullary TXB2 was important to the development of DOCA-salt induced hypertension. 20852048: This study was conducted to determine the contribution of CYP1B1 to hypertension and associated pathophysiological changes produced by DOCA (30 mg/kg) given subcutaneously per week with 1% NaCl + 0.1% KCl in drinking water to uninephrectomized rats for 6 wk. 2,3',4,5'-Tetramethoxystilbene prevents deoxycorticosterone-salt-induced hypertension: contribution of cytochrome P-450 1B1. These data suggest that CYP1B1 contributes to DOCA-salt-induced hypertension and associated pathophysiological changes, most likely as a result of increased ROS production and ERK1/2 and p38 MAPK activity, and could serve as a novel target for the development of agents like TMS to treat hypertension. Reactive oxygen species (ROS) contribute to various models of hypertension, including deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 21126972: METHODS AND RESULTS: Angiotensin II-induced hypertension increased the presence of activated (CD86(+)) dendritic cells in secondary lymphatic tissues. Blockade of B7-dependent costimulation with CTLA4-Ig reduced both angiotensin II- and deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 21748534: Emblica officinalis exerts antihypertensive effect in a rat model of DOCA-salt-induced hypertension: role of (p) eNOS, NO and oxidative stress. We determined whether hydroalcoholic lyophilized extract of EO may influence DOCA/HS-induced hypertension by modulating activity of (p) eNOS and endogenous antioxidants. Our results demonstrate that EO reduces oxidative stress, prevents development and progression of hypertension as well as cardiac and renal hypertrophy in DOCA/HS-induced hypertension via modulation of activated eNOS, endogenous antioxidants, serum NO and electrolyte levels. Emblica officinalis (EO) has antioxidant properties that could improve redox-sensitive vascular, cardiac and renal changes associated with deoxycorticosterone acetate/1% NaCl high salt (DOCA/HS)-induced hypertension. 21971354: Using wild-type mice with deoxycorticosterone acetate (DOCA) salt-induced HTN and intravital microscopy, we observed significant increases in the adhesion of both leukocytes and platelets in cerebral venules, compared with uninephrectomized control mice, without an accompanying increase in blood-brain barrier permeability. Cerebral microvascular inflammation in DOCA salt-induced hypertension: role of angiotensin II and mitochondrial superoxide. 22001745: We studied the effects of chronic treatment with epicatechin on blood pressure, endothelial function, and oxidative status in deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 22258333: BACKGROUND: We have shown that the ouabain-sensitive alpha2 Na,K-ATPase is required for adrenocorticotropic hormone (ACTH)-induced hypertension and gestational blood pressure regulation. These findings indicate that the underlying mechanisms of hypertension induced by DOCA-salt treatment are different from those of ACTH-induced hypertension. 22266490: Thus the experiment clearly showed that diosmin acts as an antihypertensive agent against DOCA-salt induced hypertension. The present study was aimed to evaluate the antihypertensive effect of diosmin in deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. 22386933: The present study was designed to evaluate the antihypertensive and antioxidant effect of morin, a flavonoid against deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. These results suggest that morin acts as an antihypertensive and antioxidant agent against DOCA-salt induced hypertension. 22467300: Systolic blood pressures did not differ between wild-type (WT) and Alox15(-/-) mice between 8-12 wk of age, but Alox15(-/-) mice exhibited resistance toward both N(G)-nitro-L-arginine-methyl ester (L-NAME)- and deoxycorticosterone acetate (DOCA)/high-salt-induced hypertension. Injection of WT PM, a primary source of Alox15 protein, into Alox15(-/-) mice abolished their resistance toward L-NAME-induced hypertension. On the other hand, WT mice acquired resistance to L-NAME-induced hypertension after depletion of macrophages by clodronate injection. 22507914: In the present research work, for the first time we are reporting the genesis of VaD by deoxycorticosterone acetate (DOCA)-salt induced experimental hypertension. Experimental hypertension induced vascular dementia: pharmacological, biochemical and behavioral recuperation by angiotensin receptor blocker and acetylcholinesterase inhibitor. It may be concluded that DOCA-salt hypertension induces VaD in rats. Furthermore, we have also investigated the beneficial effect of telmisartan, an angiotensin II type 1 receptor blocker (ARB) and donepezil, an acetylcholinesterase inhibitor (AChEI), on DOCA-salt hypertension induced VaD in rats. ARBs and AChEIs may be considered as potential pharmacological agents for the management of hypertension induced VaD. 22666794: In the studied conditions (e.g., post-myocardial infarction, deoxycorticosterone acetate salt-induced hypertension, chronic N-nitro-L-arginine methyl ester treatment, and streptozotocin-induced diabetes), a positive correlation between force or plateau tetanic tension and myosin ATPase activity was observed. 22731503: This study has been designed to investigate the role of phosphatidyl-inositol 3-kinase-gamma (PI3Kgamma) in deoxycorticosterone acetate salt (DOCA) hypertension induced vascular endothelium dysfunction. Wistar rats were uninephrectomised and DOCA (40 mg.(kg body mass)(-1), subcutaneous injection) was administered twice weekly for 6 weeks to produce hypertension. 23033370: We sought to identify the key chemokine receptors associated with macrophage infiltration into the vascular wall during deoxycorticosterone acetate (DOCA)/salt-induced hypertension in mice and to evaluate the impact of pharmacological inhibition of these receptors on blood pressure and leukocyte accumulation. Intervention with a CCR2 antagonist, INCB3344 (30 mg/kg per day, IP), 10 days after the induction of hypertension with DOCA/salt treatment, reduced the aortic expression of CCR2 mRNA and completely reversed the DOCA/salt-induced influx of macrophages. 23108654: Previously, we showed that the cytochrome P450 1B1 inhibitor 2,3',4,5'-tetramethoxystilbene reversed deoxycorticosterone acetate (DOCA)-salt-induced hypertension and minimized endothelial and renal dysfunction in the rat. Cytochrome P450 1B1 gene disruption minimizes deoxycorticosterone acetate-salt-induced hypertension and associated cardiac dysfunction and renal damage in mice. 23108791: Effect of combination of renin inhibitor and Mas-receptor agonist in DOCA-salt-induced hypertension in rats. 23489008: Etoricoxib attenuates effect of antihypertensives in a rodent model of DOCA-salt induced hypertension. 23569947: OBJECTIVE: To determine the protective effect of morin, a flavonoid against deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. CONCLUSIONS: These findings indicate that morin exhibits strong antihypertensive effect against DOCA-salt induced hypertension. Effect of morin against DOCA-salt induced hypertension was evaluated by measuring blood pressure and performing biochemical estimations and histopathological examination of renal tissues. 24246383: Neuron-specific PRR knockout prevents the development of deoxycorticosterone acetate-salt-induced hypertension, possibly through diminished angiotensin II formation. PRR knockout in neurons prevented the development of deoxycorticosterone acetate-salt-induced hypertension as well as activation of cardiac and vasomotor sympathetic tone. Thus, PRR knockout in the brain is expected to prevent angiotensin II formation and development of deoxycorticosterone acetate-salt-induced hypertension. 24379186: Apolipoprotein E-knockout mice with deoxycorticosterone acetate salt-induced hypertension were placed on a high-cholesterol diet and exhibited exaggerated leukocyte and platelet adhesion responses in cerebral microvessels. 24937386: The present study was designed to evaluate the interactions of PPARalpha and GLUT4 in a model of hypertensive renal injury by studying deoxycorticosterone acetate (DOCA)-salt induced hypertension in wild-type (WT) and PPARalpha knockout (KO) mice. 25234650: Resveratrol treatment (50 mg/l in drinking water) prevented DOCA salt-induced hypertension, but did not improve endothelial dysfunction. Resveratrol affects histone 3 lysine 27 methylation of vessels and blood biomarkers in DOCA salt-induced hypertension. 25421983: In summary, PRO20 binds to both mouse and human PRRs and decreases angiotensin II formation and hypertension induced by either prorenin or DOCA-salt. 25519733: DOCA-salt-induced hypertension was reduced in SL mice, with hACE2 overexpression in the brain. 25621930: Plasma PCSK9 concentrations were increased by 2.8 fold in DOCA-salt-induced hypertension. 25885968: The present study investigated whether the central blockade of endogenous AT2-R augments deoxycorticosterone acetate (DOCA)/salt-induced hypertension in both male and female rats. To determine the effect of central AT2-R on DOCA/salt-induced hypertension, male and female rats were intracerebroventricularly (icv) infused with AT2-R antagonist, PD123,319, during DOCA/salt treatment. Brain endogenous angiotensin II receptor type 2 (AT2-R) protects against DOCA/salt-induced hypertension in female rats. 26195912: Formulation SJT-HT-03 (250 mg/kg, p.o.), was evaluated using two kidney one clip (2K1C) model and deoxycorticosterone acetate (DOCA)-salt-induced hypertension model using the enalapril (10 mg/kg, p.o.) and hydrochlorothiazide (5 mg/kg, p.o.) as a reference standard drug in respective models. 26597823: Transgenic mice expressing dominant-negative PPARgamma (S-P467L) in smooth muscle cells were more prone to deoxycorticosterone acetate-salt-induced hypertension and mesenteric arterial dysfunction compared with nontransgenic controls. 27334059: The DOCA-salt treatment induced hypertension in both genotypes, as observed by increases in systolic blood pressure. In conclusion, the results of this study suggest that the presence of KLF5 in postn-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension. 28143892: Activation of TRPV4 by dietary apigenin antagonizes renal fibrosis in deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 28411074: Based on the similarity in the anatomic characteristics of renal artery between pigs and humans, this study was undertaken to establish a low-dose sustained-release DOCA-induced hypertension model in pigs. Low-dose sustained-release deoxycorticosterone acetate-induced hypertension in Bama miniature pigs for renal sympathetic nerve denervation. Traditional high-dose deoxycorticosterone acetate (DOCA)-induced hypertension pig model has some problems due to extensive end-organ damage. Low-dose sustained-release DOCA is able to induce hypertension in pigs. 28431181: METHODS: Intracranial aneurysms were induced with a combination of a single elastase injection into the cerebrospinal fluid and deoxycorticosterone acetate salt-induced hypertension in mice. 2963066: These results suggest that chronic administration of L-5-HTP provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. 30290168: Administering DOCA and offering saline to uninephrectomized rats, induced hypertension and associated abnormalities of diastolic dysfunction, CV and renal hypertrophy and fibrosis via activating local renin angiotensin system. To address this, we aimed to determine the effect of deoxycorticosterone acetate (DOCA) -salt (sodium chloride)-induced hypertension on the alterations in renin-angiotensin system, leading to CV and renal dysfunction in uninephrectomized male Sprague Dawley rats. 30366037: In the present study, the effects of LXR agonist GW3965 on vascular reactivity and expression of functional proteins in DOCA-Salt induced hypertension were examined. 30458302: ERS inhibition in DOCA-salt induced hypertension was observed to have reduced systolic blood pressure, improved endothelial dysfunction, enhanced plasma nitric oxide (NO) level, reduced protein expressions of phosphorylated-double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase (pPERK), 78 kDa glucose-regulated protein (GRP78), Inositol trisphosphate receptor1 (IP3R1) and Epidermal growth factor receptor (EGFR), increased expressions of endoplasmic reticulum Ca2+-ATPase2 (SERCA2) and B cell lymphoma2 (Bcl2) in vessels. Inhibition of endoplasmic reticulum stress protected DOCA-salt hypertension-induced vascular dysfunction. 30872813: DOCA-salt hypertension was induced by DOCA (20 mg/kg s.c., twice weekly) administration plus 1% NaCl and 0.2% KCl solutions in drinking water for 12 weeks. We investigated the therapeutic effect of MH-76 and MH-79, which are non-quinazoline alpha1-adrenoceptor antagonists with an additional ability to stimulate the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP)/K + pathway, on deoxycorticosterone acetate (DOCA)-salt induced hypertension in rats. 31065896: PROCEDURES: After baseline renal magnetic resonance imaging (MRI), 24 out of 30 uninephrectomized Sprague-Dawley rats with DOCA-salt-induced hypertension were divided equally into four groups. 31514180: Here, we examined the effects of flaxseed powder, which includes all flaxseed components, flaxseed oil, composed mainly of ALA, flaxseed lignan, and flaxseed fiber, on hypertension and renal damage induced by deoxycorticosterone acetate (DOCA)-salt. 3420163: Treatment with either dose of nicotinic acid did not, however, prevent either the renal hypertrophy characteristic of DOCA-salt-induced hypertension in rats or their reduced renal concentrating ability during a 24-hour dehydration; nor did treatment with nicotinic acid reduce the excessive ingestion of saline characteristic of chronic treatment with DOCA. Chronic dietary administration of either l-tryptophan (5.0%) or nicotinic acid (5.0%) reduced the elevated blood pressure of rats with established, deoxycorticosterone-acetate (DOCA)-salt-induced hypertension without affecting either body weight or cardiac hypertrophy. Effect of chronic dietary treatment with nicotinic acid on the development and maintenance of deoxycorticosterone-acetate-salt-induced hypertension. These results suggest that increased production of nicotinic acid resulting from dietary administration of tryptophan may play a role in the protective effect of tryptophan against the development of DOCA-salt-induced hypertension. In contrast, treatment with the higher dose of nicotinic acid prevented the excessive loss of sodium into urine characteristic of DOCA-salt-induced hypertension when the rats were loaded (3% of body weight, i.p.) with a hypotonic (0.075 M) saline solution. 3621037: These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. Chronic dietary administration of tryptophan prevents the development of deoxycorticosterone acetate salt induced hypertension in rats. 466431: No significant changes in DA content were observed in any region of the brain following induction of hypertension by the three different methods. NA content increased significantly in various areas: the increase of NA in the pons-medulla was common to all procedures inducing hypertension. In two substrains, selected from the Hebrew University strain, for their respective sensitivity (H) or immunity (N) to hypertension induced by DOCA--salt treatment, there were no significant increases in NA or DA in any part of the brain following DOCA--salt treatment. Noradrenaline (NA) and dopamine (DA) distribution in different brain areas was assayed following induction of hypertension. 6279507: In hypertension induced by deoxycorticosterone acetate (DOCA)-salt treatment, as in Dahl genetic hypertension, there was also no difference in membrane potential (Em) between hypertensive and normotensive rats. 6488011: Hypothalamic knife cuts attenuate maintenance of deoxycorticosterone acetate-salt induced hypertension. These experiments tested the effects of knife cuts transecting neural pathways associated with the anteroventral third ventricle (AV3V) region on deoxycorticosterone acetate (DOCA)-salt induced hypertension. 7115983: In both these experiments although BAPN lowered blood pressure it did not affect the hypertension-induced hypertrophy of the aorta. BAPN suppressed the rise in blood pressure during the developing phase of deoxycorticosterone acetate-salt-induced hypertension and in this model the compound also prevented the accompanying aortic hypertrophy. 7581242: This DOCA-salt-induced hypertension was markedly suppressed by feeding a sesamin-containing diet. Protection against deoxycorticosterone acetate-salt-induced hypertension and cardiovascular hypertrophy. 7780646: Role of endothelin-1 and the ETA receptor in the maintenance of deoxycorticosterone acetate-salt-induced hypertension. To search for a possible role for endothelin-1 (ET-1) in deoxycorticosterone acetate (DOCA)-salt-induced hypertension, we examined changes in concentration of ET-1 in vascular and renal tissue in DOCA-salt hypertensive rats and evaluated the antihypertensive effect of the ETA receptor antagonist, FR139317. In addition, our study indicates the pathophysiological importance of increased endogenous ET-1 in the maintenance of DOCA-salt-induced hypertension, through interaction of the peptide with ETA receptors. 7810723: Myocardial fibrosis has been investigated in 3-, 16-, and 24-mo-old normal rats and also in 24-mo-old rats subjected to deoxycorticosterone acetate (DOCA)-salt treatment-induced-hypertension. 8587444: In addition, our study suggests the pathophysiologic importance of ET-1 and the ETA receptor in DOCA-salt-induced hypertension but not in SHR, in SHR-SP, in 2K1C renal hypertension, and in LNA-induced hypertension. 8628104: We also suggest that at least in part, ET-1 and ETA receptors are involved in renal hemodynamic abnormalities in DOCA-salt-induced hypertension. Thus, it seems likely that endogenous ET-1 is responsible for the maintenance of DOCA-salt-induced hypertension. The augmentation of renal ET-1 production may possibly have a function in the development and maintenance of DOCA-salt-induced hypertension. 8888962: This study demonstrates the effects of hypertension produced by deoxicorticosterone acetate (DOCA) and salt load on the extensor digitorum longus (EDL) and soleus muscles of the rat. 8924521: Enhanced ET-1 gene expression in blood vessels of rats with hypertension induced by deoxycorticosterone acetate (DOCA)-salt has been previously demonstrated. 9369284: Four-week DOCA-salt treatment induced hypertension associated with cardiac hypertrophy. 9667071: The renal AT1 receptors appear to be up-regulated in early stages of DOCA-salt-induced hypertension as well. 9798534: Overexpression of Gi-proteins precedes the development of DOCA-salt-induced hypertension: relationship with adenylyl cyclase. CONCLUSIONS: These results indicate that the enhanced expression of Gi alpha-2 and Gi alpha-3 precedes the development of blood pressure in DOCA-salt-induced hypertension. 9931125: DOCA-salt (volume expansion) or aortic coarctation (renin-dependent) induced similar hypertension and left ventricular hypertrophy (LVH) in 129/SvEvTac and B2-KO mice, suggesting that kinins do not play an essential role in the development of DOCA-salt- or aortic coarctation-induced hypertension. Effect of ACE inhibitor on DOCA-salt- and aortic coarctation-induced hypertension in mice: do kinin B2 receptors play a role? Using normal 129/SvEvTac mice and mice lacking the bradykinin B2 receptor gene (B2-KO), we investigated whether (1) the hypertensinogenic effect of DOCA-salt or aortic coarctation is enhanced in B2-KO mice and (2) the chronic antihypertensive and antihypertrophic effects of an ACEi (ramipril, 4 mg. kg-1. d-1) are mediated by B2 receptors in aortic coarctation (6 weeks)- and DOCA-salt (4 weeks)-induced hypertension. Thus, in mice, kinins acting via B2 receptors do not participate in (1) maintenance of normal basal blood pressure, (2) establishment and maintenance of hypertension induced by DOCA-salt or aortic coarctation, and (3) chronic antihypertensive and cardiac antihypertrophic effects of ACEi in DOCA-salt and aortic coarctation hypertension. 14685807: In conclusion, the bioactivity associated with the AChE-peptide sequence may account for the non-cholinergic actions of AChE, whilst its neurotrophic-apoptotic-necrotic spectrum of action may be involved in the aetiology of neurodegenerative disorders such as Alzheimer's disease. 16772751: The accumulation of evidence implicating AChE in the pathogenesis of AD raises the question of whether, in addition to their palliative actions, inhibitors of this enzyme are able to act as disease-modifying agents. 18669022: Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) are the key enzymes in pathogenesis of Alzheimer's disease (AD), which is characterized by a deficit in central cholinergic transmission. 20026160: Therefore, we initiated a study to screen the methanol extracts prepared from the aerial parts of 33 Turkish Scutellaria species for their acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inhibitory activities, which are the key enzymes taking place in pathogenesis of Alzheimer's disease. 20689242: BACKGROUND: Several studies implicate acetylcholinesterase (AChE) in the pathogenesis of Alzheimer's disease (AD), raising the question of whether inhibitors of AChE also might act in a disease-modifying manner. 20732375: Since, acetylcholinesterase and butyrylcholinesterase enzymes are taking place in pathogenesis of Alzheimer's disease, in vitro anticholinesterase activity of the essential oil and the extract was also studied spectrophotometrically. 21384354: Therefore, the extracts were also evaluated against acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), which are chief enzymes in the pathogenesis of AD. 21762104: Cholinesterase enzyme family consisting of acetylcholinesterase (AChE) and butrylcholinesterase (BChE) is important in pathogenesis of Alzheimer's disease (AD), explained by \cholinergic hypothesis\. 25951978: Cholinesterases, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), have a role in cholinergic deficit which evidently leads to Alzheimer's disease (AD). 26527154: Acetyl cholinesterase (AChE) and butyrylcholinesterase (BChE) are two types of cholinesterase enzymes that have been identified in vertebrates that are responsible for Alzheimer's disease and related dementia. 26832327: Acetylcholinesterase (AChE) is an important enzyme in the pathogenesis of Alzheimer's disease (AD). 27801451: Hyperactivity of acetylcholinesterase (AChE) in the brain is the immediate cause of Alzheimer's disease (AD), which is one of the most prevalent fatal diseases afflicting numerous older people. 29303784: Acetylcholinesterase (AChE) is an enzyme that metabolises the ACh at synaptic cleft resulting in Alzheimer's disease. 30316049: Acetylcholinesterase (AChE) is one of the major cholinergic enzymes, and there is no report to show the relationship between cAbeta accumulation and peripheral AChE alteration in early stage of AD pathogenesis. 30530106: In the present study, 26 novel O-alkylcoumarin derivatives were synthesized and have been tested at 100 uM for their in vitro inhibitory potential against acetylcholinesterase (AChE) and butyrlcholinesterase (BChE) targets which are the key enzymes playing role in the pathogenesis of Alzheimer's disease. 31002611: Previous studies showed that some mushrooms are highly efficient in inhibiting acetylcholinesterase and tyrosinase, the increased activity of which can trigger the development of Alzheimer and Parkinson diseases. 31639294: Previous studies have shown that fascaplysin might act on acetylcholinesterase and beta-amyloid (Abeta) to produce anti-AD properties. 10805411: The hypertension was induced by oral administration of NO synthase inhibitor N(G)-nitro-L-arginine methylester (L-NAME, 50 mg/kg/day) to normotensive rats for 8 weeks. 10872554: L-NAME-hypertension was induced by oral administration of 100 mg/kg per day of L-NAME twice daily for 4 weeks using 4-week-old male Wistar rats. 10954000: METHODS: Hypertension, in Sprague-Dawley rats was induced by the oral administration of the arginine analog N(omega)-nitro-L-arginine methyl ester (L-NAME) in their drinking tap water for a period of 4 weeks. Enhanced expression of Gi proteins in non-hypertrophic hearts from rats with hypertension-induced by L-NAME treatment. 14508194: Exogenous H2S effectively prevented the development of hypertension induced by l-NAME. METHODS: Hypertension in Wistar rats was induced by the oral administration of the l-arginine analog, NG-nitro-l-arginine methyl ester (l-NAME) in their drinking water for a period of 6 weeks. 1476186: We have found that the infusion of both glycyrrhizic acid, an active principle of licorice, and carbenoxolone, a synthetic analogue, into a lateral ventricle of the brain [intracerebroventricular (icv)] of a rat, at a dose less than that which has an effect when infused subcutaneously, produces hypertension. While the oral administration caused saline polydipsia and polyuria typical of chronic systemic mineralocorticoid excess, the icv licorice derivatives produced hypertension without affecting saline appetite. Furthermore, the hypertension produced by the oral administration of carbenoxolone or glycyrrhizic acid is blocked by the icv administration of RU 28318, an MR antagonist, at a dose below that which has an effect on blood pressure when infused subcutaneously. They also suggest that more is involved in licorice-induced hypertension than only inhibition of 11 beta-HSD. 1526064: Dietary NG-nitro-L-arginine induces sustained hypertension in normotensive Wistar-Kyoto rats. Prolonged oral administration of NG-nitro-L-arginine (L-NNA) for a period of 5 weeks in 8 week old male normotensive Wistar-Kyoto (WKY) rats (n = 10), induced hypertension in all animals. 16710099: CONCLUSIONS: L-NAME treatment leads to hypertension, proteinuria and renal fibrosis. METHODS: 36 Sprague-Dawley rats were divided into a control group and an experimental group, in which hypertension was induced by oral administration of L-NAME (100 mg/kg/day). 19152678: A 83-year-old woman presented with a 25-year history of hypertension which was long-standing, uncontrolled, severe hypertension because of irregular oral administration of antihypertensive drug underwent an echocardiographic examination as part of an evaluation of hypertension. 19498093: Hypertension was induced by oral administration of the nonselective NOS inhibitor l-NAME (25 mg/kg day) for 6 wk. 25103225: Oral administration of bisphenol A induces high blood pressure through angiotensin II/CaMKII-dependent uncoupling of eNOS. 26890104: Hypertension was induced by oral administration of the nonselective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME, 25 mg/kg/day) for 6 weeks and systolic blood pressure was measured by the tail-cuff method. 29996172: Hypertension was induced by oral administration of nitric oxide synthase inhibitor, N-nitro L-arginine-methyl-ester (L-NAME), at 40 mg/kg body weight to the male Wistar rats for 14 consecutive days. There is a growing global interest in hypertension due to its associated complications including renal dysfunction in patients. 31472272: MATERIALS AND METHODS: Hypertension and diabetes were induced by oral administration of sucrose (15%) and ethanol (40 degrees ) at doses of 1.5 g/kg and 5 g/kg respectively for 30 days, followed by an intravenous injection of streptozotocin (STZ; 40 mg/kg). 32532282: CONCLUSION: We conclude that CX3CR1-microglia represses the nNOS signaling pathway and promotes chronic inflammation in fructose-induced hypertension. METHODS: The hypertensive rat model was used to study the role of CX3CR1-microglia in NTS inflammation following hypertension induction by oral administration of 10% fructose water. 32985250: Hypertension was induced by the oral administration of L-NAME (60 mg/kg) for 6 weeks. 36362975: Hypertension was induced by oral administration of L-NAME in drinking water for four weeks at 40 mg/kg/day. 36678530: Hypertension was induced by oral administration of L-NAME (40 mg/kg) for two weeks. 6373587: These results suggest that DX-induced hypertension in rats is associated with inhibition of prostaglandin synthesis leading to increased sensitivity in the vascular response to norepinephrine. Glucocorticoid hypertension was induced by oral administration of dexamethasone (DX) in male Wistar rats. 7843755: In the present studies, we produced chronic nitric oxide blockade by oral administration of the L-arginine analogue NG-nitro-L-arginine methyl ester, which produced sustained hypertension and increased renal vascular resistance in conscious rats. These findings indicate the following: (1) Hypertension induced by chronic nitric oxide blockade due to substituted L-arginine analogue cannot be acutely reversed with excess L-arginine, suggesting that the maintenance of the hypertension is not solely caused by competitive inhibition of nitric oxide production; (2) in contrast, the kidney remains responsive to L-arginine whereas the renal vasodilator response to glycine is abolished in this model of hypertension. 9128216: Hypertension in Sprague-Dawley rats was induced by the oral administration of the arginine analog N(omega)-nitro-L-arginine methyl ester (L-NAME) in their drinking tap water for a period of 4 weeks. 10609168: Corticosteroid-induced hypertension was only noted in 2 cases. There was a discrepancy between the low frequency of corticosteroid induced hypertension and the broad use of topical corticosteroids in cases of uveitis. 10625095: There is increasing evidence that the intrauterine milieu and corticosteroid exposure play a role in the etiology of hypertension. 10773515: This patient had ischemic heart disease, corticosteroid-induced hypertension, diabetes mellitus, and a difficult airway. 11152234: Calcineurin inhibitors and corticosteroids induce hypertension in renal, cardiac, liver, bone marrow, and lung transplant recipients. 11835800: CONCLUSIONS: Topical application of corticosteroid may cause corticosteroid hypertension and corticosteroid glaucoma after PRK, and visual function damage may occur in a few eyes. 12109923: It is not known to what extent corticosteroids induce hypertension in patients with RA. 12929904: About 3% of our hypertensive patients have high blood pressure induced by corticosteroids. In conclusion, a work-up for corticosteroid-induced hypertension is indicated in patients with hypokalaemic hypertension and in those with severe hypertension even in the absence of hypokalaemia, and in hypertensive patients with a family history of cardiovascular diseases. 14406950: [The role of corticosteroids in etiology of arterial hypertension]. 15341497: Corticosteroids induce endothelial dysfunction, hypertension, hyperlipidaemia and diabetes mellitus, and impair fibrinolysis. 1560165: Corticosteroids can induce hypertension, which reportedly remits as the drug is withdrawn. 15839366: A significant number of transplant recipients suffer from posttransplant hypertension in part because of corticosteroid and calcineurin inhibitor use. 1592452: Pressor responsiveness in corticosteroid-induced hypertension in humans. 16307204: OBJECTIVES: Corticosteroids can induce hypertension and inhibit collagen synthesis in the blood vessel wall. 18215783: CS may cause hypertension, development of cardiac chamber hypertrophy (CCH), and left ventricular outflow tract obstruction (LVOTO). 18370695: Corticosteroids can induce glucose intolerance, hypertension, hyperlipidemia, and weight gain. Cyclosporine and tacrolimus can induce glucose intolerance, hypertension, and hyperlipidemia. 21692837: The incidence of adverse effects was low, with one patient developing CS-induced hypertension (5%). 23629578: Paracetamol and corticosteroids induce hypertension, while steroids also adversely affect the heart from metabolic change as well as fluid retention. 24731552: Since melatonin is a potent antioxidant and has been known to regulate blood pressure, we examined the beneficial effects of melatonin therapy in preventing prenatal dexamethasone-induced programmed hypertension. Although antenatal corticosteroid is recommended to accelerate fetal lung maturation, prenatal dexamethasone exposure results in hypertension in the adult offspring. 25184914: They are treated mainly with systemic corticosteroids, which may provoke osteoporosis; atherosclerosis, higher blood pressure, insulin resistance, glucose intolerance, hyperlipidemia and abdominal obesity. 25683700: Because the majority of hypertensive patients were under corticosteroid treatment, the iatrogenic cause of hypertension cannot be excluded. 25810066: The role of sustained release isosorbide mononitrate on corticosteroid-induced hypertension in healthy human subjects. There is evidence implicating abnormalities in the nitric oxide (NO) pathway in the development of glucocorticoid-induced hypertension (GC-HT). 29765616: This study aimed to quantify the risk of new diabetes, hypertension, cataracts, osteoporosis and avascular necrosis that is attributable to cumulative corticosteroid exposure in SLE. 29800813: By identifying candidate proteins underlying sex-specific mechanisms, our results could lead to novel offspring sex-specific interventions to prevent hypertension induced by antenatal corticosteroids and postnatal HF intake in both sexes. Postnatal high-fat diet sex-specifically exacerbates prenatal dexamethasone-induced hypertension: Mass spectrometry-based quantitative proteomic approach. We found that postnatal HF diet increased vulnerability of prenatal DEX-induced hypertension in male but not in female adult offspring. 3246279: [Role of corticosteroid hormones in the pathogenesis of arterial hypertension]. 492574: [The clinical value of corticosteroid-induced intraocular hypertension in subjects belonging to glaucomatous families]. 7070755: The ultrastructure of the trabecular meshwork of the anterior chamber angle after corticosteroid-induced hypertension was studied with TEM. 8205462: New mechanisms for corticosteroid-induced hypertension. 9284410: In this review hypertensive disorders caused by adrenal cortical hormones is briefly stated. 12635375: [Our experience in the surgical treatment of the arterial hypertension due to endocrine disturbances]. This study is trying to expose our experience in the surgical treatment for adrenal tumors which produce arterial hypertension, experience gained over a period of 25 years. 13358959: [Hypertension due to adrenal tumor in an infant]. 13562726: Hypertension due to adrenal tumor (pheochromocytoma); case report. 1937678: Excess production of aldosterone secondary to an adrenal tumor or bilateral hyperplasia is a known, but infrequent, cause of hypertension. 20662337: We report an eleven month old child presenting to us as Cushing syndrome with hypertension due to left adrenal tumor. 22007678: Blood pressure remained normal despite the discontinuation of antihypertensive drugs, further supporting that the adrenal tumor was indeed the cause of high blood pressure. 23255991: One 21-year-old woman, 24 weeks pregnant, with hypertension and Cushing's syndrome due to a left adrenal tumour, underwent laparoscopic adrenalectomy followed by hydrocortisone replacement. 28872770: Hormone-secreting adrenal tumours cause severe hypertension and high rates of poor pregnancy outcome; a UK Obstetric Surveillance System study with case control comparisons. 471769: [Isotope scan using labelled cholesterol in the diagnosis of hypertension due to adrenal tumors (author's transl)]. 8582113: In a 19 month period from June 1993 to December 1994, 60 patients (mean age 54.8 +/- 1.5 years s.e.m.; 32 males, 28 females) underwent unilateral laparoscopic adrenalectomy by one of us (JCR) for the treatment of hypertension due to primary aldosteronism (n = 48), phaeochromocytoma (n = 3) and cortisol-producing adenoma (n = 1) or to remove adrenal massess incidentally discovered on abdominal computerized tomography scanning ('incidentaloma') performed for other reasons (seven adenomas without biochemical evidence of excessive steroid hormone or catecholamine secretion and one carcinoma autonomously producing cortisol). Laparoscopic adrenalectomy for adrenal tumours causing hypertension and for 'incidentalomas' of the adrenal on computerized tomography scanning. 10022029: By mediating an enhanced receptor-coupled response, such as increased proximal tubular sodium reabsorption during sodium loading, a genetic abnormality of renal alpha 2-adrenoceptors may contribute to some of the pathophysiologic derangements leading to hypertension in Dahl salt-sensitive rats. 10596451: The possible role of alpha 1D-adrenoceptors in the genesis/maintenance of hypertension is discussed in this review. 1325516: CONCLUSION: Our findings indicate that PIH is characterized by an exaggerated response of platelet alpha 2-adrenoceptor density to a rise in blood pressure and that this alteration could be significant in the pathogenesis of hypertension. 14656925: Among these GPCRs are adrenoceptors and angiotensin receptors that contribute to the pathogenesis of hypertension through their vasoconstrictive and growth effects. 16636200: Sequence variations in the human alpha2 adrenergic receptor genes (ADRA2A and ADRA2C) have been implicated as a cause of hypertension in blacks. 2471890: Thus, the present study demonstrates that there is a specific loss of alpha 2-adrenoceptors in the medulla oblongata of SHR and SHRSP that may be partly involved in the pathogenesis of spontaneous hypertension. 2891422: Is there a role for renal alpha 2-adrenoceptors in the pathogenesis of hypertension? 29097625: Autoantibodies (AAs) against angiotensin AT1 receptor (AT1-AAs) and alpha1-adrenergic receptor (alpha1-AAs) are important in the pathogenesis of hypertension. 2994833: Thus, the present study suggests an important role for hypothalamic alpha 1-adrenoceptors in the pathogenesis of spontaneous hypertension. 3401352: Thus an alteration of tissue noradrenaline content and/or adrenergic receptors in heart and kidney might be involved in the pathogenesis of hypertension. 9406660: Nitric oxide (NO) synthase inhibition in sheep using NG-nitro-L-arginine following blockade of alpha- and beta-adrenoceptors and cholinoceptors causes hypertension, but minor changes, if any, in pulmonary pressures or heart rate. 15696696: Modified hemoglobins such as intermolecular or intramolecular cross linked hemoglobins have side effect to cause hypertension by scavenging nitro oxide (NO) which is produced by endothelial cells, because the size of these hemoglobins are small enough to go to the adjacent place near endothelial surface. 16182764: Renal failure with arterial hypertension, due to CNI side-effects, is a major cause of morbidity and mortality after OLT. 18706002: Adverse effects, drug interactions, inter-individual variation in drug metabolism, and underlying causes of hypertension that differ between patients require individualized therapy. 1972206: This type of antihypertensive agent would be expected to exhibit fewer side effects with efficacy, directed towards the etiology of hypertension. 19874251: Mecamylamine (Inversine), the first orally available antihypertensive agent launched in the 1950s, is rarely used today for hypertension because of its widespread ganglionic side effects at antihypertensive doses (25 - 90 mg/day). 21896146: * This class of drugs, however, is currently used mainly as fourth-line (or beyond) drug therapy for hypertension because of side effects of drowsiness, fatigue, and dry mouth. 23124953: Sympathetic hyperactivity has long been recognized as a major contributor to resistant hypertension, but radical sympathectomy was abandoned several decades ago due to its significant side effects. Hypertension is a leading cause of cardiovascular morbidity and mortality. 24990369: However, the clinical application to treat hypertension was disappointing because of the side effects, including liver toxicity and fluid retention. 30755327: No significant differences were found in the following parameters: the rates of diarrhea, glucose intolerance (or diabetes mellitus), gastrointestinal syndrome, as well as hypertension because of adverse effects (p>0.05). 3154313: Angiotensin converting enzyme (ACE) inhibition is increasingly used as monotherapy for hypertension, especially because of the minimal side effects. 38605140: Although the treatment of HT aims to improve life prognosis, the use of antihypertensive agents can impair QOL because of adverse effects and lifestyle changes associated with long-term medication use. 6366659: The present data suggest that 1) maternal and fetal prolactin levels do not differ significantly between normal and abnormal pregnancies, 2) the decidua is the principal source of amniotic fluid prolactin, and 3) the significantly lower levels of prolactin in amniotic fluid of pregnancies complicated by hypertension or polyhydramnios are probably due to adverse effects of these conditions on the synthesis and release of prolactin by decidua. 7048882: Of the 323 patients who received pindolol alone for the treatment of mild to moderate hypertension, only 20 (6.2%) were withdrawn from the study because of side effects. 8292559: This study tested the hypothesis that the adverse effects of cyclosporine (Cy) are accelerated in animals with induced hypertension. 20066010: Since these secretases mediate proteolytic processing of numerous proteins, little success has been achieved to treat AD by secretase inhibitors because of inevitable undesired side effects. Dysregulation of beta-site APP-cleaving enzyme (BACE) and/or gamma-secretase leads to anomalous production of amyloid-beta peptide (Abeta) and contributes to the etiology of Alzheimer's disease (AD). 20190429: To date, acetylcholinesterase (AChE) inhibitors have been clinically effective drugs for the palliative treatment of Alzheimer's disease, but their clinical efficacy is limited, mainly due to their adverse effects on peripheral organs. 24053611: EXPERT OPINION: Amyloid-based immunotherapy for AD is a novel method with potential; however, some clinical trials were terminated because of the adverse effects. 28065587: Thus far, phosphodiesterase-4 (PDE4) inhibitors have not been approved for application in Alzheimer's disease (AD) in a clinical setting due to severe side effects, such as nausea and vomiting. 28788095: Tacrine (THA), the first clinically effective acetylcholinesterase (AChE) inhibitor and the first approved drug for the treatment of Alzheimer's disease (AD), was withdrawn from the market due to its side effects, particularly its hepatotoxicity. 32709074: Recent clinical trials of synthetic compounds for the treatment of AD have failed because of their adverse effects or lack of efficacy. 33534126: Though several drug candidates have been developed in the management of AD, an alternative option is still required due to serious adverse effects of the former. 33596779: Development of ABT-736 for Alzheimer's disease was discontinued due to severe adverse effects (AEs) observed in cynomolgus monkey toxicity studies. 3387586: Changes in hepatic metabolism in AD may be relevant not only for drug metabolism and the development of side effects, but also for the pathogenesis of AD. 37156292: Exposure to exogenous chemicals may exert adverse effects on cognitive function, and we discovered 15 chemicals in human hair that may contribute to the pathogenesis of Alzheimer's disease. 10415373: Furthermore, angiotensin II may have neurotoxic effect to use as the pressor agent for induced hypertension after cerebral ischemia. Mild phenylephrine-induced hypertension treatment (21+/-4 mmHg) during post-cerebral ischemia-reperfusion improved the survival ratio and reduced cerebral edema, which was also associated with an increase in local CBF and a recovery of brain energy metabolism. However, intense phenylephrine-induced hypertension, angiotensin II-induced hypertension, or hypotension worsen the survival rate and produced extra cerebral edema, that were also associated with deterioration of brain energy metabolism. 1069437: The sensitivity and reproducibility of the method are exemplified and discussed in regard to its applicability in diagnosis of organic arterial obliterations, e.g. in Raynaud's phenomenon as well as to its usefulness in evaluation of reconstructive arterial surgery and medical treatment with respectively thrombolytic (Brinase, Astra) and microhaemorheologic agents (Venoruton, Zyma; Arwin, Knoll) or those with an influence on systemic haemodynamic factors as in induced hypertension. 10853686: BACKGROUND: Under systemic hypertension induced by angiotensin II (AII) infusion, an attenuated vasoconstrictive response to the infusion in tumours was observed and a marked increase in tumour blood flow was observed in comparison with that in normal tissues. The phenomenon was absent when hypertension was provoked by other vasoconstrictive agents such as norepinephrine or endothelin-1. 11703402: In the rat, blockade of the RAS in the first weeks of life by pharmacological agents reduces glomerular number and has been shown to cause hypertension in adult life. 12217256: We remain uncertain of the mechanism whereby these agents cause hypertension, and therefore remain uncertain of the ideal treatment; however, the search for a mechanism has taken us from the organ level to intracellular effects of the agents. Especially ironic, however, for those caring for kidney transplant patients has been the finding that these breakthrough agents are toxic to the kidney and can cause hypertension. 1299423: Effect of calcium blocking agents of the verapamil series on the myocardium mitochondrial activity in experimentally induced arterial hypertension. 1498343: Deoxycorticosterone acetate (DOCA) is an agent commonly used to induce hypertension in experimental animals. 15017527: Impaired autoregulation of glomerular filtration rate (GFR); demonstrated with some blood pressure-lowering agents implies disturbances in the downstream transmission of the systemic blood pressure into the glomerulus, leading to capillary hypertension or hypotension depending of the level of blood pressure. 15861508: Topical phenylephrine, an agent used to facilitate nasotracheal intubation and prevent nasal mucosal bleeding, can cause severe hypertension in some patients, secondary to its stimulation of alpha-adrenergic receptors. 17418121: These results indicate that chronic administration of agents that induce hypertension can also produce changes in the subcellular localization in p47(phox) in dmNTS neurons. 18025637: Although an infrequent complication of selective serotonin reuptake inhibitor therapy, it is important that ophthalmologists are aware that these agents can cause hypertension because this class of drugs is widely prescribed. 19218474: The possible mechanisms of Epo-induced hypertension are examined with in vivo animal and in vitro data, as well as pathophysiological human studies in both normal subjects and CKD patients. Arterial hypertension induced by erythropoietin and erythropoiesis-stimulating agents (ESA). 19388463: Exposures to those agents may cause circulatory diseases (arterial hypertension, ischemic heart disease), symptoms of lower and upper spine or renal calculosis. 20838932: The most widely used agents to induce hypertension were phenylephrine (48%) and norepinephrine (39%). 21584715: These agents are all known to frequently cause hypertension, their most common side-effect. 21884028: AIMS: Erythropoietin stimulating agents (ESAs) is an active area of clinical investigation in heart failure (HF) but can cause hypertension and higher hemoglobin concentrations (Hb) that have been associated with adverse outcomes. 2317107: Because high blood pressure is a risk factor for left ventricular hypertrophy and cardiovascular mortality in this patient population, use of an agent that may cause high blood pressure requires careful monitoring. 25217090: Hypertension induced by chemotherapeutic and immunosuppresive agents: a new challenge. 26931476: Our aim is to provide an overview of the latest Federal Drug Administration (FDA) approved VEGF inhibitors and TKI's causing hypertension so that others managing patients on these treatments may easily recognize hypertension attributable to these agents and feel comfortable and confident in providing appropriate management and treatment of this side effect. Update of Targeted Therapy-Induced Hypertension: Basics for Non-Oncology Providers. This manuscript focuses on hypertension induced by vascular endothelial growth factor (VEGF) inhibitors and tyrosine kinase inhibitors (TKI). 27048353: The choice of agent is usually driven by underlying etiology of hypertension, profile of its side effects, and clinician's preference. 3113166: Leakage of HRP occurred in both cerebral hemispheres in response to hypertension induced by the three pressor agents, but the leakage was greater on the lesioned side in response to epinephrine and norepinephrine, while in the case of angiotensin-induced hypertension side-to-side differences in permeability alterations were not observed. Unilateral locus ceruleus lesion enhances leakage of radioiodinated human serum albumin into the ipsilateral cerebral cortex of rats with norepinephrine-induced hypertension. 31286941: Therefore, RA would be an alternative strategy for improving skeletal muscle glucose transport and protecting against ANG II-induced hypertension and hyperglycemia. Angiotensin II (ANG II) is a potent agent that generates hypertension and oxidative stress. 33186593: These agents induce adverse hepatorenal effects, hypertension, and gastric ulcers. 35568958: However, many of these agents can cause hypertension resulting in major adverse cardiovascular event. 3731504: It is concluded that hypertension in SHR is caused by a circulating hypertensive agent produced in kidneys and adrenals, the secretion of which can be suppressed by volume or salt depletion. 3880068: The apparent discrepancy and reversal of order of potency for IOP responses may be related to the hypothesis that the net ocular hypotensive effect of adrenergic agents is the summation of the initial hypertension and the delayed hypotension produced by these agents. 4304137: This transmittable agent is probably identical with the factor that produces salt hypertension and is associated with the salt-excreting mechanism. 696877: Because vasopressin is one of the most potent naturally occurring pressor agents, and because of its importance in the regulation of blood volume and composition, we have undertaken a study of the role of vasopressin in the pathogenesis of the hypertension in the Okamoto-Aoki spontaneously hypertension (SH) rat. 7382891: The outstanding features of pre-eclampsia are hypertension and impairment of renal function which are likely due to an agent released by the placenta. 8384950: The present study was undertaken to test whether insulin acts as a pressor agent and causes hypertension in rats. 9385294: Hypertension may coexist with various other conditions and may be induced by various pressor agents. 12446934: Other studies show complex interactions between nAChR, nicotinic agonists, and agents implicated in AD etiology. 14657205: In addition, because many neurodegenerative diseases are associated with increased oxidative and inflammatory responses, an attempt was made to include studies on PLA2 in cerebral ischemia, Alzheimer's disease, and neuronal injury due to excitotoxic agents. 17047367: Processing of the amyloid precursor protein (APP) by beta- and gamma-secretases leads to the generation of amyloid-beta (Abeta) peptides, which are the toxic agents in the pathogenesis of Alzheimer's disease. 17920304: Amyloid beta peptide (Abeta) is considered one of the main agents of Alzheimer's disease pathogenesis. 18093473: A-beta is indicated to be the primary agent in the pathogenesis of AD. 18631951: During the past dozen years, several agents have been approved that enhance cognition and global function of AD patients, and recent advances in understanding AD pathogenesis has led to the development of numerous compounds that might modify the disease process. 19233290: Soluble oligomers and fibrillar deposits of amyloid beta (Abeta) are key agents of Alzheimer's disease pathogenesis. 2197055: Aluminum has also been implicated as a toxic agent in the etiology of Alzheimer's disease, Guamiam amyotrophic lateral sclerosis, and parkinsonism-dementia. 22124704: These findings suggest that Wnt signaling can protect neural cells against apoptosis induced by toxic agents, which are relevant to the pathogenesis of Alzheimer's and Huntington's diseases. 23161037: Alzheimer's disease (AD) is the sixth leading cause of all deaths in the United States, and the fifth leading cause of death in Americans aged 65 and older. During the past years, several agents have been approved that enhance cognition and global function of AD patients, and recent advances in understanding AD pathogenesis has led to the development of numerous compounds that might modify the disease process. 23526599: The amyloid-beta peptide (Abeta) is widely considered to be the major toxic agent in the pathogenesis of Alzheimer's disease, a condition which afflicts approximately 36 million people worldwide. 24448248: The amyloid-beta peptide (Abeta) is widely considered to be the major toxic agent in the pathogenesis of Alzheimer's disease, a condition which afflicts approximately 36 million people worldwide. 26248483: Herein, we reviewed the evidence stemming from the development of diabetes agent-induced AD animal model. 28098204: Low molecular weight oligomers of amyloid-beta (Abeta) have emerged as the primary toxic agents in the etiology of Alzheimer disease (AD). 2884783: So far, however, there is no proof that Alzheimer's disease is caused by an unconventional agent. 29905953: Amyloid-beta peptide (Abeta) accumulation and aggregation have been considered for many years the main cause of Alzheimer's disease (AD), and therefore have been the principal target of investigation as well as of the proposed therapeutic approaches (Grasso [2011] Mass Spectrom Rev. In recent years, actors such as metal ions, oxidative stress, and other cofactors have been proposed as possible co-agents or, in some cases, main causative factors of AD. 30550626: Amyloid beta is an inherently disordered peptide that can form diverse neurotoxic aggregates, and its 42-amino-acid isoform is believed to be the agent responsible for Alzheimer's disease (AD). 31876280: In this review, based on the latest experimental data on structure-function properties of chemically modified amyloid-beta isoforms, the concept of the origin and the mechanism of action of amyloid-beta with isomerized Asp7 residue, as a molecular agent of Alzheimer's disease pathogenesis, is presented. Advances in the research of molecular factors involved in the onset and progression of Alzheimer's disease, have led to the creation of several pathogenesis concepts of the most common neurodegenerative disease in the world, and amyloid, cholinergic, and neuroinflammatory hypotheses became leading. 32431878: A beta aggregates, especially the low-molecular weight oligomers, are the primary toxic agents in AD pathogenesis. 32991975: Biological evaluation of naturally occurring Bulbocodin D as a potential multi-target agent for Alzheimer's disease.In recent years, with the in-depth understanding of the pathogenesis of Alzheimer's disease (AD) and the development of advanced pharmacological technology, \multi-target\ strategy has recently attracted the wide interest of scientists. 34502472: Abeta(1-42) peptide is a neurotoxic agent strongly associated with the etiology of Alzheimer's disease (AD). 10373218: Blood pressures of Sprague-Dawley rat dams were manipulated during gestation with continuous intracerebroventricular infusions of vehicle, aldosterone, 11alpha-hydroxyprogesterone, or carbenoxolone at doses known to produce hypertension with no renal effects or with subcutaneous infusions of larger, equally hypertensinogenic doses that produce systemic effects. 10831247: The subcommissural organ is not highly permeable and does not have fenestrated capillaries, but new evidence indicates that it may be involved in the hypertension produced by aldosterone acting on the brain. 11004715: Primary aldosteronism is a disorder characterised by hypertension and hypokalaemia due to autonomous aldosterone secretion from the adrenocortical zona glomerulosa. 12110505: Although the aldosterone-responsive segments of the nephron together reabsorb <10% of the filtered Na+, certain single-gene defects that affect the epithelial Na+ channel (ENaC) in the luminal membrane of the collecting duct (CD) or its regulation by aldosterone cause severe hypertension, whereas others cause salt wasting and hypotension. 12384457: Thus aldosterone and salt treatment in uninephrectomized rats led to severe hypertension and the development of a vascular inflammatory phenotype in the heart, which may represent one mechanism by which aldosterone contributes to myocardial disease. Aldosterone induced severe hypertension at 4 wk [systolic blood pressure (SBP), 210 +/- 3 mmHg vs. vehicle, 131 +/- 2 mmHg, P < 0.001], which was partially attenuated by eplerenone (SBP, 180 +/- 7 mmHg; P < 0.001 vs. aldosterone alone and vehicle). 12782645: Endothelin A (ETA) receptor blockade has prevented vascular remodeling in aldosterone and salt-induced hypertension. 12860833: Aldosterone is now suggested to be a more common cause of hypertension than previously believed and has been linked to myocardial fibrosis, independent of its hypertensive effects. 1334353: Kallikrein-kinin,enkephalin, renin-aldosterone and catecholamine systems in the vanadate (as vanadyl)-induced arterial hypertension. 13759045: [On the intervention of the angiotensin-aldosterone system in the pathogenesis of arterial hypertension]. 14304759: IMPORTANCE OF ALDOSTERONE IN PATHOGENESIS OF EDEMA AND HYPERTENSION IN KIDNEY DISEASE. 14510903: Primary aldosteronism, diagnosed by the aldosterone to renin ratio, is a common cause of hypertension. 15351948: Primary aldosteronism is a disorder characterized by hypertension and hypokalemia due to aldosterone secretion out of renin-angiotensin control. 15458970: The intracerebroventricular, but not subcutaneous, infusion of 0.3 microg/h trilostane effectively blocked the increase in systolic blood pressure and reversed the hypertension produced by drinking 0.9% saline. Salt-induced hypertension in the Dahl inbred salt-sensitive (SS/jr) rat is associated with normal to low levels of circulating aldosterone, yet it is abrogated by the central infusion of mineralocorticoid receptor antagonists. These studies suggest that the synthesis in the brain of a mineralocorticoid receptor agonist, probably aldosterone, is responsible in part for the salt-induced hypertension of the inbred Dahl SS/jr rat. To test the hypothesis that de novo synthesis of aldosterone in the brain has a pathophysiological role in the salt-induced hypertension of the SS rat, the 3beta-steroid dehydrogenase antagonist trilostane was infused continuously intracerebroventricularly or subcutaneously in two different cohorts of Dahl SS/jr rats, one female, the other male, during and after the development of salt-induced hypertension. 15478626: Elevation of aldosterone leads to systemic hypertension through its action on the mineralocorticoid receptor (MR) in the kidney. 15980941: Moreover, excessive formation of aldosterone in glucocorticoid-remediable hypertension leads to severe hypertension. Several monogenic hypertensive disorders are caused by genetic mutations leading to the deranged function and/or regulation of renal tubular NaCl transport, such as mutations of the renal epithelial Na+ channel (ENaC) in Liddle syndrome, of the kinase WNK1 (with no K) in Gordon syndrome, and of the mineralocorticoid receptor, or of 11beta-hydroxysteroid dehydrogenase. 16211209: This study examined the role of aldosterone and its interplay with the renin-angiotensin system in the pathogenesis of hypertension. 16256010: In primary and secondary aldosteronism, aldosterone synthesis continues despite volume expansion and causes hypertension. 16426574: These observations indicate that ENaC and SGK1 are abnormally regulated by aldosterone in salt-sensitive hypertensive rats, suggesting that disturbance of the aldosterone regulation would be one of factors causing salt-sensitive hypertension. 16680076: Thus, aldosterone directly causes the dysregulation of endothelial cell function, which may be partly responsible for high blood pressure and atherosclerosis. 16801482: Thus, hypertension because of excess autonomous aldosterone secretion features an early and more prominent renal damage than PH. 17215648: It was previously thought that aldosterone produced hypertension primarily by promoting sodium retention with consequent hypervolemia. 17218415: The present findings suggest that the Ang II-dependent pathway resulting from vascular angiotensin-converting enzyme up-regulation and Ang II-independent pathway are both involved in the underlying mechanisms resulting in the development of hypertension, vascular inflammation, and oxidative stress induced by aldosterone. 18039981: A not-so-modest proposal that a \modest\ increase in aldosterone causes hypertension and more. 18710464: OBJECTIVE: Evidence suggests that high levels of aldosterone lead to hypertension and increased risk of cardiovascular disease. 187612: These studies suggest that a steroid other than aldosterone, 18-OH-DOC, or DOC may be the cause of the ACTH-induced hypertension in this patient. Evidence for an unidentified ACTH-induced steroid hormone causing hypertension. 18828652: Resistant hypertension is frequently the result of excessive aldosterone production, a situation easily treated. 19296925: Primary aldosteronism is caused by autonomous secretion of aldosterone by the adrenal cortex which results in hypertension with clinically, biochemically and therapeutically distinct features. 19574489: About 60% are functional tumors with hormonal secretions and clinical manifestations due to specific hormone secretions: Cushing's syndrome due to cortisone, virilizing tumor due to androgens, feminizing tumor due to estrogens, or hypertension due to aldosterone. 19814640: Our data showed that NHE1 inhibitor reduced aldosterone-induced glomerulosclerosis but not hypertension in 5/6 nephrectomized rats. 19837774: Aldosterone synthesis in brains of SS rats is greater than in SD rats and is important in the genesis of their salt-sensitive hypertension. 19850745: Aldosterone infusion results in left ventricular hypertrophy (LVH) and hypertension and may involve profibrotic and proinflammatory mechanisms. 1996630: However, mespirenone given in combination with aldosterone reversed the hypertension caused by aldosterone in a dose-dependent manner. 21112947: In the present studies, we tested the hypothesis that ANG II and Aldo interact centrally in Aldo- and ANG II-induced hypertension in male rats. These results suggest that ANG II and Aldo interact in the brain in a mutually cooperative manner such that the functional integrity of both brain AT1R and MR are necessary for hypertension to be induced by either systemic ANG II or Aldo. Many studies have implicated both angiotensin II (ANG II) and aldosterone (Aldo) in the pathogenesis of hypertension, the progression of renal injury, and cardiac remodeling after myocardial infarction. In ANG II-induced hypertension, icv infusion of RU28318 significantly reduced the increase in BP. Central interactions of aldosterone and angiotensin II in aldosterone- and angiotensin II-induced hypertension. 21298576: Mineralocorticoid receptors (MR) and epithelial sodium channels (ENaC) in the brain mediate central aldosterone-induced sympathetic hyperactivity and hypertension. 21814209: Angiotensin II and aldosterone of peripheral origin act in the brain to activate this cascade, increasing sympathetic outflow and leading to hypertension. 2192823: Experiments were performed to test the hypothesis that Na retention and Na in the diet are not required to initiate central aldosterone induced hypertension. 22000559: To test the hypothesis that aldosterone can cause hypertension in a manner that does not involve renal sodium retention, we administered eplerenone, a specific aldosterone antagonist, to oligo-anuric chronic hemodialysis patients who had HTN. 22026130: In the present study, the effect of a subdose of fasudil, a selective ROCK inhibitor, on systemic hypertension and myocardium fibrosis induced by aldosterone was investigated in uninephrectomized Sprague-Dawley rats (SD). 22184340: Overproduction of aldosterone in the adrenal gland can lead to hypertension, a major cause of heart disease and stroke. 22266731: CONCLUSION: Long-term infusion of aldosterone results in hypertension and profibrotic cardiovascular responses in rats fed a normal sodium diet, which were mediated by oxidative stress. 22808456: In these rats, the stress-induced elevation of aldosterone secretion was most pronounced, which indicates an important contribution of this hormone to the pathogenesis of stress-dependent arterial hypertension. 2316642: The chronic intracerebroventricular (icv) infusion of aldosterone in rats and dogs elevates the blood pressure within 10-14 days at doses far below those that produce hypertension systemically. 2333987: However, RU 26752 administered with aldosterone significantly prevented the hypertension produced by aldosterone alone. 2354554: Studies in the rat and the dog have shown that infusion of aldosterone for several weeks into the cerebral ventricles (ICV) can produce hypertension at doses that do not have an effect when infused systemically. 2375419: These results suggest that ANG II-induced hypertension in the rat is sodium dependent, that plasma aldosterone does not play a major role in ANG II-induced hypertension in the rat, and that a small chronic increase in circulating ANG II does not necessarily lead to a detectable sustained increase in PAC. Initial experiments demonstrated that a 1-h infusion of 10 ng/min angiotensin II (ANG II) into rats causes an increase in plasma aldosterone concentration (PAC) and that chronic administration of aldosterone alone to rats on increased sodium intake causes hypertension. 23785797: Recent advances in research into salt-sensitive hypertension revealed that mineralocorticoid receptor activities independent of aldosterone induce both salt-sensitive hypertension and organ damage, which is closely related to oxidative stress. Although novel therapeutic agents have become available and blood pressure tends to be lowered, the morbidity and mortality rates of hypertension-induced renal failure or stroke in Japan have not decreased in recent decades. 24048492: The combination of excess aldosterone and salt loading induces hypertension and cardiac damage. 24251173: About 60% are functional tumors secreting hormones, with its consequent clinical manifestations, the Cushing's syndrome due to cortisone, virilization due to androgens, feminization due to estrogens, or hypertension due to aldosterone. 25029123: Chronic RAS (renin-angiotensin system) activation by both AngII (angiotensin II) and aldosterone leads to hypertension and perpetuates a cascade of pro-hypertrophic, pro-inflammatory, pro-thrombotic and atherogenic effects associated with cardiovascular damage. 25353961: Hypertension and diastolic dysfunction induced by aldosterone were abolished by treatment with PASE. 25443574: Increased volume expansion, aldosterone concentration, mineralocorticoid receptor activity, arterial stiffness, and sympathetic nervous system activity are central to the pathogenesis of aTRH and are targets of therapies. 26340408: Primary aldosteronism accounts for 5%-10% of hypertension and in a third of cases is caused by autonomous aldosterone production by adenomas (APA). 26854589: Overproduction of cortisol is related to Cushing's disease, whereas overproduction of aldosterone leads to hypertension and end-organ damage such as cardiac and renal hypertrophy. 26876814: The adverse effect of excess aldosterone on insulin metabolic signaling has generated increasing interest in the role of hyperaldosteronism in the pathogenesis of insulin resistance and resistant hypertension. 2698926: We conclude that it is unlikely that either aldosterone or the weak mineralocorticoids corticosterone, 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone play a specific role in the pathogenesis of hypertension in Cushing's disease. 2755272: A C19 steroid, 19-hydroxyandrostenedione (19-OHAD), an amplifier of the mineralocorticoid effects of aldosterone, is known to cause hypertension in rats during chronic administration. 27592201: Hypertension and diastolic dysfunction induced by aldosterone were abolished by treatment with PRO80. 27733768: Excess production of aldosterone (Ald) results in hypertension as well as ASCVD. 27781210: Excess aldosterone can cause the dysregulation of the renin-angiotensin-aldosterone system (RAAS) and lead to hypertension. 27906749: Sodium and potassium in the pathogenesis of hypertension: focus on the brain. RECENT FINDINGS: Animal studies point to a small increase in plasma and cerebrospinal fluid (CSF) [Na], a small decrease in CSF [K], and increased levels of circulating angiotensin II, aldosterone, and endogenous ouabain as the central signals evoking hypertension. 28368454: Excess ALDO that is inappropriate for salt intake status causes cardiac hypertrophy, inflammation, fibrosis, and hypertension. 28978980: In conclusion, BM ameliorated tubulointerstitial damage in the Ald- and salt-induced hypertension model through suppression of both ROS production and intrarenal renin-angiotensin system activation. 29030398: Primary aldosteronism, a condition in which too much aldosterone is produced and that leads to hypertension, is often initiated by an aldosterone-producing adenoma within the zona glomerulosa of the adrenal cortex. 29273276: These findings suggest that aldosterone concurrently modulates microvascular and macrovascular function from the very early stages of essential hypertension and is dynamically implicated in the pathogenesis of hypertensive vascular disease. 29391190: Activation of mineralocorticoid receptor (MR) is evoked by aldosterone, and it induces hypertension and cardiovascular disease when it's concomitant with excessive salt loading. 29655877: INTERPRETATION: Our results suggest that resistant hypertension is commonly a salt-retaining state, most likely due to inappropriate aldosterone secretion. 29884931: Angiotensin II and aldosterone are overexpressed during hypertension and lead to hypertension development and its cardiovascular complications. 3004430: The presence of such sites could explain syndromes of mineralocorticoid excess where even trace amounts of an unusual aldosterone analogue, with little affinity for the classical mineralocorticoid receptor, can nevertheless produce hypertension through the intervention of an entirely new and abundant receptor system. 30153065: Excess aldosterone causes cardiac hypertrophy, fibrosis, inflammation and hypertension. 30571230: Lack of Suppression of Aldosterone Production Leads to Salt-Sensitive Hypertension in Female but Not Male Balb/C Mice. 30678858: The importance of maintaining tight control over aldosterone secretion is demonstrated by cases of dysregulation, which can result in severe hypertension and significantly increased cardiovascular risk. 31024637: Herein we present the case of a patient who developed multiple end-organ damage due to unrecognized and uncontrolled hypertension caused by an aldosterone-producing adrenal adenoma. 31397984: Excess aldosterone leads to arterial hypertension with suppressed renin, frequently associated to hypokalemia. 31409916: Primary aldosteronism is characterized by inappropriate overproduction of aldosterone by adrenal lesions and leads to hypertension. 31738186: Primary aldosteronism (PA) results from renin-independent production of aldosterone and is a common cause of hypertension. 3536587: Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. 3553487: Hypermineralocorticoid hypertension is usually due either to aldosterone or deoxycorticosterone excess. 3943493: Intracerebroventricular infusion of aldosterone induces hypertension in rats. A dose of aldosterone that was too small to produce changes in blood pressure when infused systemically was found to produce hypertension without polydypsia/polyuria when infused intrathecally. 4285923: On the role of renin-angiotensin system with special relation to aldosterone for the etiology of hypertension. 436781: An incremental change in circulating PRL, corticosterone, and aldosterone as early as 2 months of age, when blood pressure levels are beginning to rise, suggests that there may be some connection between the genetically programmed pathogenesis of the spontaneous hypertension and the progressively increasing (with age) sensitivity of the pituitary-adrenal axis to stress. 6339119: The present paper adds further evidence for the hypertensinogenic effects of amplifiers of the action of aldosterone and suggests the importance of amplifiers of the action of aldosterone in the etiology of human hypertension. 6396982: The importance of plasma vasopressin and aldosterone in the pathogenesis of hypertension seems to be probable but not yet unanimously proved. 7411808: Elevated levels of aldosterone may have been responsible for the severe hypertension, while hypercalcemia may have had a synergistic effect on the arteriolar response to circulating vasoactive peptides. 9782547: Primary aldosteronism is a rare cause of hypertension caused by increased aldosterone secretion. 10219973: Abnormal processing of amyloid precursor protein (APP), in particular the generation of beta-amyloid (Abeta) peptides, has been implicated in the pathogenesis of Alzheimer's disease. 10589538: Genetic evidence strongly supports the view that Abeta amyloid production is central to the cause of Alzheimer's disease. 10670439: Further studies are required to determine the clinical significance of these physiological changes in plasma amyloid precursor protein and the implications for Alzheimer's disease pathogenesis. The deposition of beta amyloid is a critical event in the pathogenesis of Alzheimer's disease. 10818502: The beta-amyloid (A beta) peptide is believed to play a central role in the pathogenesis of AD. 10899442: Although there remains controversy as to whether Abeta deposited as classic amyloid or a smaller, aggregated, form causes AD, the relevance of studying the amyloid deposits has certainly been proven. 11019859: Chemical and conformational early modifications of the beta-amyloid peptide are critical steps in AD pathogenesis and have been widely investigated. 11145990: Converging lines of evidence implicate the beta-amyloid peptide (Ass) as causative in Alzheimer's disease. 11181832: A large body of evidence suggests that an increase in the brain beta-amyloid (Abeta) burden contributes to the etiology of Alzheimer's disease (AD). 11388427: Microglial activation induced by beta-amyloid (A beta) is an important cellular response in the pathogenesis of Alzheimer's disease (AD). 11455613: Microglial interaction with beta-amyloid: implications for the pathogenesis of Alzheimer's disease. 11475420: Recent studies suggest melatonin, due to its antioxidant and free-radical-scavenging actions, may play a role in the neuroprotection against amyloid, which is implicated in the pathogenesis of Alzheimer's disease (AD). 11496136: The beta-amyloid peptide (A beta) is a key player in the pathogenesis of Alzheimer's disease. 11602326: Substantial evidence suggests that the accumulation of beta-amyloid (Abeta)-derived peptides contributes to the aetiology of Alzheimer's disease (AD) by stimulating formation of free radicals. 11701593: Here, we report a family (family GB) in which early-onset Alzheimer's disease was caused by a novel presenilin 1 mutation (L282V). Nevertheless, in > 90% of cases of Alzheimer's disease amyloid is also deposited in cerebral blood vessel walls (congophilic amyloid angiopathy; CAA) but its role in Alzheimer's disease pathogenesis remains enigmatic. This was unusually severe CAA reminiscent of the Flemish amyloid precursor protein (A692G) mutation we reported previously, which causes Alzheimer's disease and/or cerebral haemorrhages. Cerebral amyloid angiopathy is a pathogenic lesion in Alzheimer's disease due to a novel presenilin 1 mutation. 11818564: beta-amyloid (A beta), derived form the beta-amyloid precursor protein (APP), is important for the pathogenesis of Alzheimer's disease (AD), which is characterized by progressive decline of cognitive functions, formation of A beta plaques and neurofibrillary tangles, and loss of neurons. 11848621: Investigation of the interactions of nerve cells with human apolipoprotein E (apoE), beta-amyloid (Abeta), and their complex, which are known to be included in senile plaques, is necessary to clarify the functional role of apoE in the pathogenesis of Alzheimer's disease. 11886820: Aggregation of amyloid peptide (Abeta) has been identified as a major feature of the pathogenesis of Alzheimer's disease. 11967228: Moreover, our findings indicate that beta-sheet breaker peptides provide a valuable tool for evaluating further the importance of amyloid in the etiology of AD and suggest that these peptides or some of their derivatives might be good candidates for AD treatment. 12119153: The amyloid and tangle cascade hypothesis is the dominant explanation for the pathogenesis of Alzheimer's disease (AD). 12214051: The biogenesis and degradation/clearance of Abeta amyloid lies at the centre of the pathogenesis of Alzheimer's disease. 12423367: While BACE1 processes the amyloid precursor protein (APP) at a key step in generating the beta-amyloid peptide and presumably causes Alzheimer's disease (AD), BACE2 has not been demonstrated to be directly involved in APP processing, and its physiological functions remain to be determined. 12496118: The amyloid precursor protein (APP) is the precursor of the beta-amyloid peptide (Abeta), which is centrally related to the genesis of Alzheimer's disease (AD). 12598899: Amyloid precursor protein (APP) processing and the generation of beta-amyloid peptide (Abeta) are important in the pathogenesis of Alzheimer's disease. 12600718: Increased formation of the beta-amyloid peptide (Abeta) is a central event in the pathogenesis of Alzheimer's disease (AD). 12751917: The evidence indicates that abnormal processing and extracellular deposition of the longer form of the beta-amyloid (Abeta) peptide (Abeta(1-42), a proteolytic derivative of the amyloid precursor protein [APP]) is implicated in the pathogenesis of Alzheimer's disease. This research strongly supports the notion that abnormal Abeta processing is essential to the pathogenesis of Alzheimer's disease and provides a crucial platform for the development and detailed testing of potential treatments in experimental models before each of these approaches can be proposed as a therapy for Alzheimer's disease. 12821522: The accumulation of beta-amyloid (A beta) in neuritic plaques is thought to be causative for the progression of Alzheimer's disease (AD). 12970358: Increased production and deposition of the 40-42-amino acid beta-amyloid peptide (Abeta) is believed to be central to the pathogenesis of Alzheimer's disease. 13130516: Current Alzheimer's disease (AD) research has established the fact that excessive genesis of Abeta derived from amyloidogenic processing of beta-amyloid (Abeta) precursor protein is fundamental to AD pathogenesis. 14511676: Deposition of amyloid in the brain is important in the pathogenesis of Alzheimer's disease (AD), but it remains to be determined if deposition is due to increased production or decreased clearance of fibrillogenic forms of beta-amyloid (Abeta). 14640701: Deposition of beta-amyloid (Abeta) is considered an important early event in the pathogenesis of Alzheimer's disease (AD). 14713297: Beta-amyloid (Abeta) peptide has been suggested to play important roles in the pathogenesis of Alzheimer's disease (AD). 15071107: Multiple lines of evidence implicate beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD), but the mechanisms whereby Abeta is involved remain unclear. 15099019: The formation of amyloid-containing senile plaques and tau-rich neurofibrillary tangles are central events in Alzheimer disease (AD) pathogenesis. 15181252: We will continue to investigate the effect of apoE isoform and Abeta conformation on the structural and functional interactions between these two proteins in relation to the pathogenesis of AD. 15189029: Recent studies have indicated that the most important role of beta-amyloid peptide (Abeta) in the etiology of Alzheimer's disease may not be in plaque formation but in the formation of soluble, metastable Abeta(1-42) neurotoxic intermediates (called ADDLs). 15240683: Human formyl peptide receptor-like 1 and its mouse homologue formyl peptide receptor 2 (FPR2) are G protein-coupled receptors used by a number of exogenous and host-derived chemotactic peptides, including the 42 aa form of beta amyloid peptide, a causative factor of Alzheimer's disease. 15340356: Cerebral accumulation of beta-amyloid peptide (A beta) is a central event in the pathogenesis of Alzheimer's disease (AD). 15452193: gamma-Secretase inhibitors reduce brain beta-amyloid peptide (Abeta), which is believed to be a major contributor in the etiology of AD. 15474359: Understanding the molecular mechanism of beta-amyloid (Abeta) generation is crucial for Alzheimer's disease pathogenesis as well as for normal APP function. 15565529: According to the beta-amyloid cascade hypothesis, the accumulation of beta-amyloid (Abeta) deposits as amyloid plaques in the patient's brain is the primary event in the pathogenesis of Alzheimer's disease (AD). The majority of known APP and presenilin mutations responsible for familial early onset AD affect APP processing causing overproduction of Abeta, especially Abeta42. 15974916: Previous studies from our lab also showed that TGF-beta1 can reduce accumulation of beta-amyloid peptide (Abeta), which appears to be central to Alzheimer's disease (AD) pathogenesis, and we therefore initiated a search for small molecule chemical compounds that could mimic this effect. 16170650: Genetic evidence indicates a central role of cerebral accumulation of beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD). 16271725: Polymerization of the soluble beta-amyloid peptide into highly ordered fibrils is hypothesized to be a causative event in the development of Alzheimer's disease. 16289381: Accumulation of the beta-amyloid peptide (Abeta) is a primary event in the pathogenesis of Alzheimer's disease (AD). 16420415: Considering the deleterious role of beta-amyloid (Abeta) in the aetiology of Alzheimer's disease (AD), we investigated green and black tea extracts and flavan-3-ols (present as monomers and dimers in green and black forms, respectively) against toxicity induced by Abeta-derived peptides using primary cultures of rat hippocampal cells as model. 16539391: Activation of alpha-secretase upon PKC stimulation by ligands causes increased degradation of the amyloid precursor protein (APP), resulting in enhanced secretion of sAPPalpha and reduced deposition of beta-amyloid peptide (Abeta), which is implicated in the pathogenesis of Alzheimer's disease. 16542055: The amyloid hypothesis, which states that beta-amyloid (Abeta) aggregates cause the onset and progression of Alzheimer's disease (AD), is a leading proposal to explain AD aetiology. 16581185: Production and accumulation of beta-amyloid peptide (Abeta) is central to the pathogenesis of AD. 16624948: Increasing evidence links intraneuronal beta-amyloid (Abeta42) accumulation with the pathogenesis of Alzheimer's disease (AD). 16626708: In addition to the role of beta-amyloid peptide (Abeta) in the pathogenesis of AD, reduced glucose oxidative metabolism and decreased mitochondrial activity have been suggested as associated factors. 1669714: Amyloid precursor protein (APP) and beta A4 amyloid in the etiology of Alzheimer's disease: precursor-product relationships in the derangement of neuronal function. 16723396: beta-Amyloid (Abeta) polypeptide plays a critical role in the pathogenesis of Alzheimer's disease (AD), which is characterized by progressive decline of cognitive functions, formation of Abeta deposits and neurofibrillary tangles, and loss of neurons. 16762454: beta-Amyloid (Abeta) is a hydrophobic peptide that drives the pathogenesis of Alzheimer's disease (AD) due to its aberrant aggregation. 16822591: Cerebral accumulation of beta-amyloid peptide (Abeta) is a central event in the pathogenesis of Alzheimer's disease (AD). 16908985: The accumulation of the beta-amyloid peptide (Abeta) is a central event in the pathogenesis of Alzheimer's disease (AD). 16945610: BACKGROUND: Growing evidence suggests that oxidative damage caused by the beta-amyloid peptide in the pathogenesis of Alzheimer's disease may be hydrogen peroxide mediated. 16962711: Recent studies indicate that the deposition of beta-amyloid (Abeta) is related in the pathogenesis of Alzheimer's disease (AD), but the underlying mechanism is still not clear. 17013614: A contributing factor to the pathology of Alzheimer's disease is the generation of reactive oxygen species, most probably a consequence of the beta-amyloid (Abeta) peptide coordinating copper ions. 17050537: Understanding the intracellular transport of the beta-amyloid precursor protein (APP) is a major key to elucidate the regulation of APP processing and thus beta-amyloid peptide generation in Alzheimer disease pathogenesis. 17086547: Based on the central dogma of beta-amyloid (Abeta) as a key seeding event in the pathogenesis of Alzheimer disease (AD), immunoneutralization strategies have been actively pursued both in AD and in models of AD as a potential means for treating AD. 17287054: Beta-amyloid peptide (AbetaP) aggregation, an essentially early event in Alzheimer's disease (AD) pathogenesis, became a target for therapeutics. 17374949: Evidence supports an important role for beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD). 17517969: Subcutaneous administration of G-CSF into two different beta-amyloid (Abeta)-induced AD mouse models substantially rescued their cognitive/memory functions. 17531157: The involvement of beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD) has been well documented. 17553417: BACE initiates the production of beta-amyloid (Abeta), the likely cause of Alzheimer's disease (AD). 17566645: Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is a key protease in the generation of beta-amyloid, an important trigger protein in the pathogenesis of AD. 17620492: BACKGROUND: Deposition of the beta-amyloid peptide Abeta(42) is thought to be an important initial step in the pathogenesis of Alzheimer disease (AD). 17650113: The beta amyloid (Abeta) cascade has been at the forefront of the hypothesis used to describe the pathogenesis of Alzheimer's disease (AD). 17722071: To elucidate whether myricetin could counter the progress of AD, we examined the effects of myricetin on neurotoxicity induced by beta-amyloid (A beta), a component of senile plaques in the AD brain. 17907956: The ageing brain becomes increasingly less able to destroy or eject toxic amyloid (A) beta42 peptide byproducts of normal neuronal activity that consequently accumulate to induce Alzheimer's disease (AD). 18167346: Amyloid formation may mediate aberrant protein interactions that culminate in neurodegeneration in Alzheimer, Huntington, and Parkinson diseases and in prion encephalopathies. 18304698: The amyloid precursor protein (APP) is the source of beta-amyloid, a pivotal peptide in the pathogenesis of Alzheimer's disease (AD). 18357680: While such amyloid mechanism contributes to Alzheimer's pathological conditions, recent studies from a number of laboratories suggest that defective axonal transport may represent an early stage in AD pathogenesis because axonal swellings and reduced axonal transport were observed before apparent AD hallmarks. 18395981: Amyloid precursor protein (APP) is a precursor protein for beta-amyloid, an important trigger protein in the pathogenesis of AD. 18413473: Most of these mutations may also cause cognitive impairment, but the Arctic APP mutation is the only known intra-beta-amyloid mutation to date causing the more typical clinical picture of Alzheimer disease. Clinical and neuropathological features of the arctic APP gene mutation causing early-onset Alzheimer disease. 18422968: The interaction of the beta-amyloid peptide (Abeta) with neuronal membranes could play a key role in the pathogenesis of Alzheimer's disease. 18452319: Extracellular beta-amyloid (A beta) deposit is considered as one of the primary factors that induce Alzheimer's disease (AD). 18473932: Beta-amyloid (Abeta)likely plays a pivotal role in the etiology of Alzheimer's disease (AD). 18855672: In line with the growing body of evidence of the pivotal role of the beta-amyloid peptide (Abeta) in the pathogenesis of AD, alternative classes of drugs targeting mainly the formation or the aggregation of Abeta are actively pursued by the pharmaceutical industry, as they could positively modify the course of AD, stopping or slowing down disease progression. 19270530: Extracellular accumulation of beta-amyloid peptide has been reported to be a major cause of Alzheimer disease (AD) and large numbers of autophagic vacuoles accumulate in the brain of AD patient. 19360426: Beta-amyloid (Abeta) is thought to be a key contributor to the pathogenesis of Alzheimer disease (AD) in the general population and in adults with Down syndrome (DS). 19572401: Deposition of beta-amyloid (A beta) is considered as an important early event in the pathogenesis of Alzheimer's Disease (AD), and reduction of A beta levels by various therapeutic approaches is actively being pursued. 19594760: BACKGROUND AND PURPOSE: Orally administered withanoside IV (a compound isolated from the roots of Withania somnifera) improved memory deficits in mice with a model of Alzheimer's disease induced by the amyloid peptide Abeta(25-35). 19610108: The significance of intracellular beta-amyloid (Abeta(42)) accumulation is increasingly recognized in Alzheimer's disease (AD) pathogenesis. 19631265: The role of beta-amyloid (A beta) in the pathogenesis of Alzheimer's disease (AD) is frequently reported in the literature. 19634775: A wide range of diseases are associated with amyloidosis such as Alzheimer's disease, multiple myeloma, other plasma cell disorders, and chronic inflammation, either as a cause, or result, of amyloid production. 19657023: Recent evidence supports an important role for intraneuronal beta-amyloid in the pathogenesis of Alzheimer's disease. 19678545: The neurotoxicity induced by beta-amyloid (Abeta), which is one of the major causes of Alzheimer's disease (AD), leads to synaptic loss and subsequent neuronal death. 19699263: The neurotoxicity of aggregated beta-amyloid (Abeta) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD). 19794916: In Alzheimer's disease tauopathy is considered secondary to amyloid, and the duality obscures their relation and the definition of their respective contributions. 19827625: Anomalous accumulation of beta-amyloid peptide in cerebral neurons plays central role in pathogenesis of Alzheimer's disease (AD). 19843960: The beta-amyloid (Abeta) peptide is associated with the pathogenesis of Alzheimer's disease (AD). 19903023: Genetic and biological studies provide strong support for the hypothesis that accumulation of beta amyloid peptide (Abeta) contributes to the etiology of Alzheimer's disease (AD). 19957250: Withanamides in Withania somnifera fruit protect PC-12 cells from beta-amyloid responsible for Alzheimer's disease. 20074226: Beta-amyloid (Abeta) peptides are thought to play a major role in the pathogenesis of Alzheimer's disease. 20101562: Increased beta-amyloid (Abeta) production and its aggregation to the oligomeric state is considered to be a major cause of Alzheimer's disease (AD). 20101719: The design of future immunomodulatory approaches that are more focused is dependent on addressing a number of questions, including when is the best time to start immunization, what are the most appropriate targets for vaccination, and is amyloid central to the pathogenesis of Alzheimer's disease or is it critical to target tau-related pathology also. 20164555: Controversy still exists about the amyloid pathway as the initiating mechanism or a mere consequence of the events leading to AD. 2025422: Hypothesis regarding amyloid and zinc in the pathogenesis of Alzheimer disease: potential for preventive intervention. 20306540: Although Alzheimer's disease (AD) is characterized by the extracellular deposition of fibrillar aggregates of beta-amyloid (Abeta), transient oligomeric species of Abeta are increasingly implicated in the pathogenesis of AD. 20348021: Research in genetics, pathology, epidemiology, biochemistry, and cell biology, as well as in animal models, suggests that cholesterol, its transporter in the brain, apolipoprotein E, amyloid precursor protein, and amyloid-beta all interact in AD pathogenesis. 20362424: Beta-amyloid (Abeta) aggregation, believed to be responsible for Alzheimer's disease, is monitored using its intrinsic fluorescence decay. 20429609: Deposition of beta-amyloid (Abeta) is considered an important early event in the pathogenesis of Alzheimer's disease (AD), and reduction of Abeta levels in the brain could be a viable therapeutic approach. 20456003: Presenilin 1 (PS1) is a key component of the gamma-secretase complex in the generation of beta-amyloid (Abeta), an important trigger protein in the pathogenesis of AD. 20583856: Inhibiting the PAS is desirable for prevention of aggregation of the amyloid peptide Abeta, a major causative factor in the progression of Alzheimer's disease (AD). 20637185: In AD, activated microglia may facilitate the clearance of beta-amyloid (Abeta), a neurotoxic component in AD pathogenesis. 20665950: Galantamine, which is currently used in the treatment of patients with Alzheimer's disease (AD), has been shown to have a neuroprotective effect against beta-amyloid (Abeta) peptide-induced toxicity, which is involved in the pathogenesis of AD. 20674676: The neurotoxicity of aggregated beta-amyloid (Abeta) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD). 20675873: [Involvement of beta-amyloid in the etiology of Alzheimer's disease]. 20972410: Accumulation of the beta-amyloid peptide (Abeta) is generally believed to be central to the induction of Alzheimer's disease, but the relevant mechanism(s) of toxicity are still unclear. 21222605: Proteolytic processing of APP to generate beta-amyloid, the principle component of amyloid plaques, can occur in membrane rafts, implicating them in the pathogenesis of Alzheimer's disease (AD). 21233670: The first article on Alzheimer's disease (AD) outlines the major evidence available to date that links Abeta-amyloid peptide as a proximal cause of AD. 21270904: beta-Amyloid (Abeta) over-expression and tau hyperphosphorylation are considered to be the central events in the pathogenesis of Alzheimer's disease (AD). 21315759: Metabolism of beta-amyloid peptide (Abeta) is closely associated with the pathology and etiology of Alzheimer's disease (AD). 21318523: A large body of evidence suggests a causative role of beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (reviewed in refs. 1 and 2). 21395066: [Formation and participation of nano-amyloids in pathogenesis of Alzheimer's disease and other amyloidogenic diseases]. 21472290: Excessive accumulation of beta-amyloid (Abeta) has been proposed as a pivotal event in the pathogenesis of Alzheimer's disease. 21476939: The beta-amyloid (Abeta) peptide, which plays a crucial role in the pathogenesis of Alzheimer's disease, alters hippocampal-dependent synaptic plasticity and memory and mediates synapse loss through the CREB signaling pathway. 21480689: The production of beta-amyloid is thought to be a major and early contributor to the pathogenesis of AD. 21504387: Solanezumab is a monoclonal antibody that binds to beta-amyloid (Abeta), a protein that plays a key role in the pathogenesis of AD. 21706413: beta-amyloid (Abeta) and copper play important roles in the pathogenesis of Alzheimer's disease (AD). 21839813: It is recognized that the main trigger of Alzheimer disease related neurodegeneration is beta-amyloid peptide, which subsequently generates different metabolic disorders in neuron and finally leads to neuronal death. 21897007: These results support the idea that a link between glucose dysmetabolism and the amyloid pathway may exist in the pathogenesis of AD. 21961303: Excess production and accumulation of beta-amyloid peptide (betaAP) are central for pathogenesis of Alzheimer's disease. 22031884: Impaired beta-amyloid secretion in Alzheimer's disease pathogenesis. 22042506: Beta-amyloid peptide (Abeta), a major protein component of senile plaques, has been considered as a critical cause in the pathogenesis of Alzheimer's disease (AD). 22202113: Generation of Amyloid peptide (Abeta) is at the beginning of a cascade that leads to Alzheimer's disease. 22288451: Solanezumab (LY2062430) is a humanized monoclonal antibody that binds to the central region of beta-amyloid, a peptide believed to play a key role in the pathogenesis of Alzheimer's disease (AD). 22342932: It has been more than a century since the first evidence linking the process of amyloid formation to the pathogenesis of Alzheimer's disease. 22351073: Generation of amyloid peptide (Abeta) is at the beginning of a cascade that leads to Alzheimer's disease (AD). 22702727: beta-Amyloid peptide (1) (Abeta) aggregates are toxic to neuron and the main cause of Alzheimer's disease (AD). 22727791: AIMS: Multiple lines of evidence have implicated beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD). 22833976: BACKGROUND: Excessive accumulation of beta-amyloid (Abeta) has been proposed as a pivotal event in the pathogenesis of Alzheimer's disease. 23036978: The abnormal production and accumulation of beta-amyloid peptide (Abeta), which is produced from amyloid precursor protein (APP) by the sequential actions of beta-secretase and gamma-secretase, are thought to be the initial causative events in the development of Alzheimer's disease (AD). 23134284: CONTEXT: The beta-amyloid (Abeta) peptide aggregation with accompanying oxidative stress plays the major role in the pathogenesis of Alzheimer's disease (AD). 23300647: Beta-amyloid (Abeta ) neurotoxicity is important in Alzheimer's disease (AD) pathogenesis. 23383341: Unraveling the normal physiologic role of beta-amyloid is likely crucial to understanding the pathogenesis of Alzheimer's disease. 23420027: IMPORTANCE: Current hypothetical models emphasize the importance of beta-amyloid in Alzheimer disease (AD) pathogenesis, although amyloid alone is not sufficient to account for the dementia syndrome. 23512986: The extracellular accumulation of beta-amyloid peptide is a key trigger in the pathogenesis of Alzheimer's disease (AD). 23516302: Alzheimer's disease is thought to be caused by beta-amyloid peptide (Abeta)-dependent synaptic dysfunction. 23662474: At current review we represented state-of-art views on the processes of production and aggregation of betaAP in organism, cellular and molecular mechanisms of betaAP influence on physiological functions of excitable cells, the role of betaAP in pathogenesis of neurodegenerative diseases (Alzheimer's disease and others), as well as the results of our own studies in this field. 23794448: Amylin amyloid formation in the wall of cerebral blood vessels may also induce failure of elimination of Abeta from the brain, thus contributing to the etiology of AD. 23942088: BACKGROUND: Beta-amyloid (Abeta) protein is a key factor in the pathogenesis of Alzheimer's disease (AD) and it has been reported that mitochondria is involved in the biochemical pathway by which Abeta can lead to neuronal dysfunction. 24162852: Notably, CD36 is also a receptor for modified lipoproteins and beta-amyloid, and has been implicated in the pathogenesis of atherosclerosis and of Alzheimer's disease. 24277156: The current study was carried out to investigate the effects of chronic administration of pioglitazone, a PPAR-gamma agonist, on cognitive impairment in an animal model of Alzheimer's disease induced by beta-amyloid. 24287378: The toxicity of amyloid beta-peptide (Abeta) has been implicated as a critical cause in the development of AD, and Abeta-amyloid-induced toxicity is typically associated with apoptosis. 24491999: The dark sides of amyloid in Alzheimer's disease pathogenesis. Many evidences are starting to cast doubt on Abeta as the primary causative factor in AD. 24985739: The disruption of Abeta homeostasis, which results in the accumulation of neurotoxic amyloids, is the fundamental cause of Alzheimer's disease (AD). 25066110: Implicating the role of lycopene in restoration of mitochondrial enzymes and BDNF levels in beta-amyloid induced Alzheimer's disease. 25108368: Aberrant accumulation of beta-amyloid (Abeta) is thought to be an early event in a biological cascade that eventually leads to Alzheimer's disease (AD). 25639816: An interesting target is the beta-amyloid peptide (Abeta), whose accumulation and progressive deposition into amyloid plaques are key events in AD aetiology. 25686760: Even in Alzheimer disease, which is thought to be primarily caused by amyloid, vascular pathology, such as small vessel disease, may be of greater importance than amyloid itself in terms of influencing the disease course, especially in older individuals. 25686800: Extracellular beta-amyloid peptide accumulation is reported as a major cause in Alzheimer's disease (AD) pathogenesis; large numbers of autophagic vacuoles accumulate in patients' brains. 25714795: Alzheimer's disease (AD) and Parkinson's disease (PD) are caused by beta-amyloid (Abeta) and alpha-synuclein (alphaS), respectively. 26073444: Aggregation of beta-amyloid (Abeta) is central to the pathogenesis of Alzheimer's disease (AD). 26244661: Autophagy is a vital pathway for the removal of beta-amyloid peptide (Abeta) and the aggregated proteins that cause Alzheimer's disease (AD). 26411291: Although amyloids are best known for their role in the etiology of diseases such as Alzheimer's, Parkinson's, and diabetes by forming toxic protein aggregates, our findings show that cells can utilize amyloid-like protein aggregates to function as central regulators of gametogenesis. 26440073: The accumulation of extracellular beta-amyloid (Abeta) is crucial in AD pathogenesis, and Abeta-initiated secondary pathological processes could independently lead to neuronal degeneration and pathogenesis in AD. 26594145: Strong evidence showed neurotoxic properties of beta amyloid (Abeta) and its pivotal role in the Alzheimer's disease (AD) pathogenesis. 26618706: RESULTS: 55% of the experts assigned a dominant role to amyloid, and 32% attributed a similar role to amyloid and tau in AD pathogenesis. OBJECTIVE: To assess the role attributed to amyloid in AD pathogenesis by Italian dementia experts, and whether this modulates the impact of amyloid PET results in their diagnostic workup. 26786779: Accumulation of oxidized proteins, and especially beta-amyloid (Abeta), is thought to be one of the common causes of Alzheimer's disease (AD). 26883101: The processing of amyloid beta precursor protein (APP) to beta-amyloid peptide (Abeta) is one of the critical events in the pathogenesis of AD. 27018282: beta-Amyloid (Abeta) oligomers may play an important role in the early pathogenesis of Alzheimer's disease: cognitive impairment caused by synaptic dysfunction. 27071404: Protein misfolding, aggregation and deposition in the brain, in the form of amyloid, are implicated in the etiology of several neurodegenerative disorders, such as Alzheimer's, Parkinson's and prion diseases. 27072891: The processing of amyloid precursor protein (APP) into beta-amyloid peptide (Abeta) is a key step in the pathogenesis of Alzheimer's disease (AD), and trafficking dysregulations of APP and its secretases contribute significantly to altered APP processing. 27072999: Because of the increased lifetime of phosphorylated beta-amyloid aggregates, phosphorylation can promote the spreading of beta-amyloid in Alzheimer pathogenesis. 27106205: Several lines of evidence indicate that beta amyloid (beta-A) production, neurofibrillary tangles and neuroinflammation are interrelated in the pathogenesis of Alzheimer's disease (AD). 27303604: INTRODUCTION: To study the effect of gallic acid (GA) on hippocampal long-term potentiation (LTP) and histological changes in animal model of Alzheimer disease (AD) induced by beta-amyloid (Abeta). 27318146: The misfolding and accumulation of the protein fragment beta-amyloid (Abeta) is an early and essential event in the pathogenesis of Alzheimer's disease (AD). 27481595: Given its role in the formation of amyloids leading to Alzheimer's disease, it has been a major therapeutic target for intervention and has been a challenge in the past and the progress has been very slow. 27634977: This review examines the possible role of the gut in the dissemination of amyloids, the role of the gut microbiota in the regulation of the gut-brain axis, the potential amyloidogenic properties of gut bacteria, and the possible impact of nutrients on modulation of microbiota composition and amyloid formation in relation to the pathogenesis of Alzheimer disease. 27710900: Misfolded beta-sheet-rich protein aggregates termed amyloid, deposit in vivo leading to debilitating diseases such as Alzheimer's, prion and renal amyloidosis diseases etc. 27867033: The prevailing beta-amyloid (Abeta)-cascade hypothesis is the most classical Alzheimer's disease (AD) pathogenesis. 27922847: The objective of this article is to review the recent findings about the metabolism of apolipoprotein E (ApoE) and amyloid beta and other possible mechanisms by which ApoE contributes to the pathogenesis of Alzheimer's disease. 28261990: AIMS: Axonal degeneration is a pathological symbol in the early stage of Alzheimer's disease (AD), which can be triggered by amyloid-? 28271324: Beta-amyloid peptide (Abeta) induced neurotoxicity is considered as a hallmark of the pathogenesis of Alzheimer's disease (AD). 28320296: Here we (i) highlight the latest data on mechanisms of amyloid formation and further discuss a hypothesis on the amyloid cascade as a primary mechanism of AD pathogenesis and (ii) review the evolutionary aspects of amyloidosis, which allow new insight on human-specific mechanisms of dementia development. 28352309: According to the findings of the observed study, AS has a marked protective effect on Abeta-induced AD pathology, and the underlying mechanism may be associated with the alleviation of the mitochondrial injuries, the anti-inflammatory activities, and the influence on the expression levels of apoptosis-associated proteins. The present study aimed to investigate the effects of asiaticoside (AS) on the pathology and associated mechanisms of beta-amyloid (Abeta)-induced Alzheimer's disease (AD) in rats. 28509380: OBJECTIVE: The aim of this study is to examine the hypotheses stating the importance of amyloid or of its oligomers in the pathogenesis of Alzheimer's disease (AD). RESULTS: The importance of amyloid in the pathogenesis of AD is well established, yet accepting it as the main cause for AD is problematic, because amyloid-centric treatments have provided no clinical benefit and about one-third of cognitively normal, older persons have cerebral amyloid plaques. 28592267: BACKGROUND: ?-Amyloid peptide (A?) oligomers are initial factors used to induce Alzheimer's disease (AD) development, and A? monomers have normal physiological function. 28756148: Excessive accumulation of beta-amyloid (Abeta) has been proposed as a pivotal event in the pathogenesis of AD. 28774853: Maintenance of normal biochemical levels in brain tissue demonstrated the potential of these coated MWCNTs in reducing beta-amyloid induced AD. 28815614: The amyloid hypothesis suggests that the progressive accumulation and deposition of central nervous system (CNS) amyloid with aging is the proximate cause of Alzheimer's disease (AD). 28866757: Experimental data suggest that the cerebrospinal fluid (CSF) dynamic is involved in the clearance of beta-amyloid, a key event in the pathogenesis of Alzheimer's disease (AD). 28900376: Also, various experimental and clinical studies are in progress to prove exercise role in the beta-amyloid (Abeta) pathology as a most prevailing hypothesis explaining AD pathogenesis. 2890206: Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD. 28993924: The role of beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD) is still considered crucial. 29158049: We therefore evaluated the effects of tanshinone IIA (TIIA) and cryptotanshinone (CRY) (the two major lipophilic compounds of Danshen) in a non-genetic mouse model of beta-amyloid (Abeta)-induced AD, which is mainly characterized by reactive gliosis and neuro-inflammation in the brain. 29191087: Deranged beta-amyloid (Abeta) trafficking across the blood-brain barrier is known to be a critical element in the pathogenesis of AD. 29311595: Excessive accumulation of beta-amyloid (Abeta) is thought to be a major causative factor in the pathogenesis of Alzheimer's disease (AD). 29427089: However, the role of ER stress in beta-amyloid (Abeta)-induced AD pathology remains elusive, and data obtained from different animal models and under different experimental conditions are sometimes controversial. 29444819: BACE1 initiates the generation of the beta-amyloid peptide, which likely causes Alzheimer's disease (AD) when accumulated abnormally. 29966723: beta-Amyloid (Abeta) plays an important role in the early pathogenesis of Alzheimer's disease (AD). 30126231: Increasing evidence suggests that amyloid formation, i.e., self-assembly of proteins and the resulting conformational changes, is linked with the pathogenesis of various neurodegenerative disorders such as Alzheimer's disease, prion diseases, and Lewy body diseases. 30127003: Amyloid peptide-related inflammation is thought to be an important aspect of AD pathogenesis. 30220236: By affirming markers of abnormal Abeta and tau proteins as the essential pathobiological signature of Alzheimer's disease, the Framework tacitly reinforces the amyloid (Abeta) cascade as the leading theory of Alzheimer pathogenesis. In light of recent evidence that the cascade is driven by the misfolding and templated aggregation of Abeta and tau, we believe that an empirically grounded Standard Model of Alzheimer's pathogenesis is within reach. 30232325: In Alzheimer's disease (AD), the canonical Wnt inhibitor Dickkopf-1 (Dkk1) is induced by beta-amyloid (Abeta) and shifts the balance from canonical towards non-canonical Wnt signalling. 30483749: Cytotoxicity of beta-Amyloid (Abeta) is a major contributor to the pathogenesis of Alzheimer's disease. 30572184: beta-Amyloid (Abeta) accumulation is an early event of Alzheimer's disease (AD) pathogenesis. 30723404: Effects of BIS-MEP on Reversing Amyloid Plaque Deposition and Spatial Learning and Memory Impairments in a Mouse Model of beta-Amyloid Peptide- and Ibotenic Acid-Induced Alzheimer's Disease. 30786665: Alzheimer's disease neuropathologic change (ADNC) in the form of ?-amyloid (A?) deposits is important not only in the pathogenesis of Alzheimer's disease (AD) and Down's syndrome (DS) but also as a 'co-pathology' in disorders such as dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and chronic traumatic encephalopathy (CTE). 30868421: Does HIV infection contribute to increased beta-amyloid synthesis and plaque formation leading to neurodegeneration and Alzheimer's disease? 30936829: Literary evidence depicts that aggregated beta-amyloid (Abeta) leads to the pathogenesis of Alzheimer's disease (AD). 30946834: Beta-amyloid (Abeta) has pivotal functions in the pathogenesis of Alzheimer's Disease (AD). 30959405: beta-amyloid (Abeta) plays an essential role in the pathogenesis of Alzheimer's disease (AD). 31095505: Accumulation of beta-amyloid peptide (Abeta) is regarded as a primary cause of Alzheimer's disease (AD). 31108937: beta-site APP-cleaving enzyme 1 (BACE1) initiates amyloid precursor protein (APP) cleavage and beta-amyloid (Abeta) production, a critical step in the pathogenesis of Alzheimer's disease (AD). 31164812: Alzheimer's disease (AD) is one of the most common neurodegenerative diseases, and beta-amyloid (Abeta) plays a leading role in the pathogenesis of AD. 31193333: They are infectious such as prions or noninfectious such as beta-amyloid (Abeta) fibrils causing Alzheimer's disease (AD). 31211853: The abnormal accumulation of beta-amyloid peptide (Abeta) is recognized as a central component in the pathogenesis of Alzheimer disease. 31299145: Tracing the GSAP-APP C-99 Interaction Site in the beta-Amyloid Pathway Leading to Alzheimer's Disease. 31301179: Pretreatment with QCR potentiates the action of Sita in Abeta induced AD in rats. Activation of Nrf2 signaling by sitagliptin and quercetin combination against beta-amyloid induced Alzheimer's disease in rats. 31332160: Beta-amyloid (Abeta) peptide accumulation is considered as a primary cause of AD pathogenesis, with defective autophagy in patients' brains. 31458243: During the early stages of beta amyloid (Ab) peptide aggregation, toxic oligomers form which have been recognized as a likely cause of Alzheimer's disease. 31482248: Beta amyloid (Abeta) peptide aggregation and phosphorylated tau protein accumulation are considered as one of the causes for AD. 31629115: Beta-amyloid (Abeta) peptide accumulation has long been implicated in the pathogenesis of Alzheimer's disease (AD). 31639294: Previous studies have shown that fascaplysin might act on acetylcholinesterase and beta-amyloid (Abeta) to produce anti-AD properties. 31722781: Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. 31876283: Zinc ions and glycosaminoglycans (GAGs) are found in amyloid deposits and are known to modulate the beta-amyloid peptide (Abeta) aggregation, which is thought to be a key event in the pathogenesis of Alzheimer's disease (AD). 32035959: Sodium tanshinone IIA sulfonate protects against Abeta 1-42 -induced cellular toxicity by modulating Abeta-degrading enzymes in HT22 cells.beta-Amyloid (Abeta) plays an important role in the pathogenesis of Alzheimer's disease (AD). 32046518: This study investigated the mechanism which postulates that intraneuronal accumulation of amyloid aggregates for pathogenesis of AD. 32350803: CONCLUSIONS: The current ATN model of AD does not specify the subtype of beta-amyloid to be considered, which may be overlooking the differential roles that these two subtypes serve in the pathogenesis of AD. 32353422: The fibrillar peptide beta-amyloid (Abeta) has a chief function in the pathogenesis of AD. 32508629: Emerging evidence reveals that an aberrant accumulation of beta-amyloid (Abeta) is the main reason of Alzheimer's disease (AD) pathogenesis. 32831200: Dickkopf-1 Overexpression in vitro Nominates Candidate Blood Biomarkers Relating to Alzheimer's Disease Pathology.BACKGROUND: Previous studies suggest that Dickkopf-1 (DKK1), an inhibitor of Wnt signaling, plays a role in amyloid-induced toxicity and hence Alzheimer's disease (AD). 3288032: Theories pertinent to the origins of brain amyloid and its role in the pathogenesis of Alzheimer disease are discussed in relation to theories of the cause of this dementia. 32907613: Peroxiredoxin 6 mediates protective function of astrocytes in Abeta proteostasis.BACKGROUND: Disruption of beta-amyloid (Abeta) homeostasis is the initial culprit in Alzheimer's disease (AD) pathogenesis. 33092519: Amyloid-beta peptides slightly affect lifespan or antimicrobial peptide gene expression in Drosophila melanogaster.BACKGROUND: Beta-amyloid peptide (Abeta) is the key protein in the pathogenesis of Alzheimer's disease, the most common age-related neurodegenerative disorder in humans. 33186671: With this viewpoint article, we aim to challenge the traditional view of amyloid as the leading cause of AD. 33480241: Injection of ?-amyloid peptide (A?1-42) into the lateral ventricle was used to induce AD in rats. 33509204: Despite extensive research on the amyloid-based mechanism of AD pathogenesis, the underlying cause of AD is not fully understood. 34123738: Amyloid and tau protein abnormalities have been identified as the main causes of Alzheimer's disease but exact mechanisms remain to be revealed. 34299592: Beta (beta)-amyloid (Abeta) is a causative protein of Alzheimer's disease (AD). 34488020: These three amyloidogenic proteins forming amyloids under physiological conditions (pH 7.4 and 37C) served as model and are thought to be the causative proteins of AD, type 2 diabetes, and insulin-derived amyloidosis, respectively. 34520451: Synthesis of human amyloid restricted to liver results in an Alzheimer disease-like neurodegenerative phenotype. 35109309: BACKGROUND: The amyloid channel theory readily explains primary molecular damage induced by beta-amyloid (Abeta) but cannot interpret multiple major phenomena associated with Alzheimer's Disease such as autophagy failure and decreased metabolism. 36420978: Betaeta-amyloid (Abeta) is a neurotoxic protein that deposits early in the pathogenesis of preclinical Alzheimer's disease. 36856252: Effect of silibinin and trans-chalcone in an Alzheimer's disease-like model generated by insulin amyloids. 37774681: Our integrative analysis provides an organizing framework for targeting circuit dysfunction, neuroinflammation, and amyloid production early in AD pathogenesis. 38352874: Methods: Here, we evaluated the in vivo role of microglia-selective and full body inflammasome signalling in several mouse models of ss-amyloid-induced AD neuropathology. 38473975: An extensive body of genetic evidence suggests soluble aggregates of beta-amyloid (Abeta) as the primary neurotoxin in the pathogenesis of AD. New data suggest that the aggregation of misfolded native proteins initiates and drives the pathogenic cascade that leads to Alzheimer's disease (AD) and other age-related neurodegenerative disorders. Understanding the distinct roles of soluble and insoluble amyloid aggregates on AD pathogenesis has been the key missing piece of the Alzheimer's puzzle. 7491048: Our study suggests that the size of cortical area affected by beta-amyloid deposition is an important factor in the clinical manifestation of dementia, and lends support to the possibility that beta-amyloid is central to the aetiology of AD. 7565212: Amyloid, aluminium and the aetiology of Alzheimer's disease. 7708775: Normal control fibroblasts exposed to 10 nM beta-amyloid, the same concentration that induced AD-like K+ changes in control fibroblasts, showed a similar decrease in Cp20. 7750567: The non-enzymatic glycosylation of beta-amyloid is implicated in the aetiology of Alzheimer's disease. 7763339: Consequences of the molecular mechanism of amyloid formation for the understanding of the pathogenesis of Alzheimer's disease and the development of therapeutic strategies. 7812796: These observations have direct consequences for the interpretation of Alz-50 staining in diagnostic usage and for the assessment of Alzheimer's disease-like changes induced by beta-amyloid in experimental animal brains. 7822152: PURPOSE: Increased immunoreactivity (IR) of beta-amyloid and the amyloid-associated proteins tau and amyloid precursor protein (APP) in the brain have been linked to the pathogenesis of neurodegenerative disorders such as Alzheimer's disease. 8131745: Accumulation of the amyloid A beta peptide, which is derived from a larger precursor protein (APP), and the formation of plaques, are major events believed to be involved in the etiology of Alzheimer's disease. 8146663: In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation. Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels. 8159255: We probed serial and near serial sections of cerebellum from 13 Alzheimer's disease (AD), 10 older Down's syndrome (DS) patients, and 9 age-matched, non-AD controls, using single and double labeling immunohistochemistry to investigate the pathologic consequences of beta-amyloid or A4 (A beta) deposits in cerebellum and their relationship to Purkinje cells (PCs). 8185566: Besides the neurotoxic properties of beta-amyloid (beta A4), apolipoprotein E polymorphism seems to play an important role in the pathogenesis of sporadic Alzheimer's disease (AD). 8489324: CONCLUSION: The results of the study indicate the importance of neurofibrillary degeneration, not the deposition of amyloid, in the pathogenesis of Alzheimer's disease. 8604204: Amyloid, aluminum and the aetiology of Alzheimer's disease. 8606673: Amyloid, aluminium and the aetiology of Alzheimer's disease. 8706841: The overproduction of beta-amyloid (A beta) appears to be a primary cause of Alzheimer's disease (AD). 8740984: Four genes have thus far been implicated in the etiology of Alzheimer's disease (AD). The occurrence and effects of the mutations in APP and the fact that the epsilon 4 allele of ApoE are genetic risk factors point to the hypothesis that the extracellular deposition of beta-amyloid is the key initiating event in the pathogenesis of AD. 8761337: Soluble beta-amyloid induces Alzheimer's disease features in human fibroblasts and in neuronal tissues. 8997415: The importance of the beta-amyloid peptide in the pathogenesis of AD has been strengthened by the identification of pathogenic mutations in the APP gene on chromosome 21. 9116244: Since administration of anti-inflammatory drugs has been reported to possibly slow the progression of Alzheimer's disease, an effort was made to define effector functions induced by beta-amyloid (A beta) which may be inhibited by these drugs. 9168112: Although most of the molecular mechanisms involving beta-amyloid and APP in the aetiology of Alzheimer's disease are still unclear, changes in APP metabolism may be important in the pathogenesis of the disease. 9348103: Since the identification in 1984 of the amyloid beta protein (Abeta) as the major component of senile plaques and cerebrovascular amyloid in Alzheimer's disease (AD) brains, it is well accepted that the production of this protein is a crucial factor in the pathogenesis of AD. 9399697: These findings indicate that changes in cerebral betaA4 levels contribute to temporal lobe atrophy in AD and support the possibility that betaA4 is central to the etiology of AD. Pathological and biochemical studies indicate that beta-amyloid (betaA4) deposition is a hallmark in the pathogenesis of Alzheimer's disease (AD). 9630681: Experimental evidence increasingly implicates the beta-amyloid peptide in the pathogenesis of Alzheimer's disease. 9683325: Formation of beta-amyloid and neurofibrillary tangles in the brain due to genetic or other factors is the most frequent cause of Alzheimer's disease. 9794144: The particular contribution of muscarinic receptors, beta-amyloid and tau proteins in the pathogenesis of Alzheimer's disease remains still unclear. Probably Alzheimer's disease could be due to a progressive degeneration in the relationship between the three components covered in this review. 9865931: An increased beta-amyloid (Abeta) peptide is believed to play a central role in the pathogenesis of AD. 9928821: Strong genetic evidence has been accumulated in favor of a central role of beta-amyloid precursor protein (APP) and beta-amyloid peptide (betaA4) in the pathogenesis of Alzheimer's disease (AD). 11374584: The formation of amyloid fibrils is considered to be an important step in the aetiology of Alzheimer's disease and other amyloidoses. 11570871: The assembly of the beta-amyloid peptide (Abeta) into amyloid fibrils is essential to the pathogenesis of Alzheimer's disease. 11714802: These observations provide direct evidence of the ability of beta-amyloid fibrils to trigger activation of the classical C pathway and further support the hypothesis that C activation may be a component of the pathogenesis of Alzheimer's disease. 14640676: Protofibrils are transient structures observed during in vitro formation of mature amyloid fibrils and have been implicated as the toxic species responsible for cell dysfunction and neuronal loss in Alzheimer's disease (AD) and other protein aggregation diseases. 15980593: Elucidating the structural properties of early intermediates (protofibrils) on the fibril formation pathway of Abeta and alpha-synuclein, the structural relationship among the different intermediates and their relationship to the structure of the amyloid fibrils is critical for understanding the roles of amyloid fibril formation in the pathogenesis of Alzheimer's and Parkinson's diseases. 16178030: Mutations in AbetaPP cause deposition of Abeta amyloid fibrils in brain parenchyma and cerebral vessels, resulting in Alzheimer's disease (AD) and/or cerebral amyloid angiopathy (CAA). 16186179: Protein aggregation--and, more specifically, amyloid fibril formation--has been implicated as a primary cause of neurodegeneration in Alzheimer's disease, Parkinson's disease, and related disorders, but the mechanism by which this process triggers neuronal death is unknown. 16233815: Structure of beta-amyloid fibrils and its relevance to their neurotoxicity: implications for the pathogenesis of Alzheimer's disease. 22271749: Amyloid fibrils are known to be responsible for diseases such as Alzheimer's disease. 22468636: The misfolding and aggregation of amyloid-beta (Abeta) peptides into amyloid fibrils in solution and on the cell membrane has been linked to the pathogenesis of Alzheimer's disease. 22528091: The elucidation of the structure of amyloid fibrils and related aggregates is an important step towards understanding the pathogenesis of diseases such as Alzheimer's and Parkinson's, which feature protein misfolding and/or aggregation. 23415897: The formation of amyloid beta (Abeta) fibrils is crucial in initiating the cascade of pathological events that culminates in Alzheimer's disease. 23506133: The misfolding and aggregation of amyloid-beta (Abeta) peptides into amyloid fibrils is regarded as one of the causative events in the pathogenesis of Alzheimer's disease (AD). 23650245: Amyloid fibril formation is a critical step in Alzheimer's disease (AD) pathogenesis. 24247242: The interconversion of monomers, oligomers, and amyloid fibrils of the amyloid-beta peptide (Abeta) has been implicated in the pathogenesis of Alzheimer disease. 25343100: Aggregation of Abeta under the form of amyloid fibrils has long been considered central to the pathogenesis of AD. 25874995: The misfolding and aggregation of amyloid beta (Abeta) peptides into amyloid fibrils are key events in the amyloid cascade hypothesis for the etiology of Alzheimer's disease (AD). 26206266: Finally, the surface-enhanced Raman scattering (SERS) activity of these HNS was investigated by using thioflavin T, a biomarker of the beta-amyloid fibril formation, responsible for Alzheimer's disease. 28750656: Although amyloid fibrils were originally considered responsible for AD pathogenesis, recent convincing evidence strongly implicates soluble oligomeric Abeta as the primary neurotoxic species driving disease progression. 29107146: The NABi blocks Abeta-fibril formation in vitro and in vivo and prevents neuronal cell death, a hallmark of AD pathogenesis. 29704282: Taken together, this study illustrates dysfunction of hippocampal silent synapse in the rodent model of AD, which might result from the impairments of actin cytoskeleton and postsynaptic scaffolding proteins induced by amyloid fibrils. 30264484: Beta-secretase 1 (BACE-1) is an aspartyl protease implicated in the overproduction of beta-amyloid fibrils responsible for Alzheimer disease. 30979271: The formation of amyloid fibrils is considered to be one of the main causes for many neurodegenerative diseases, such as Alzheimer's, Parkinson's or Huntington's disease. 31291354: Accumulation of amyloid beta (Abeta) peptides, the major component of amyloid fibrils in senile plaques, is one of the main causes of Alzheimer's disease. 34480905: Accumulating evidence indicates that amyloid oligomers, not amyloid fibrils, are the most toxic species that causes Alzheimer's disease (AD) and Parkinson's disease (PD). 35213966: The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer's Disease. 35458686: Alzheimer's disease is understood to be caused by amyloid fibrils and oligomers formed by aggregated amyloid-beta (Abeta) peptides. 36297599: Senile plaques composed of amyloid beta (Abeta) fibrils are considered the leading cause of Alzheimer's disease (AD). 36305141: Alzheimer's disease is caused by extracellular amyloid fibrils containing the peptide Amyloid beta (Abeta) accumulating in the brain. 8621479: Polymerization of amyloid beta-peptide (Abeta) into amyloid fibrils is a critical step in the pathogenesis of Alzheimer's disease. 9689467: The aggregation of soluble A beta into insoluble amyloid fibrils is believed to be an important step in the pathogenesis of Alzheimer's disease (AD) and the prevention of this process therefore seems to be a promising strategy for the treatment of AD. 31901901: A novel rhamnoside derivative PL402 up-regulates matrix metalloproteinase 3/9 to promote Abeta degradation and alleviates Alzheimer's-like pathology.The accumulation of amyloid-beta (Abeta), considered as the major cause of Alzheimer's disease (AD) pathogenesis, relays on the rate of its biosynthesis and degradation. 31951717: Amyloid beta is of particular interest as its oligomerization and aggregation are major events in the etiology of Alzheimer's disease, and it is known that interactions between the peptide and bioavailable metal cations have the potential to significantly damage neurons. 32061803: The response of astrocytes to the presence of Abeta as well astrocytic and microglial interaction and inflammatory cytokine release is also discussed, highlighting a cyclical behaviour of these cells in contributing to AD pathogenesis. 32144141: Thus, we reveal the Abeta-burdened neuron as a primary proinflammatory agent, implicating the intraneuronal accumulation of Abeta as a significant immunological component in the AD pathogenesis. 32146679: Microglial dysregulation, pertaining to impairment in phagocytosis, clearance and containment of amyloid-beta (Abeta), and activation of neuroinflammation, has been posited to contribute to the pathogenesis of Alzheimer's disease (AD). 32154567: Neuronal Aquaporin 1 inhibits amyloidogenesis by suppressing the interaction between beta-secretase and amyloid precursor protein.The accumulation of amyloid beta (Abeta) is a characteristic event in the pathogenesis of Alzheimer's disease (AD). 32165044: Defective immune cell-mediated clearance of amyloid-beta (Abeta) and Abeta-associated inflammatory activation of immune cells are key contributors in pathogenesis of Alzheimer's disease (AD). 32229231: Nanogold neuroprotection in human neural stem cells against Amyloid-beta-induced mitochondrial dysfunction.Alzheimer's disease (AD) is a neuronal dementia with progressive memory loss. 32238175: CONCLUSIONS: Overall, our RNA-seq data provide a valuable resource for future investigations into the roles of microglia and astrocytes in aging- and amyloid-beta-induced AD pathologies. 32244832: The cerebral accumulation of amyloid-beta (Abeta) is a critical molecular event in the pathogenesis of AD. 32381118: Amyloid-beta (Abeta) is suggested to play a pivotal role in the pathogenesis of AD, and clearance of Abeta from the brain becomes a main therapeutic strategy for AD. 32403399: Amyloid-beta and tau proteins are triggers for AD pathogenesis, and usually used as AD candidate biomarkers in the clinical research. 32525440: Fluid transport in the perivascular space by the glia-lymphatic (glymphatic) system is important for the removal of solutes from the brain parenchyma, including peptides such as amyloid-beta which are implicated in the pathogenesis of Alzheimer's disease. 32559516: Amyloid beta (Abeta) is an intricate molecule that interacts with several biomolecules and/or produces insoluble assemblies and eventually the nonphysiological depositions of its alternate with normal neuronal conditions leading to Alzheimer's disease (AD). Revisiting the role of brain and peripheral Abeta in the pathogenesis of Alzheimer's disease. 32569471: Neuroprotective Effects of Triterpenoids from Camellia japonica against Amyloid beta-Induced Neuronal Damage.Alzheimer's disease (AD), a neurocognitive impairment affecting human mental capacity, is related to the accumulation of amyloid-beta peptide (Abeta) and the hyperphosphorylation of tau protein. 32588983: An agnostic reevaluation of the amyloid cascade hypothesis of Alzheimer's disease pathogenesis: The role of APP homeostasis.OBJECTIVE: To reassess the role of amyloid beta (Abeta) and the amyloid precursor protein (APP) system in the pathogenesis of Alzheimer's disease (AD). 32599720: Evaluation of Amyloid beta 42 Aggregation Inhibitory Activity of Commercial Dressings by A Microliter-Scale High-Throughput Screening System Using Quantum-Dot Nanoprobes.The aggregation and accumulation of amyloid beta (Abeta) in the brain is a trigger of pathogenesis for Alzheimer's disease. 32601313: Analyzing microglial-associated Abeta in Alzheimer's disease transgenic mice with a novel mid-domain Abeta-antibody.The mechanisms of amyloid-beta (Abeta)-degradation and clearance in Alzheimer's disease (AD) pathogenesis have been relatively little studied. 32649026: Alzheimer's Disease risk modifier genes do not affect tau aggregate uptake, seeding or maintenance in cell models.Alzheimer's disease (AD) afflicts millions of people worldwide and is caused by accumulated amyloid beta and tau pathology. 32725265: Increasing activity of post-synaptic kinase p38gamma that targets T205 in tau reduced memory deficits in symptomatic Abeta-induced AD models. 32804091: APOE-E4 reduces the levels of neuronal cholesterol, interferes with the transportation of cholesterol, impairs repair of synapses, decreases the clearance of neurotoxic peptide amyloid-beta (Abeta), and promotes the deposition of amyloid plaque, and eventually may cause development of AD. 32816241: Dimethyl Fumarate Mitigates Tauopathy in Abeta-Induced Neuroblastoma SH-SY5Y Cells.Alzheimer's disease pathogenesis is measured by two key hallmarks viz extracellular senile plaques composed of insoluble amyloid beta (Abeta) and neurofibrillary tangles composed of hyperphosphorylated tau, resulting in microtubule destabilization, synaptic damage and neurodegeneration. 32832007: Amyloid beta - (A beta -) induced mitochondrial dysfunction may be a primary process triggering all the cascades of events that lead to AD. 32926328: 5-N-ethyl Carboxamidoadenosine Stimulates Adenosine-2b Receptor-Mediated Mitogen-Activated Protein Kinase Pathway to Improve Brain Mitochondrial Function in Amyloid Beta-Induced Cognitive Deficit Mice.Alzheimer's disease (AD) is a progressive neurodegenerative disorder with loss in memory as one of the cardinal features. 32949547: Cerebral amyloid angiopathy can cause life-threatening brain haemorrhages; yet, there is no proof that the transmission of amyloid beta can also lead to Alzheimer's dementia. 32985682: Gut amyloid-beta induces cognitive deficits and Alzheimer's disease-related histopathology in a mouse model. 32993092: Lupeol, a Plant-Derived Flavonoid, Protects Mice Brains against Abeta-Induced Oxidative Stress and Neurodegeneration.Alzheimer's disease (AD) is a progressive neurodegenerative disorder that represents 60-70% of all dementia cases. 33014538: Besides extracellular deposition of amyloid beta and formation of phosphorylated tau in the brains of patients with Alzheimer's disease (AD), the pathogenesis of AD is also thought to involve mitochondrial dysfunctions and altered neurotransmission systems. 33059154: Cobalt(III) Schiff base complexes stabilize non-fibrillar amyloid-beta aggregates with reduced toxicity.The aggregation of amyloid-beta (Abeta) is believed to be foundational to the pathogenesis of Alzheimer's disease (AD). 33106917: Amyloid-beta (Abeta) plays a pivotal role in the pathogenesis of Alzheimer's disease (AD) and has been regarded as the main therapeutic target for AD. 31949779: The abnormal accumulation and deposition of amyloid-beta peptide (Abeta) in senile plaques and cerebral vasculature is widely recognized to be the most likely culprit in the pathogenesis of AD. 31991578: AD mutations contribute to the generation of toxic amyloid beta (Abeta) peptides and the formation of cerebral plaques, leading to the formulation of the amyloid cascade hypothesis for AD pathogenesis. 32028683: Amyloid-beta (Abeta) peptides play a crucial role in the pathogenesis of Alzheimer's disease (AD). 32046252: Interaction of Abeta42 with Membranes Triggers the Self-Assembly into Oligomers.The self-assembly of amyloid beta (Abeta) proteins into oligomers is the major pathogenic event leading to Alzheimer's disease (AD). 32142821: Abeta-ganglioside interactions in the pathogenesis of Alzheimer's disease.It is widely accepted that the abnormal self-association of amyloid beta-protein (Abeta) is central to the pathogenesis of Alzheimer's disease, the most common form of dementia. 32210564: Purpose: Amyloid-beta protein (Abeta) is one of the causative proteins of Alzheimer's disease. 32272441: Multiple lines of evidence indicate that amyloid beta (Abeta) peptide is responsible for the pathological devastation caused in Alzheimer's disease (AD). 32307772: Identification of calcium and integrin-binding protein 1 as a novel regulator of production of amyloid beta peptide using CRISPR/Cas9-based screening system.The aberrant metabolism of amyloid beta peptide (Abeta) has been implicated in the etiology of Alzheimer disease (AD). 32354467: Successive cleavage of beta-amyloid precursor protein by gamma-secretase.gamma-Secretase is a multimeric aspartyl protease that cleaves the membrane-spanning region of the beta-carboxyl terminal fragment (betaCTF) generated from beta-amyloid precursor protein. gamma-Secretase defines the generated molecular species of amyloid beta-protein (Abeta), a critical molecule in the pathogenesis of Alzheimer's disease (AD). 32372339: BACKGROUND: Acetylcholine deficiencies in hippocampus and cortex, aggregation of beta-amyloid, and beta-secretase over activity have been introduced as main reasons in pathogenesis of Alzheimer's disease. 32444869: Amyloidogenic processing of Alzheimer's disease beta-amyloid precursor protein induces cellular iron retention.The proteolytic cleavage of beta-amyloid precursor protein (APP) to form the amyloid beta (Abeta) peptide is related to the pathogenesis of Alzheimer's disease (AD) because APP mutations that influence this processing either induce familial AD or mitigate the risk of AD. 32580638: Herein, using both molecular dynamics and quantum mechanics, the binding mechanisms of APOE4 leading to the AD are unraveled and now available for drug design. Salt bridges for the APOE correct folding are missing in APOE4, resulting in an increased deposition of the amyloid-beta peptide, compared to APOE3, which can lead to the AD. 32683653: Amyloid-beta (Abeta) peptides play a significant role in the pathogenesis of Alzheimer's disease (AD). 32733240: The Neuroprotective Action of Amidated-Kyotorphin on Amyloid beta Peptide-Induced Alzheimer's Disease Pathophysiology. 32848600: Major efforts in AD drug were devoted to the interference with the production and accumulation of amyloid-beta peptide (Abeta), which plays a causal role in the pathogenesis of AD. 32973471: Studies focused on nonpharmacological treatment for AD have been developed to act on brain plasticity and minimize the neurotoxicity caused by the amyloid-beta (Abeta) peptide. 32975365: Evidence that in Down syndrome (DS), a population markedly predisposed to develop early onset AD, increased APP gene dose is necessary for both AD neuropathology and dementia points to normalization of the levels of the amyloid precursor protein (APP) and its products as a route to further define AD pathogenesis and discovering novel treatments. NEW/UPDATED HYPOTHESIS: We hypothesize that the increase in APP gene dose in DS initiates a process in which increased levels of full-length APP (fl-APP) and its products, including beta-CTF and possibly Abeta peptides (Abeta42 and Abeta40), drive AD pathogenesis through an endosome-dependent mechanism(s), which compromises transport of neurotrophic signals. Moreover, upregulation of fl-APP protein and products may drive downstream events that dysregulate tau homeostasis and inflammatory responses that contribute to propagation of AD pathogenesis. 32990912: Amyloid beta protein (Abeta) deposition is the main pathogenesis of AD, and many studies have shown that Abeta accumulation is toxic to neurons, leading to the inflammatory reaction, neuronal apoptosis, and neurofibrillary tangles. 33010207: Aggregation, fibril formation, and deposition of amyloid beta (Abeta) protein are believed to be the central pathogeneses of Alzheimer's disease (AD). 33066971: This study investigated whether early-life and chronic exposure to DEHP affects AD via the toxicity of amyloid-beta (Abeta), which has been implicated in the pathogenesis of AD, using Caenorhabditis elegans AD models (strains CL4176 and CL2006). 33074279: Excess aggregation of amyloid beta peptide (Abeta) is a fatal cause of Alzheimer's disease (AD), which leads to physiological toxicity. 33132896: Accumulation of amyloid beta is a key event in Alzheimer's disease pathogenesis. 33189440: Further spatial memory assays in Abeta-induced AD model showed that 22 enhanced the ability of learning and memory. 33208229: The accumulation and aggregation of amyloid-beta (Abeta) are critical factors in the pathogenesis of Alzheimer's disease (AD). 33224974: Particularly, the aggregation of misfolded amyloid- beta and hyperphosphorylated tau and alpha -synuclein are linked to the pathogenesis of AD and PD, respectively. 33225679: The accumulation and deposition of beta-amyloid (Abeta) is one postulated cause of Alzheimer's disease (AD). 33238667: [Roles of amyloid-beta in the pathogenesis of cerebral amyloid angiopathy and Alzheimer's disease should be clarified]. 33258115: A variety of findings from in vitro experiments and animal models support the hypothesis that one contribution to pathogenesis in Alzheimer's disease (AD) is enhanced phosphorylation of tau protein, which may be triggered by amyloid beta (Abeta) and mediated by impaired activity of the PI3K/Akt signaling pathway. 33279620: The amyloid beta protein cascade hypothesis places the formation of amyloid beta protein aggregates on the first position in the complex pathological cascade leading to neurodegeneration, and therefore AD might be considered to be a protein-misfolding disease. 33310049: In the present study, we tested whether pinoresinol reduces learning and memory and excitatory synaptic deficits in an amyloid beta (Abeta)-induced AD-like mouse model. 33353018: We evaluated the effects of a grain diet rich in anthocyanins in a mouse model of Alzheimer's disease induced by amyloid-beta (Abeta) and a transgenic mouse model of Parkinson's disease (PD) with overexpression of human alpha-synuclein. 33359145: Accumulating evidences suggest that amyloid beta (Abeta)-peptide plays a key role in pathogenesis of Alzheimer's disease (AD) through aggregation and deposition into plaques in neuronal cells. 33386802: Such stress provides the activation energy needed to induce conformational changes of both Abeta and tau within the lower brain and brainstem region, producing unique neurotoxic oligomer molecule conformations that induce AD. 33400522: Cu, Zn, and amyloid-beta (Abeta) peptides play an important role in the etiology of Alzheimer's disease (AD). 33401892: Cu 2+ -mediated amyloid beta-protein (Abeta) aggregation is implicated in the pathogenesis of Alzheimer's disease, so it is of significance to understand Cu 2+ -mediated conformational transitions of Abeta. 33414705: Misfolding and extracellular aggregation of Amyloid-beta (Abeta) peptides are recognized as the main cause of AD progression, leading to the formation of toxic Abeta oligomers and to the deposition of beta-amyloid plaques in the brain, representing the hallmarks of AD. 33426095: Amyloid beta peptides (A beta 1-42) have been found to be associated with the cause of Alzheimer's disease (AD) and dementia. 33495810: The generation of beta-amyloid protein (Abeta) is considered a key step in the pathogenesis of Alzheimer's disease (AD) and the regulation of its production is an important therapeutic strategy. 33503934: Aggregation of amyloid-beta (abeta) peptides into toxic oligomers, fibrils, and plaques is central in the molecular pathogenesis of Alzheimer's disease (AD) and is the primary focus of AD diagnostics. 33508037: Intraneuronal rise of amyloid beta in its oligomeric forms (iAbetaOs), has been linked to the pathogenesis of AD by disrupting cytosolic Ca2+ homeostasis. 33535469: Amyloid beta (Abeta) peptide is an important pathological factor that triggers the progression of AD through accumulation and aggregation, which leads to AD-related pathologies that consequently affect cognitive functions. 33560154: Areas covered : Considering the significance of Abeta and Tau in AD pathogenesis, these proteins have currently been adopted as the core biomarkers of AD, and their quantification has provided precise diagnostic information to develop next-generation AD therapeutic approaches. 33571523: Beta-amyloid (Abeta) has been recognized as an early trigger in the pathogenesis of Alzheimer's disease (AD) leading to synaptic and cognitive impairments. 33571524: gamma-secretase is responsible for the proteolysis of amyloid precursor protein (APP) into amyloid-beta (Abeta) peptides, which are centrally implicated in the pathogenesis of Alzheimer's disease (AD). 33624157: METHODS: For the induction of Alzheimer's disease, amyloid beta (Abeta) 1-42 was injected in the CA1 region of the hippocampus. 33716668: (Dys)regulation of Synaptic Activity and Neurotransmitter Release by beta-Amyloid: A Look Beyond Alzheimer's Disease Pathogenesis. 33727592: Amyloid plaques are small (~ 50 MUm), highly-dense aggregates of amyloid beta (Abeta) protein in brain tissue, supposed to play a key role in pathogenesis of Alzheimer's disease (AD). 33750486: Ovariectomized Sprague-Dawley rats were fed high-fat(H-F) or H-P diets for two weeks, and then they had a hippocampal infusion of beta-amyloid(25-35) for 4 weeks to induce AD and an injection of monoidoacetate(MIA) into the articular cartilage to induce osteoarthritis. We hypothesized that Alzheimer's-like disease (AD) exacerbates osteoarthritis and that intermittent fasting(IMF) with a high-protein(H-P) diet would enhance memory function and relieve osteoarthritis symptoms in estrogen-deficient animals with surgically induced AD and osteoarthritis. 33785017: BACKGROUND: Alzheimer's disease (AD), an age-related neurodegenerative disorder and a serious public health concern, is mainly caused by beta-amyloid (Abeta)-induced toxicity. 33803769: The aggregation of amyloid beta (Abeta) peptides and deposition of amyloid plaques are implicated in the pathogenesis of Alzheimer's disease (AD). 33828600: AD was induced by amyloid-beta (Abeta 1-42 ) (10 MUg/2 MUL, intracerebroventricular injection, icv) and then BVS at 20, 40, and 80 mg/kg were injected intraperitoneally (ip) in six equal intervals over 21 days. 33845371: Here, we review novel findings that have shifted our understanding of the role of Abeta in the pathogenesis of Alzheimer's disease. 33848635: The imbalance between production and clearance of amyloid beta (Abeta) peptides and their resulting accumulation in the brain is an early and crucial step in the pathogenesis of Alzheimer's disease (AD). 33851209: Amyloid formation and the deposition of the amyloid-beta peptide are hallmarks of Alzheimer's disease pathogenesis. 33875089: Recent studies found that the cellular uptake of extracellular amyloid beta (Abeta) peptides can lead to a build-up of intracellular Abeta in certain neuronal cells, which consequently lead to the onset of AD pathogenesis. 33876786: A comparative study of the effects of phosphatidylserine rich in DHA and EPA on Abeta-induced Alzheimer's disease using cell models. 33898246: In the present study, we report that SST has preventive effects on memory impairment and neuronal cell changes in an Abeta-induced AD-like mouse model. Korean traditional herbal formula Soshiho-tang attenuates memory impairment and neuronal damage in mice with amyloid-beta-induced Alzheimer's disease. 33908427: The accumulation of toxic soluble oligomers of the amyloid-beta peptide (Abeta) is a key step in the pathogenesis of Alzheimer's disease. 33935701: Here, we investigated the neuroprotective effects of F. erecta Thunb. against cognitive deficit and neuronal damage in a mouse model of amyloid-beta (Abeta)-induced AD. Leaves Ameliorate Cognitive Deficit and Neuronal Damage in a Mouse Model of Amyloid-beta-Induced Alzheimer's Disease. 33967797: Alzheimer's disease (AD) is one of the most common neurodegenerative diseases and accumulating evidences suggest a key role of amyloid-beta (Abeta) peptide in the pathogenesis of AD. 33976546: The amyloid cascade hypothesis, claiming that excess production or reduced clearance of amyloid-beta (Abeta) and its aggregation into amyloid plaques, was accepted for a long time as the main cause of AD. 33977265: Accumulation of amyloid beta peptides is thought to initiate the pathogenesis of Alzheimer's disease. 34006557: As amyloid-beta (Abeta) is regarded as the core pathological change and the trigger mechanism of AD, anti-Abeta therapy may be an effective therapy. 34051062: An emerging concept is that the amyloid-beta (Abeta) peptide, which was until recently deemed a major player in the cause of AD, may instead modulate synaptic plasticity and protect against excitotoxicity. The link between Abeta-mediated synaptic plasticity and Abeta trafficking is central for understanding AD pathogenesis and remains a perplexing relationship. Based on existing literature, as a signaling molecule, Abeta is proposed to modulate its own turnover and synaptic plasticity through what is currently believed to be the cause of AD: the transient formation of pore-like oligomers. 34053209: Treadmill Running Improves Spatial Learning Memory Through Inactivation of Nuclear Factor Kappa B/Mitogen-Activated Protein Kinase Signaling Pathway in Amyloid-beta-Induced Alzheimer Disease Rats. 34078792: Amyloid beta (Abeta) is one of the causative proteins of AD. 34080759: The relationship between neuronal loss and Abeta deposits is one of the fundamental questions in the pathogenesis of AD. 34084446: The excessive production and deposition of amyloid-beta (Abeta) is one of the most important etiologies of Alzheimer's disease (AD). 34086399: The aggregation and deposition of amyloid beta (Abeta) peptide onto neuronal cells, with consequent cellular membrane perturbation, are central to the pathogenesis of Alzheimer's disease (AD). 34099032: BACKGROUND: The aggregation of amyloid beta (Abeta) is central in the pathogenesis of Alzheimer's disease (AD). 34133880: The aggregation of amyloid beta (Abeta) peptide with subsequent formation of fibrils which deposit in senile plaques is considered one of the key triggers of Alzheimer's disease (AD). 34151790: Sustained Hippocampal Neural Plasticity Questions the Reproducibility of an Amyloid-beta-Induced Alzheimer's Disease Model. 34280181: Oligomers of the amyloid beta-protein (Abeta) have been implicated in the pathogenesis of Alzheimer's disease (AD) through their toxicity towards neurons. 34285489: Purpose: Amyloid-beta (Abeta) is a brain protein that causes Alzheimer's disease. 34286787: Additionally, they were able to inhibit the aggregation of amyloid-beta, one of the hallmarks in AD pathogenesis, and to exhibit considerable antioxidant capacity. 34294676: Failures of clinical trials targeting amyloid-beta protein (Abeta), a key trigger of AD, have been explained by drug inefficiency regardless of the mechanisms of amyloid neurotoxicity, which are very difficult to address by available technologies. 34299316: In addition, since toxic aggregates of amyloid-beta (Abeta) have been proposed as one of the major causes of the disease, the mechanism of clearing Abeta is also required to be investigated to reveal the etiology of AD clearly. Dyshomeostasis of these redox-active metal ions in the brain could cause Alzheimer's disease (AD). 34343891: The accumulation of amyloid beta (Abeta) peptides in the human brain leads to AD. 34407949: Synapse loss at early stages of Alzheimer's disease is thought to be induced by beta-amyloid (Abeta) pathology. 34411643: Chemical inhibition of sEH by TPPU, a selective sEH inhibitor, alleviated spatial learning and memory deficits, and elevated levels of neurotransmitters in Abeta-induced AD mice. In this study, we evaluated the vital role of sEH in amyloid beta (Abeta)-induced AD mice, and revealed a possible molecular mechanism for inhibition of sEH in the treatment of AD. The results showed that the sEH expression and activity were remarkably increased in the hippocampus of Abeta-induced AD mice. 34446574: Using mixed gender human temporal cortex and cultured hippocampal neurons from rats we further show that this balance is perturbed during Alzheimer's disease (AD) because of amyloid beta (Abeta)-driven reduction in Ly6h, with severe reduction leading to increased phosphorylated tau and alpha7-mediated neurotoxicity. 34502282: To investigate its therapeutic effects on AD pathology, we administered aripiprazole to 5xFAD AD model mice and examined beta-amyloid (betaA)-induced AD-like phenotypes, including betaA production, neuroinflammation, and cerebral glucose metabolism. 34628876: BACKGROUND: Alzheimer's disease (AD) is a progressive dementia, and beta-amyloid (Abeta) accumulation is widely regarded as the primary pathogenesis of AD. 34654465: METHODS: We examined relationships between CSF p-Tau/Abeta 40 , and CSF Abeta 42 /Abeta 40 , Abeta PET, and white matter hyperintensities (WMH) as well as vascular risk factors in 149 cognitively unimpaired and 52 impaired individuals who were presumably not on the Alzheimer's disease (AD) pathway due to negative Abeta status on both CSF and PET. 34669098: Moreover, plant-based foods containing flavonoids were previously reported to show neuroprotective effects by modulating self-aggregation of amyloid-beta (Abeta)/or tau peptide into oligomers and fibrils, associated with the pathogenesis of AD. 34671708: According to the glymphatic hypothesis, in physiological conditions, cerebrospinal fluid flows primarily during sleep and serves to remove metabolic wastes like the amyloid-beta and tau proteins whose accumulation is believed to cause Alzheimer's disease. 34677321: Abnormal amyloid beta protein (Abeta) accumulation is believed to be the most common cause of AD. 34695393: This study explored the effects of chronic stimulation of 5-HT4R on cognition, memory, long-term potentiation (LTP), paired-pulse ratio (PPR), and neuronal apoptosis in a rat model of amyloid-beta (Abeta)-induced AD. 34715093: Here we investigate the potential of concurrent exercise to prevent recognition memory deficits in an Alzheimer's disease-like model induced by the hippocampal beta-amyloid (Abeta) injection in Wistar rats. 34733055: Background: Alzheimer's disease (AD), a prevalent neurodegenerative disease with progressive dementia and neurotransmission (NT)-dysfunction-related complications in older adults, is known to be caused by abnormal Amyloid-beta (Abeta) peptide and associated amyloid plaques in the brain. 34789556: Erratum: Medeiros et al., \Connecting TNF-alpha Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid beta Protein\. 34798299: Coenzyme Q10, which scavenges FA, was shown to ameliorate Abeta-induced AD pathological phenotypes, thus suggesting a causative relation between FA toxicity and AD. 34801648: In our study, our established 3D gelatin scaffold model and a well characterized in vivo (APP/PS1) murine model of AD were used to directly investigate the molecular, biochemical and behavioural effects of neuronal stem cell exposure to Abeta to improve understanding of the in vivo etiology of AD. 34832029: Amyloid beta (Abeta) is a transmembrane protein known to play a major role in the pathogenesis of AD. 34838849: MAIN METHODS: Neuroblastoma cell line SH-SY5Y was treated with beta-amyloid (Abeta) to induce AD-like pathological changes, which serves as Alzheimer's disease model. 34856900: However, given the well-described role of misfolding peptides, particularly beta-amyloid (Abeta), in the pathogenesis of AD, the need for a broad-based conceptualization of AD, coalescing different theories into a single harmonized explanation emerges as a viable alternative. 34861133: Mounting evidence suggests that amyloid-beta (Abeta) and vascular etiologies are intertwined in the pathogenesis of Alzheimer's disease (AD). 34867177: Amyloid beta (Abeta) and alpha-synuclein are two of the most investigated proteins, whose pathological aggregation and spreading are crucial to the pathogenesis of AD and PD, respectively. 34878807: The main pathological phenomena of AD are the accumulation of beta-amyloid (Abeta), neurofibrillary tangles, and neuroinflammation, however, the specific molecular mechanism of pathogenesis of AD is not fully clear. 34943094: The abnormal extracellular accumulation and deposition of the peptide amyloid-beta (Abeta) is considered as an early toxic event in AD pathogenesis, which initiates a series of events leading to neuronal dysfunction and death. 34971171: Fibroblast Growth Factor 21 and Autophagy Modulation Ameliorates Amyloid beta-Induced Alzheimer Disease Pathology in Rats. 35013124: All together, these findings suggest that L1-70 contributes to the clearance of Abeta in AD, thereby adding a novel perspective in understanding AD pathogenesis. 35019536: Two major amyloid-beta peptide (Abeta) variants, Abeta 42 and Abeta 40 , play a pivotal role in the etiology of AD and the concentration ratio of which (i.e., Abeta 42 %) has been suggested to be the superior biomarker for AD. 35043380: Amyloid-beta-induced Alzheimer's disease (AD) and its further complications are well-established models in preclinical studies and demonstrated by many researchers. Avicularin Attenuates Memory Impairment in Rats with Amyloid Beta-Induced Alzheimer's Disease. 35108926: Transport across the BBB is an important mediator of beta-amyloid (Abeta) accumulation in the brain and a contributing factor in the pathogenesis of Alzheimer's disease (AD). 35109138: Microglia, specialized phagocytic cells of the brain, likewise play a critical role in the clearance of cellular debris, particularly amyloid beta, which is involved in the pathogenesis of Alzheimer's disease. 35109187: Increasing activity of post-synaptic kinase p38gamma that targets T205 in tau reduced memory deficits in symptomatic Abeta-induced AD models. 35122611: Optimal Formula of Angelica sinensis Ameliorates Memory Deficits in beta-amyloid Protein-induced Alzheimer's Disease Rat Model. 35134462: PINK1 regulates mitochondrial fission/fusion and neuroinflammation in beta-amyloid-induced Alzheimer's disease models. 35148068: Abnormal aggregation and subsequent fibrillogenesis of amyloid-beta protein (Abeta) can cause Alzheimer's disease (AD). 35156141: For the purpose of discovering potential inhibitors of beta-amyloid (BACE1), which is a crucial element in Alzheimer's disease (AD) pathogenesis, an in silico study of naturally occurring compounds was performed using precise computational approaches. 35212149: Here, we aim to refocus the amyloid cascade hypothesis on its original premise that the accumulation of amyloid beta (Abeta) peptide is the primary and earliest event in AD pathogenesis as based on current evidence, initiating several pathological events and ultimately leading to AD dementia. 35214143: Neurofibrillary tangles (NFTs) composed of tau rather than senile plaques composed of Abeta are correlated with AD pathogenesis. 35281253: The aggregation of beta-amyloid peptide (Abeta) is one potential cause for Alzheimer's disease (AD). 35294796: INTRODUCTION: Amyloid beta (Abeta) is a brain protein that causes Alzheimer's disease (AD). 35306343: Here, we analyzed the process of aggregation and accumulation of amyloid beta (Abeta), which causes the development of Alzheimer's disease (AD), by real-time 3D imaging under physiological conditions using a quantum dot nanoprobe that we previously developed. 35372522: The cytotoxic self-aggregation of beta-amyloid (Abeta) peptide and islet amyloid polypeptide (IAPP) is implicated in the pathogenesis of Alzheimer's disease (AD) and Type 2 diabetes (T2D), respectively. 35443153: Amyloid-beta and tau are key molecules in the pathogenesis of Alzheimer's disease, but it remains unclear how these proteins interact to promote disease. 35443198: The present study was aimed to evaluate the effect of HIIT exercise and ecdy consumption synergistically on the changes in learning and memory functions, activities of hippocampal antioxidant enzymes, and neuronal population after AD induced by Abeta in male rats. 35459147: These observations have given rise to the theory that Abeta is the primary trigger of AD, and induces proinflammatory activation of immune brain cells (i.e., microglia), which culminates in neuronal damage and cognitive decline. 35474400: The accumulation of amyloid-beta at the neuronal sites is a major pathological hallmark involved in the etiology of Alzheimer's disease. 35531555: The development of hQC inhibitors could prevent the self-aggregation of Abeta peptides, resulting in impeding AD. 35631608: Subsequently, beta-amyloid (Abeta) was added into the brain-on-a-chip system to generate an AD-on-a-chip model, and toxic effects on neurons and the degeneration of synapses were observed. 35656096: While AD research is dominated by protein/peptide-centric research based on the amyloid hypothesis, a theory that designates dysfunction in beta-amyloid production, accumulation, or disposal as the primary cause of AD, many studies focus on metabolomics as a means of understanding the biological processes behind AD progression. 35663520: In this paper, we follow up with our preliminary biological studies that showed that Repeated electromagnetic field stimulation (REMFS) decreased the toxic amyloid-beta (A beta ) levels, which is considered to be the cause of Alzheimer's disease (AD). 35666692: These studies will enhance the physicochemical understanding of the structural changes of Abeta at the heterogeneous interfaces and the mechanism of Alzheimer's disease pathogenesis. 35741166: Accumulation of aggregated amyloid-beta (Abeta) in the brain is considered the first pathological event within the pathogenesis of Alzheimer's disease (AD). 35742862: Disposition of amyloid beta (Abeta) into the perivascular space of the cerebral cortex has been recently suggested as a major source of its clearance, and its disturbance may be involved in the pathogenesis of cerebral amyloid angiopathy and Alzheimer's disease. 35759136: Alzheimer's disease (AD) is a type of dementia characterized by the deposition of amyloid beta, a causative protein of AD, in the brain. 35762411: Excessive accumulation of amyloid-beta (Abeta) is the leading cause of Alzheimer's disease (AD). 35928227: C99 is the immediate precursor for amyloid beta (Abeta) and therefore is a central intermediate in the pathway that is believed to result in Alzheimer's disease (AD). 35956985: Anti-Inflammatory Activity of 4-(4-(Heptyloxy)phenyl)-2,4-dihydro-3 H -1,2,4-triazol-3-one via Repression of MAPK/NF-kappaB Signaling Pathways in beta-Amyloid-Induced Alzheimer's Disease Models. In this study, the neuroprotective effects of 4-(4-(heptyloxy)phenyl)-2,4-dihydro-3 H -1,2,4-triazol-3-one (W112) against beta-amyloid (Abeta)-induced AD pathology and its possible mechanism were explored both in vitro and in vivo. The results showed that W112 exhibits a neuroprotective role against Abeta-induced cytotoxicity in PC12 cells and improves the learning and memory abilities of Abeta-induced AD-like rats. 36015135: Pretreatment with the KBD formula for 14 days significantly improved the short- and long-term memory performance of Abeta-induced AD rats as assessed by the Morris Water Maze (MWM) and object-recognition tests. The main purpose of the present study was to determine the protective effect and mechanism of KBD in amyloid beta (Abeta)-induced AD rats and its toxicity profiles. 36044812: Due to the hugely important roles of neurotransmitter acetylcholine (ACh) and amyloid-beta (Abeta) in the pathogenesis of Alzheimer's disease (AD), the development of multi-target directed ligands (MTDLs) focused on cholinesterase (ChE) and Abeta becomes one of the most attractive strategies for combating AD. 36058175: CONCLUSIONS: Our findings indicate that Abeta peptide induces AD-like molecular changes at certain doses, and these changes could be detected by evaluating brain oscillations. 36084891: The present study was designed to investigate the potential protective effects of minocycline against beta-amyloid (Abeta)-induced Alzheimer's disease (AD), recognition memory decline, and the possible involved anti-apoptotic mechanisms. 36093396: Herpes Simplex Virus Infection Increases Beta-Amyloid Production and Induces the Development of Alzheimer's Disease. 36120782: BACKGROUND: Amyloid-beta (Abeta) and tau protein accumulation in the brain is thought to be one of the causes of Alzheimer's disease (AD). 36144245: The transitional expression and aggregation of amyloid beta (Abeta) are the most important causative factors leading to the deterioration of Alzheimer's disease (AD), a commonly occurring metabolic disease among older people. 36155521: The amyloid cascade hypothesis attributes a vital role to amyloid-beta protein (Abeta) in the pathogenesis of AD. 36214002: BACKGROUND: Amyloid-beta (Abeta) is important in the etiology of Alzheimer's disease (AD). 36221865: Since Abeta plays an important role in the etiology of AD, therefore Abeta-linked pathways are mainly targeted in order to develop potential AD therapies. 36284704: Amyloid beta-peptide (Abeta) misfolding into beta-sheet structures triggers neurotoxicity inducing Alzheimer's disease (AD). 36361906: Amyloid beta (Abeta) peptide is suspected to be a major cause of AD, and therefore, simultaneously blocking its formation and aggregation by inhibition of the enzymes BACE-1 (beta-secretase) and AChE (acetylcholinesterase) by a single inhibitor may be an effective therapeutic approach, as compared to blocking one of these targets or by combining two drugs, one for each of these targets. 36362046: This study could reveal the role of a highly toxic Abeta on AD pathogenesis, thereby contributing to the development of a novel therapeutic strategy targeting the toxic conformer. 36422822: New therapies under development include agents that target amyloid-beta (Abeta), a key component in AD pathogenesis. 36438603: AD was induced by intrahippocampal injection of amyloid-beta (1-42, 6 MUg), and DON was orally administrated (4 mg/kg) for 21 days. Given the promising data on the additive effect of combination therapy with donepezil (Aricept), an acetylcholinesterase inhibitor (AChEI), and regarding the similar neuronal mechanisms through which donepezil (DON) and environmental enrichment (EE) exert their enhancing effects on cognition; we asked whether simultaneous treatment with two paradigms in amyloid-beta-induced AD rats may lead to greater protection against the cognitive impairments than either treatment individually. 36510132: PirB deletion has been shown to suppress Abeta-induced synaptic dysfunction and behavioral deficits in AD model mice, implying that PirB mediates Abeta-induced AD pathology. Our findings revealed that LOTUS may be a promising therapeutic agent in counteracting Abeta-induced AD pathologies. 36544574: Oligomers of amyloid beta (Abeta) represent an early aggregative form that causes neurotoxicity in the pathogenesis of Alzheimer's disease (AD). 36549596: Naringin enhances long-term potentiation and recovers learning and memory deficits of amyloid-beta induced Alzheimer's disease-like behavioral rat model. However, the effect of naringin in AD caused by Abeta has not been clearly studied, and there are few studies on the electrophysiological aspect. 36596482: The production of amyloid beta peptide (Abeta) is an important process relating to the pathogenesis of Alzheimer disease (AD). 36610160: BACKGROUND: Neurofibrillary tangles comprising hyperphosphorylated tau are vital factors associated with the pathogenesis of Alzheimer's disease (AD). Esculentoside A (EsA), isolated from Phytolacca esculenta, exhibits pharmacotherapeutic efficacy in mice with amyloid beta-induced AD. 36623626: Hesperidin methylchalcone (HMC) hinders amyloid-beta induced Alzheimer's disease by attenuating cholinesterase activity, macromolecular damages, oxidative stress and apoptosis via regulating NF-kappaB and Nrf2/HO-1 pathways. 36630532: Impact of nanoparticles on amyloid beta-induced Alzheimer's disease, tuberculosis, leprosy and cancer: A systematic review. 36651694: Oxidative stress due to Cu 2+ -triggered aggregation of beta-amyloid protein (Abeta) and reactive oxygen species (ROS) overexpression in the brain is an important hallmark of early stages of Alzheimer's disease (AD) pathogenesis. 36674792: Alzheimer's disease (AD) is known to be caused by amyloid beta-peptide (Abeta) misfolded into beta-sheets, but this knowledge has not yet led to treatments to prevent AD. 36680733: Intriguingly, PCO treatment improved all the above-mentioned neuropathological changes in the Abeta-induced AD rats. 36704637: Overproduction and accumulation of beta-amyloid and its improper clearance can cause neurotoxicity leading to Alzheimer's disease. 36803816: The amyloid hypothesis, that established amyloid-beta (Abeta) peptide as the primary cause of Alzheimer's disease (AD) and related dementia, has driven the development of treatments for neurodegeneration for 30 years. 36816173: This study is going on to examine the effect of ghrelin on antioxidant status in the rat's model of AD induced by Abeta. The effect of ghrelin on antioxidant status in the rat's model of Alzheimer's disease induced by amyloid-beta. 36866639: It is proven that protein aggregation like amyloid beta (Abeta) is one of the critical factors causing AD and, its diagnosis in the early stages of the disease is important for the treatment or prevention of AD. 36868776: The \amyloid cascade hypothesis\ stablishes that the aggregation of the beta-amyloid protein (Abeta 42 ) is the first event that subsequently triggers AD development. 36878848: Mounting evidence suggests that the accumulation and aggregation of amyloid-beta peptides (Abeta), which constitute amyloid plaques in the brain, is critical for initiating and accelerating AD pathogenesis. 36889654: However, it has been suggested that rather than the fibrillary amyloid beta (Abeta) deposits, it is smaller, soluble Abeta aggregates that exert a neurotoxic effect and trigger AD pathogenesis. 36945328: Our preliminary biological studies showed that Repeated Electromagnetic Field Stimulation (REFMS) applying an EM frequency of 64 MHz and a specific absorption rate (SAR) of 0.4 - 0.9 W/kg decrease the level of amyloid- beta peptides (A beta ), which is the most likely etiology of AD. 36945751: In this review, we first discuss the importance of Abeta in the pathogenesis of AD, then summarize the latest progress of Abeta-related targets and compounds. 36978955: The current study aims to investigate the effect of baicalein in combination with memantine in beta-amyloid-induced AD in albino Wistar rats. The Combination of Baicalein and Memantine Reduces Oxidative Stress and Protects against beta-amyloid-Induced Alzheimer's Disease in Rat Model. 37068195: Brain-targeted lycopene-loaded microemulsion modulates neuroinflammation, oxidative stress, apoptosis and synaptic plasticity in beta-amyloid-induced Alzheimer's disease mice. 37101809: Polymerization of soluble amyloid beta (Abeta) peptide into protease-stable insoluble fibrillary aggregates is a critical step in the pathogenesis of Alzheimer's disease (AD). 37105250: Administraction of HPS ameliorated age-related symptoms such as imbalanced intestinal homeostasis, sleep disturbances, and beta-amyloid (Abeta) induced Alzheimer's disease (AD) in flies, but did not modulate neurobehavioral deficits in the AD model of tauopathy and the Parkinson's disease (PD) model of Pink1 mutation. 37173803: Remarkably, hIAPP has structural similarity with amyloid beta (Abeta) and can engage in the pathogenesis of T2DM and Alzheimer's disease (AD). 37179042: Minocycline effects on memory and learning impairment in the beta-amyloid-induced Alzheimer's disease model in male rats using behavioral, biochemical, and histological methods. This study investigated the effect of minocycline on the changes in learning and memory functions, activities of blood serum antioxidant enzymes, neuronal loss, and the number of Abeta plaques after AD induced by Abeta in male rats. 37212117: OBJECTIVE: This study was done to determine the protective effects of coenzyme Q10 (CoQ10) and high-intensity interval training (HIIT) alone and in combination for eight continuous weeks, on oxidative status, cognitive functions, and histological changes in the hippocampus in amyloid-beta (Abeta)-induced AD rats. Interestingly, pretreatment with CoQ10, HIIT, or both, could markedly improve the oxidative status and cognitive decline in the MWM and NOR tests, and hinder neuronal loss in the hippocampus of Abeta-induced AD rats. The Protective Effects of High-Intensity Interval Training Combined with Q10 Supplementation on Learning and Memory Impairments in Male Rats with Amyloid-beta-Induced Alzheimer's Disease. 37239068: Emerging evidence over the past few decades supports the critical role of Abeta and tau in AD pathogenesis and the participation of glial cells in different molecular and cellular pathways. 37245024: CONCLUSIONS: Together, these findings indicate the protective functions of the N-terminal Abeta fragments extend to reactive gliosis and gliotoxicity induced by Abeta, by preventing or reversing glial reactive states indicative of neuroinflammation and synaptic loss central to AD pathogenesis. 37263123: Effects of donepezil treatment on plasma and urine metabolites in amyloid beta-induced Alzheimer's disease rats. This study provides basic data for the effects of Abeta and donepezil on plasma and urine metabolites in Abeta-induced AD rat models. 37307834: Decades of research have demonstrated an incontrovertible role of amyloid-beta (Abeta) in the etiology of Alzheimer's disease (AD). 37348174: This study aimed to evaluate whether preconditioning MSCs with dimethyl fumarate (DMF), a Nrf2 inducer, could enhance MSC therapeutic efficacy in an amyloid-beta (Abeta 1-42 )-induced AD rat model. 37506558: The abnormal accumulation of amyloid beta protein (Abeta) is one of the most important causes of Alzheimer's disease (AD) and is usually a detecting biomarker. 37607046: Recent studies have found that beta-amyloid (Abeta) oligomers may play much more important roles than amyloid plaques in the pathogenesis of Alzheimer's disease (AD). 37609338: Microglial cGAS deletion protects against amyloid-beta induced Alzheimer's disease pathogenesis. 37619312: Dose-dependent neuroprotective effects of adipose-derived mesenchymal stem cells on amyloid beta-induced Alzheimer's disease in rats. 37626631: Amyloid-beta (Abeta) is one of the causes of Alzheimer's disease (AD), damaging nerve membranes and inducing neurotoxicity. 37628913: In conclusion, this study demonstrates the neuroprotective effects of NACA against beta-amyloid induced AD-like pathology. 37654789: The question of how Abeta relates to neurovascular function and which is the trigger for AD has recently come into sharp focus. 37663321: Aggregation of amyloid-beta peptide (Abeta) is hypothesized to be the primary cause of Alzheimer's disease (AD) progression. 37667395: However, it is still a challenge to understand the DNs of specific neurons that are vulnerable to Abeta in the pathogenesis of AD. 37718800: Probabilistic and parsimony-based arguments regarding available genetics data are used to propose that Hardy and Higgin's amyloid cascade hypothesis is valid but is commonly interpreted too narrowly to support, incorrectly, the primacy of the amyloid-beta peptide (Abeta) in driving Alzheimer's disease pathogenesis. 37728399: The accumulation of amyloid-beta (Abeta) into senile plaques and the resulting continuous oxidative stress are major pathogenic mechanisms in Alzheimer's disease (AD). 37758932: This study aimed to assess the defensive properties of rosavin against Alzheimer's disease induced by amyloid-beta, utilizing experimental models. 37853914: Sequential proteolysis of the amyloid precursor protein (APP) by gamma-secretases generates amyloid-beta (Abeta) peptides and defines the proportion of short-to-long Abeta peptides, which is tightly connected to Alzheimer's disease (AD) pathogenesis. 37905874: ABSTRACT: The aggregation of amyloid-beta peptide and tau protein dysregulation are implicated to play key roles in Alzheimer's disease pathogenesis and are considered the main pathological hallmarks of this devastating disease. 37921143: METHODS: The present study reviews the arsenic role in the generation of amyloid-beta from its precursor that leads to Alzheimer's disease through the published article from Pubmed and Scopus. 37935338: Although the validation of the long standing amyloid cascade hypothesis would seem to be at hand, what remains is the puzzling issue of why - if Abeta indeed causes AD - does removing it from the brain not stop the disease entirely. 37976283: Oligomers formed from monomers of the amyloid beta-protein (Abeta) are thought to be central to the pathogenesis of Alzheimer's disease (AD). 37983764: Amyloid-beta (Abeta) and its assemblies play important roles in the pathogenesis of Alzheimer's disease (AD). 38053635: Oligomeric amyloid beta (oAbeta) is considered a major synaptotoxic trigger for AD. 38071408: AD was induced using amyloid beta (Abeta) and confirmed through the Morris water maze (MWM) behavioural test and Congo red staining. 38143280: Amelioration of Amyloid-beta Induced Alzheimer's Disease by Bacopa monnieri through Modulation of Mitochondrial Dysfunction and GSK-3beta/Wnt/beta-Catenin Signaling. 38163326: Amyloid-beta (Abeta) forms heterogeneous oligomers, which are implicated in the pathogenesis of Alzheimer's disease (AD). 38188833: Retracted: Herpes Simplex Virus Infection Increases Beta-Amyloid Production and Induces the Development of Alzheimer's Disease. 38194817: Abnormal aggregation and fibrillogenesis of amyloid-beta protein (Abeta) can cause Alzheimer's disease (AD). 38211684: Potential links between platelets and amyloid-beta in the pathogenesis of Alzheimer's disease: Evidence from in vitro, in vivo, and clinical studies. 38242524: The undifferentiated OE-MSCs were transplanted either by intranasal (IN) or intrahippocampal (IH) injection to rat models of AD, which were induced by injecting amyloid-beta (Abeta) intrahippocampally. 38287166: Compelling genetic and biomarker evidence supports Abeta as the root cause of AD. 38344035: Aggregates of amyloid-beta (Abeta) peptides are thought to cause Alzheimer's disease. 38455162: Accumulation of beta-amyloid peptide (Abeta) induces neurotoxicity, which is the primary risk factor in the pathogenesis of Alzheimer's disease (AD). 38473727: The perivascular space has been proposed as a clearance pathway for degradation products in the brain, including amyloid beta, the accumulation of which may induce Alzheimer's disease. 38475929: BACKGROUND: Although abnormal accumulation of amyloid beta (Abeta) protein is thought to be the main cause of Alzheimer's disease (AD), emerging evidence suggests a pivotal vascular contribution to AD. 38497073: The beta-amyloid (Abeta) accumulation triggers AD pathogenesis, though clinical trials lowering Abeta have not altered disease outcomes suggesting other interacting factors to be identified for drug design of AD. 38534427: One of the most accepted theories in AD, the amyloid beta (Abeta) hypothesis, assumes that the buildup of the peptide Abeta is the root cause of AD. 38615460: This review summarizes the research on beta-hairpins in Abeta peptides and discusses the relevance of this conformation in AD pathogenesis and drug development. 12472904: The proliferation and survival of NPC in the dentate gyrus of the hippocampus was reduced in mice transgenic for a mutated form of amyloid precursor protein that causes early onset familial AD. 12476348: Studies of the pathogenic actions of mutations in presenilins and amyloid precursor protein that cause early-onset familial AD have established central roles for perturbed cellular calcium homeostasis and oxidative stress in the neurodegenerative process. The clinical presentation of patients with AD is dominated by cognitive deficits and emotional disturbances that result from dysfunction and degeneration of neurons in the limbic system and cerebral cortex. 12849363: Mutant genes for amyloid precursor protein (APP) or presenilin cause early-onset familial Alzheimer's disease (<1% of all cases) and have helped to elucidate APP processing and amyloid-peptide formation by alpha, beta, and gamma secretases. 14518509: Studies of the pathogenic mutations in presenilins 1 and 2 (PS1 and PS2) and amyloid precursor protein (APP) responsible for early onset familial AD have estabilished central roles for perturbed cellular Ca2+ homeostasis. 15565529: According to the beta-amyloid cascade hypothesis, the accumulation of beta-amyloid (Abeta) deposits as amyloid plaques in the patient's brain is the primary event in the pathogenesis of Alzheimer's disease (AD). The majority of known APP and presenilin mutations responsible for familial early onset AD affect APP processing causing overproduction of Abeta, especially Abeta42. 15987951: PDAPP transgenic mice overexpress a mutant form of human amyloid precursor protein under control of the platelet-derived growth factor promoter in CNS neurons that causes early onset, familial Alzheimer's disease in humans. 16478525: Several lines of evidence suggest that enhanced oxidative stress, inflammation, and apoptosis play important roles in the pathogenesis of AD. Mutations in the PS-1 and APP genes, which increase production of the highly amyloidogenic amyloid beta-peptide (Abeta42), are the major causes of early onset familial AD. 1791986: A mutation within exon 17 at codon 717 of the beta-amyloid protein precursor (APP) gene is one cause of early onset familial Alzheimer's disease. 18187157: Atypical early-onset Alzheimer's disease caused by the Iranian APP mutation. 18585407: To provide additional information about the effects of these oligomers on memory, the present study examined the memory of groups of rats exposed to ICV injections of the culture media (CM) of Chinese Hamster Ovary cells that were (7PA2) and were not (CHO-) transfected with a human mutation of amyloid precursor protein that appears to cause early-onset Alzheimer's disease. 19101658: AD occurs sporadically (SAD), or is caused by hereditary missense mutations in the amyloid precursor protein (APP) or presenilin-1 and -2 (PSEN1 and PSEN2) genes, leading to early-onset familial AD (FAD). 19804379: The Swedish mutation within the amyloid precursor protein (APP) causes early-onset Alzheimer's disease due to increased cleavage of APP by BACE1. 20080541: An additional copy of the beta-amyloid precursor protein (APP) gene causes early-onset Alzheimer's disease (AD) in trisomy 21 (DS). 21605030: Apo E is the major component of lipoprotein particles in the brain that mediate transport of cholesterol and other lipids between neurons and glial cells, indicating an implication of cerebral lipid metabolism in the pathogenesis of AD. Importantly, mutations in the genes of APP and the two homologous PS proteins are a major cause of familial early onset AD, indicating that the metabolism of APP and generation of Abeta play critical roles in the initiation of the disease. 21909359: Cerebrovascular integrity was characterized in Tg2576 AD model mice that overexpress the human amyloid precursor protein (APP) containing the double missense mutations, APPsw, found in a Swedish family, that causes early-onset AD. 22044463: BACKGROUND: Missense mutations in three different genes encoding amyloid-beta precursor protein, presenilin 1 and presenilin 2 are recognized to cause familial early-onset Alzheimer disease. 22491860: CONCLUSION: Our study shows that APP mutations and locus duplications are a very rare cause of EOFAD and that the contribution of common APP variants to AD susceptibility is insignificant. OBJECTIVES: More than 30 different rare mutations, including copy number variants (CNVs), in the amyloid precursor protein gene (APP) cause early-onset familial Alzheimer disease (EOFAD), whereas the contribution of common APP variants to disease risk remains controversial. 23102935: Pathogenic mutations of the APP gene, leading to early-onset Alzheimer's disease (AD) have been known for more than 20 years. 23142261: Mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) are responsible for early-onset autosomal dominant AD. 23752245: Over 200 rare and fully penetrant pathogenic mutations in amyloid precursor protein (APP), presenilin 1 and 2 (PSEN1 and PSEN2) cause a subset of early-onset familial Alzheimer's disease (EO-FAD). 23907250: Pathological amino-acid substitutions in the amyloid precursor protein (APP) and chemical gamma-secretase modulators affect the processing of APP by the gamma-secretase complex and the production of the amyloid-beta peptide Abeta42, the accumulation of which is considered causative of Alzheimer's disease. Here we demonstrate that mutations in the transmembrane domain of APP causing aggressive early-onset familial Alzheimer's disease affect both gamma- and epsilon-cleavage sites, by raising the Abeta42/40 ratio and inhibiting the production of AICD50-99, one of the two physiological APP intracellular domains (ICDs). 24838203: Mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) are responsible for early-onset autosomal dominant AD. 24964199: Swedish double mutation (KM670/671NL) of amyloid precursor protein (APP) is reported to increase toxic amyloid beta (Abeta) production via aberrant cleavage at the beta-secretase site and thereby cause early-onset Alzheimer's disease (AD). 26141474: To date, mutations in three different genes, the Amyloid precursor protein (APP), Presenilin 1 (PS1), and Presenilin 2 (PS2), have been identified as causative in early-onset AD, making predictive testing possible. 26402764: BACKGROUND: Mutations within exons 16 and 17 of the amyloid-beta protein precursor (AbetaPP) gene were the first known causes of early-onset familial Alzheimer's disease (EOFAD). 29578479: Many of these models express mutant versions of human amyloid-beta protein precursor (AbetaPP) that are associated with amyloid-beta protein (Abeta)-induced early onset familial AD. 30041064: Seizures have traditionally been related to neuronal loss in the late stages of AD as a consequence of neurodegeneration, however, recent studies indicated that seizures may contribute to the emergence of AD symptoms in early stages of the disease, mainly in familial AD. Mutations in genes encoding presenilin 1 (PSEN1), presenilin 2 (PSEN2) and amyloid precursor protein (APP) are responsible for early-onset familial AD (EOFAD). 30763650: Mutations in the genes encoding amyloid precursor protein (APP) or presenilin (PS) cause early onset familial Alzheimer's disease (AD), and sequential cleavages of the APP by beta-secretase and gamma-secretase/presenilin generate amyloid beta protein (Abeta), the major component of pathological hallmark, neuritic plaques, in brains of AD patients. 31440394: Presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP) mutations are responsible for autosomal dominant early-onset Alzheimer's disease (AD-EOAD). 31625391: Dominant mutations in APP and presenilin cause early onset familial Alzheimer's disease (FAD). 8395665: A mutation at codons 670 and 671 of exon 16 of the amyloid precursor protein has recently been identified as a cause of early onset familial Alzheimer's disease. 8811169: In early 1993, the genetic data implicating the amyloid precursor protein as one of the loci leading to early onset Alzheimer's disease were reviewed (Hardy and Duff, Annals of Medicine, 25: 437-440), together with the evidence implicating abnormal deposition of beta-amyloid as the initiating point of the process leading to the disease. 8878479: These results indicate that the presenilin mutations probably cause Alzheimer's disease through a gain of deleterious function that increases the amount of A beta42(43) in the brain. Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease. 8915610: Six different single base mutations in the APP gene have been reported causing early-onset Alzheimer's disease (age at onset < or = 65 years) or related amyloidosis in a small number of families. 9106355: Various mutations in the amyloid protein precursor and presenilin genes can lead to early onset, autosomal Alzheimer's disease. 9328472: We report a novel mutation in the amyloid precursor protein gene (APP I716V) which probably leads to familial early onset Alzheimer's disease with an onset age in the mid 50s. 9811864: The importance of the amyloid precursor protein (APP) in the pathogenesis of Alzheimer's disease (AD) became apparent through the identification of distinct mutations in the APP gene, causing early onset familial AD with the accumulation of a 4-kDa peptide fragment (betaA4) in amyloid plaques and vascular deposits. 14558486: Cerebral amyloid angiopathy (CAA), a condition affecting the elderly in a way similar to that of Alzheimer's disease, results from amyloid deposition within small and medium arteries of the cerebral leptomeninges and cerebral cortex. 14747300: Evidence is growing to link precursors of amyloid deposition in the brain and pancreas with the pathogenesis of Alzheimer disease and type 2 diabetes, respectively. 16863248: The identification and characterization of possible environmental factors that may influence amyloid deposition in vivo are important to unveil the underlying etiology of AD. According to the amyloid cascade hypothesis, diffuse plaques are initial and visual deposits in the early event of AD, leading to amyloid plaques. 1763432: Amyloid deposition as the central event in the aetiology of Alzheimer's disease. 1776729: As elucidation of the reasons behind amyloid deposition must shed some light on the pathogenesis of AD, we review the current state of knowledge on the nature of the AD amyloid protein, its origin, and its formation. At the cellular level, Alzheimer's disease (AD) must be the result of neuronal dysfunction and degeneration leading to a reduction in synaptic density. 18157656: Amyloid beta (Abeta) deposition and neurodegeneration are the two related events in the pathogenesis of Alzheimer's disease. 18547682: We propose that ASM activation is an important pathological event leading to AD, perhaps due to Abeta deposition. 19084047: Bone marrow-derived mesenchymal stem cells reduce brain amyloid-beta deposition and accelerate the activation of microglia in an acutely induced Alzheimer's disease mouse model. 20061626: The relationship between amyloid-beta (Abeta) deposition and tau-related neurofibrillary changes is a key issue in the pathogenesis of Alzheimer's disease (AD). 20538375: Despite the central role of amyloid deposition in the development of Alzheimer's disease (AD), the pathogenesis of AD still remains elusive at the molecular level. 21352095: Evidence is growing linking precursors of amyloid deposition in the brain and pancreas to the pathogenesis of AD and T2DM, respectively. 21683932: BACKGROUND: The hypothesis that amyloid deposition is the leading cause of Alzheimer's disease (AD) is supported by findings in transgenic animal models and forms the basis of clinical trials of anti-amyloid agents. 21705422: The similar topography of fibrillar amyloid-beta deposition between typical Alzheimer's disease and posterior cortical atrophy groups suggests that, although amyloid-beta accumulation plays a critical role in the pathogenesis of Alzheimer's disease, other factors such as neurofibrillary tangles may contribute to the different clinical features observed in posterior cortical atrophy. 23624169: BACKGROUND: Although it is well known that many clinical and genetic factors have been associated with beta-amyloid deposition, few studies have examined the interactions of such factors across different stages of Alzheimer's pathogenesis. 23788007: Alzheimer's disease (AD) is a consequence of degenerative brain pathology with amyloid plaque deposition and neurofibrillary tangle formation. 25662507: Considering the role of proinflammatory molecules and microglial activation in the pathogenesis of AD, the current study aimed to elucidate the effects of donepezil on microglial activation induced by amyloid deposition in transgenic mice. 26283673: The early pretangle disease phase is a focus of increasing interest because only abnormal forms of the microtubule-associated protein tau are involved at that point and, in contrast to late-stage disease when amyloid-beta deposition is present, this phase is temporally closer to the prevailing conditions that induce the pathological process underlying Alzheimer's disease. 27395454: This suggests that APOE epsilon4 facilitates amyloid deposition during the very early phase of AD pathogenesis. 27776263: The pathway leading from amyloid-beta deposition to cognitive impairment is believed to be a cornerstone of the pathogenesis of Alzheimer's disease (AD). 27996029: Accumulation of amyloid-beta (Abeta) peptides and amyloid plaque deposition in brain is postulated as a cause of Alzheimer's disease (AD). 28460142: AgNP exposure can increase amyloid beta (Abeta) deposition in neuronal cells to potentially induce Alzheimer's disease (AD) progression. This study suggested that AgNP exposure might cause Abeta deposition and inflammation for subsequent neuronal cell apoptosis to potentially induce AD progression. 28669880: Amyloid beta (Abeta) deposition is considered to be one of the primary reason to trigger Alzheimer's disease (AD). 29406914: In Alzheimer Disease, impaired vasoreactivity has been reported as the results of vascular amyloid deposition. 30958361: Abeta deposition is the most frequently hypothesized initiating factor of AD, and Abeta clearance during the pathogenesis of AD may be an optional strategy to suppress AD development. 31219699: Interestingly, knockdown of Trem2 at the early-middle stage of AD (2-6 mo) prevents synaptic loss through directly inhibiting microglial phagocytosis, whereas knockdown of Trem2 at the middle-late stage of AD (6-10 mo) accelerates synaptic dysfunction because of more severe amyloid deposition caused by the depression of microglial phagocytosis. 31223308: Increased amyloid-beta (Abeta) plaque deposition is thought to be the main cause of Alzheimer's disease (AD). Therefore, revealing the underlying mechanism of BACE1 in the pathogenesis of AD might have a significant impact on the future development of therapeutic agents targeting dementia. 32108008: Senile plaques and amyloid deposition is one of the main causes of AD, amyloid deposition isconsidered as a central event which induces the link between the production of beta amyloid and vascular changes. 32796236: Amyloid deposition can lead to Alzheimer disease and cerebral amyloid angiopathy. 33318676: According to the prevailing amyloid cascade hypothesis, amyloid-beta (Abeta) deposition in the brain is the initiating event in AD, although evidence is accumulating that this hypothesis is insufficient to explain many aspects of AD pathogenesis. 34108650: Predicting cerebral amyloid deposition is considered the key for AD diagnosis because a cerebral amyloid deposition is the hallmark of AD pathogenesis. 34405526: Amyloid-beta (Abeta) deposition in the brain has been implicated in the development of Alzheimer's disease (AD), and neuroinflammation generates AD progression. 3477820: Progressive amyloid deposition in senile plaques and cortical blood vessels may play a central role in the pathogenesis of Alzheimer disease. 34823269: Improved insight into these pathomechanisms may allow to shed light on the role of Abeta deposition as a primary vs. a secondary event in the complex pathogenesis of AD. 35575872: The pathological characteristics of Alzheimer's disease (AD) include formation of senile plaques resulting from amyloid-beta (Abeta) deposition and neurofibrillary tangles caused by tau hyperphosphorylation. The above-mentioned proteins were then evaluated in an okadaic acid (OKA)-induced AD cell model to verify the results. 35986296: CONCLUSIONS: The reciprocal effects of amyloid deposition and systemic infectious burden may lead to a vicious cycle fueling Alzheimer's disease pathogenesis. The infectious theory linked various infectious agents with the development of AD, raising the possibility that they serve as etiological causes of the disease. 36996958: Previous research has established amyloid plaque deposition as the leading cause of Alzheimer's disease (AD) pathogenesis, detected mainly in aged population. 37188840: In preclinical Alzheimer's disease, neuro-functional changes due to amyloid-beta (Abeta) deposition are not synchronized in different brain lobes and subcortical nuclei. 37864249: Impaired autophagy in plaque-associated microglia (PAM) has been reported to accelerate amyloid plaque deposition and cognitive impairment in AD pathogenesis. 37895161: While conventional pathophysiological models of AD have primarily emphasized the significance of amyloid-beta (Abeta) deposition and tau protein hyperphosphorylation, this targeted systematic review meticulously aggregates and rigorously appraises seminal contributions from the past year elucidating the complex mechanisms of H 2 S in AD pathogenesis. 38076912: Overall, this contextualized understanding of proteomic changes and their interplay with amyloid deposition provides valuable insights into the complexity of AD pathogenesis and potential biomarkers and therapeutic targets. 7651609: Rats with lesions induced by beta-peptides may be a useful animal model of amyloid deposition for investigation of the pathogenetic mechanisms leading to Alzheimer's disease. 8620894: Alzheimer's disease is a senile dementia caused by progressive neurodegeneration of the central nervous system. Here functional implications of these mutations on the processing of the precursor protein and the beta A4 amyloid deposition will be discussed with respect to the pathogenesis of Alzheimer's disease and related disorders. 9168248: Mechanisms of neurotoxicity associated with amyloid beta deposition and the role of free radicals in the pathogenesis of Alzheimer's disease: a critical appraisal. 9223085: The association of astrocytes with plaques is a well-established feature of Alzheimer's disease (AD) and has generally been interpreted as a secondary reaction to amyloid deposition or neuronal degeneration. 9399697: These findings indicate that changes in cerebral betaA4 levels contribute to temporal lobe atrophy in AD and support the possibility that betaA4 is central to the etiology of AD. Pathological and biochemical studies indicate that beta-amyloid (betaA4) deposition is a hallmark in the pathogenesis of Alzheimer's disease (AD). 9678319: CONCLUSION: Our results differ from the data from AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein and suggest that the APOE epsilon4 genotype mediates increased Abeta deposition by a mechanism that differs from that found in other genetic causes of AD. 15017581: Cerebral Abeta amyloidosis and postmenopausal hormone deficiency: roles in the genesis of Alzheimer's disease. 15265270: Atherosclerosis, vascular amyloidosis and brain hypoperfusion in the pathogenesis of sporadic Alzheimer's disease. 16399644: Neuropathological and genetic studies provide strong evidence of a key role for A beta amyloidosis in the pathogenesis of AD. 21044348: CONCLUSIONS: Our present data indicate that there is a close link between insulin deficient diabetes and cerebral amyloidosis in the pathogenesis of AD. 21426072: BACKGROUND: beta-amyloidosis and oxidative stress have been implicated as root causes of Alzheimer's disease (AD). 21911660: BACKGROUND: The amyloid hypothesis predicts that increased production or decreased clearance of beta-amyloid (Abeta) leads to amyloidosis, which ultimately culminates in Alzheimer disease (AD). 22813736: Our findings thus reveal a role of MAGL in modulating neuroinflammation and amyloidosis in AD etiology and put forth MAGL inhibitors as a potential next-generation strategy for combating AD. 24228859: CONCLUSIONS: Our study suggests that there is a close linkage of DM and cerebral amyloidosis in the pathogenesis of AD. 24373429: Despite compelling genetic evidence indicating that cerebral amyloidosis can be, at least sometimes, the primary cause of Alzheimer's disease (AD), clinical trials for symptomatic AD with amyloid-reducing agents have succeeded at target engagement but failed to cause clinical benefit. 24852227: The amyloid beta (Abeta) hypothesis posits that cerebral beta-amyloidosis is a critical early event in AD pathogenesis. We review the genetics, epidemiology and pathology of sporadic AD and give an updated account of what is currently known about the molecular pathogenesis of the disease. 28490901: Breast cancer and Alzheimer's disease (AD) are major causes of death in older women. Amyloidosis, the aggregation of amyloid proteins to form amyloid bodies, plays a central role in the pathogenesis of AD and other human neuropathies by forming intracellular fibrillary proteins. 30053949: This landmark paper laid the foundation for extensive research in the following decades that ultimately established the role of beta-amyloidosis as a player in the pathogenesis of AD. 31156159: These results provide mechanistic insight into the beneficial effects of insulin, and a possible link between insulin deficient diabetes and cerebral amyloidosis in the pathogenesis of AD. 31162811: Amyloid-like peptides are an ideal model for the mechanistic study of amyloidosis, which may lead to many human diseases, such as Alzheimer disease. 33947453: CONCLUSIONS: Our results indicate that plasma and CSF p-tau181 abnormalities associated with amyloidosis occur simultaneously in the progression of AD pathogenesis and related cognitive decline, before tau-PET turns positive. 35202955: The protective innate immune response of beta-amyloid peptide (Abeta) has been indicated as a risk factor for Alzheimer's disease (AD) due to the rapid amyloidosis. 7579788: Recent molecular biological, biochemical and immunohistochemical studies have revealed various novel facts about beta-amyloidosis including its role in the pathogenesis of Alzheimer's disease (AD). 8885836: A mechanism is proposed, whereby nicotine retards amyloidosis by preventing an alpha-helix-->beta-sheet conformational transformation that is important in the pathogenesis of Alzheimer's disease. 9099821: Based on the homology of human and monkey amyloid precursor proteins and the derived beta-amyloid peptides (A beta) the investigation of brains from old monkeys might be useful for the understanding of beta-amyloidosis in the aetiology of Alzheimer's disease. 10392370: Hypertension and virilization caused by a unique desoxycorticosterone- and androgen-secreting adrenal adenoma. 16971373: Therefore, the present studies were performed to test the hypothesis that androgens cause hypertension in SHR in part by stimulating superoxide production via NADPH oxidase. 17548721: The results strongly implicate vascular cytochrome P450 4A-derived 20-hydroxyeicosatetraenoic acid in the development of androgen-induced endothelial dysfunction and hypertension. Vascular cytochrome P450 4A expression and 20-hydroxyeicosatetraenoic acid synthesis contribute to endothelial dysfunction in androgen-induced hypertension. 18276983: We conclude that increased vascular tone brought about by downregulation of CYP2C23 and decreased levels of vasodilatory EETs and by induction of CYP4A8 and enhanced production of 20-HETE may constitute important factors in androgen-induced hypertension. Renal vascular cytochrome P450-derived eicosanoids in androgen-induced hypertension. 21722750: In this review, we will discuss the pro-hypertensive effects of 20-HETE and its role in androgen-induced vascular dysfunction and hypertension. 23641057: To examine whether androgen-independent increases in 20-HETE are sufficient to cause hypertension, we studied Cyp4a12-transgenic mice, which express the CYP4A12-20-HETE synthase under the control of a doxycycline-sensitive promoter. Although the mechanism underlying the effect of androgen on BP and cardiovascular disease is not well understood, recent studies suggest that 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE), a primary cytochrome P450 4 (Cyp4)-derived eicosanoid, may mediate androgen-induced hypertension. 25489059: We tested whether androgens induce hypertension through transcriptional regulation and signaling of protein kinase C (PKC) in the mesenteric arteries. 25526688: Androgen-induced hypertension in angiotensinogen deficient mice: role of 20-HETE and EETS. 3129324: This is consistent with the role of 11-deoxycorticosterone in the pathogenesis of androgen-induced hypertension in rats. 34874016: The purpose of this study was to evaluate the role of mTOR signaling pathway in myocardial hypertrophy in androgen-induced postmenopausal hypertension and whether mTOR inhibitors can protect the myocardium from androgen-induced interference to prevent and treat cardiac hypertrophy. 36027145: The purpose of this study was to evaluate the role of mTOR signaling pathway in myocardial hypertrophy in androgen-induced postmenopausal hypertension and whether mTOR inhibitors can protect the myocardium from androgen-induced interference to prevent and treat cardiac hypertrophy. 5527809: Effect of adrenalectomy on the development of androgen-induced hypertension. 7419267: Peripheral serum corticosteroid concentrations in relation to the rat adrenal cortical circadian rhythm in androgen-induced hypertension. 19333227: Although biologic agents are seemingly less toxic, toxic effects can also arise with their use; antiangiogenic agents result in hypertension, and EGFR inhibitors can cause severe hypersensitivity, paronychial infections, and more commonly, dermatologic rash. 20535072: Antiangiogenic agents can induce arterial hypertension, arterial and venous thromboembolism, and less frequently QTc prolongation. 21479992: Mechanisms of antiangiogenic-induced arterial hypertension. 21633924: Accumulating evidence has shown that molecular targeted agents, especially those with antiangiogenic activity cause significant hypertension which can lead to development of RPLS. 21749882: Molecular mechanisms of hypertension and heart failure due to antiangiogenic cancer therapies. 22222493: We discuss the similarity between preeclampsia and VEGF-targeted therapy-induced hypertension. Antiangiogenic-induced hypertension: the molecular basis of signaling network. 23203441: We consider two most important pathomechanisms in the development of hypertension induced by angiogenesis inhibitors. Angiogenesis-inhibitor-induced hypertension represents \crux medicorum\ as it is often pharmacoresistant to antihypertensive therapy. Therapeutic potential of nitric oxide donors in the prevention and treatment of angiogenesis-inhibitor-induced hypertension. Based on the results of experimental and clinical studies as well as on our clinical experience, we assume that NO donors could be successfully used not only for the treatment of developed angiogenesis-inhibitor-induced hypertension but also for preventive effects. 24065498: Endothelial dysfunction, an early and reversible event in the pathogenesis of atherosclerosis, is suggested to be one of the possible underlying mechanisms of hypertension caused by angiogenesis inhibitors. 24646704: Anti-angiogenic drugs that target Vascular Endothelial Growth Factor (VEGF) signaling pathways caused hypertension as an adverse effect in clinical studies. To clarify whether non-clinical research using rats can appropriately estimate the clinical risk of hypertension caused by VEGF signal inhibitors, we investigated the hemodynamic effects and pharmacokinetics (PK) of the VEGF signal inhibitors cediranib (0.1, 3, and 10 mg/kg), sunitinib (5, 10, and 40 mg/kg), and sorafenib (0.1, 1, and 5 mg/kg) in telemetered rats and examined the correlation between the non-clinical and the clinical hypertensive effect. These results represent correlations between the non-clinical and the clinical hypertensive effect of VEGF signal inhibitors, suggesting that non-clinical research using telemetered rats would be an effective approach to predict the clinical risk of hypertension caused by VEGF signal inhibitors. 24786444: Hypertension due to antiangiogenic cancer therapy with vascular endothelial growth factor inhibitors: understanding and managing a new syndrome. 25475480: Hypertension due to antiangiogenic cancer therapy with VEGF inhibitors: is autonomic nervous system toxicity another possible mechanism? 25712723: A preeclampsia-like state was induced in pregnant CD1 mice by overexpressing soluble fms-like tyrosine kinase-1, a circulating antiangiogenic protein that induces hypertension and glomerular disease resembling human preeclampsia. 26386874: NO donors could be successfully used not only for the treatment of developed angiogenesis-inhibitor-induced hypertension but also for preventive effects. 29788148: The purpose of this review was to present recent evidence regarding the incidence of HT induced by antiangiogenic agents, to analyze the pathophysiological mechanisms, and to summarize current recommendations for the management of elevated blood pressure in this field. 31593221: In this study, our aim was to determine the efficacy of selective ETA versus dual ETA/B receptor blockade for the prevention of angiogenesis inhibitor-induced hypertension and albuminuria. TRANSLATIONAL PERSPECTIVE: The endothelin (ET) system is implicated in the pathogenesis of angiogenesis inhibitor-induced hypertension and renal injury. Here we demonstrate that the development of angiogenesis inhibitor-induced hypertension and albuminuria is solely dependent on the ETA receptor and that an upregulation in PGI2 plays a previously unidentified role in the deleterious effects of angiogenesis inhibitors. 32430701: Herein, we provide a team-based approach for treatment of angiogenesis inhibitor-induced hypertension along with recommendations on monitoring and appropriate selection of anti-hypertensive agents. 32990313: However, the pathophysiological mechanisms still remain elusive and there is an urgent need to better understand exactly how anti-angiogenic drugs cause hypertension and other cardiovascular diseases (CVDs). 33706996: Anti-angiogenic drugs frequently cause hypertension. 35441670: Both low-dose and high-dose aspirin blunted angiogenesis inhibitor-induced hypertension and vascular superoxide production to a similar extent, whereas only high-dose aspirin prevented albuminuria. Differential effects of cyclo-oxygenase 1 and 2 inhibition on angiogenesis inhibitor-induced hypertension and kidney damage. In the present study we hypothesised that treatment with aspirin would prevent the development of angiogenesis inhibitor-induced hypertension and kidney damage. Collectively our findings suggest that prostanoids contribute to the development of angiogenesis inhibitor-induced hypertension and renal damage and that targeting the prostanoid pathway could be an effective strategy to mitigate the unwanted cardiovascular and renal toxicities associated with angiogenesis inhibitors. 36026868: CONCLUSIONS: In conclusion, selective COX-2 inhibition combats angiogenesis inhibitor-induced hypertension and renal toxicity. 38029870: To combat angiogenesis inhibitor-induced hypertension, dual rather than selective COX-1/2 blockade seems preferential. BACKGROUND: Anticancer angiogenesis inhibitors cause hypertension and renal injury. 11897768: Posttranscriptional control of BNP gene expression in angiotensin II-induced hypertension. In this study, the role of transcriptional mechanisms in the regulation of BNP gene expression were studied in angiotensin (Ang) II-induced hypertension by injecting DNA constructs containing the BNP promoter (-2200 to 75 bp of the transcriptional start site) linked to luciferase reporter into rat myocardium. 12900436: These results support the hypothesis that angiotensin II infusion induces persistent salt-sensitive hypertension after withdrawal of angiotensin II that may be due to downregulation of CYP2C and CYP2J epoxygenases in renal microvessels. The current study was designed to determine whether angiotensin II infusion could lead to persistent salt-sensitive hypertension and to examine involvement of renal microvascular epoxygenases in this process. 17351653: Synergistic vascular protective effects of combined low doses of PPARalpha and PPARgamma activators in angiotensin II-induced hypertension in rats. 20026758: These data indicate that early life stress sensitizes rats to an increased hemodynamic and inflammatory response during Ang II-induced hypertension. Early life stress sensitizes rats to angiotensin II-induced hypertension and vascular inflammation in adult life. 20558825: OBJECTIVE: The present study sought to investigate the protective role of OA-NO(2) in angiotensin (Ang) II-induced hypertension. From the mechanistic viewpoint, OA-NO(2) lowers Ang II-induced hypertension independently of peroxisome proliferation-activated receptor (PPAR)gamma activation. 21263125: Angiotensin (Ang) II induces hypertension by mechanisms mediated in part by adaptive immunity and T effector lymphocytes. We questioned whether Treg adoptive transfer would blunt Ang II-induced hypertension and vascular injury. T regulatory lymphocytes prevent angiotensin II-induced hypertension and vascular injury. 23129698: Ca(v)1.2 channel expression and function were compared between second-order mesenteric arteries of C57BL/6 wild-type (WT) and Ca(v)beta3(-/-) mice infused with saline (control) or angiotensin II (Ang II) for 2 weeks to induce hypertension. 23691105: We previously showed that angiotensin (Ang) II-induced hypertension is mediated by increased production of proinflammatory cytokines (PIC), including tumor necrosis factor (TNF), in brain cardiovascular regulatory centers such as the paraventricular nucleus (PVN). Presently, we tested the hypothesis that central TNF blockade prevents dysregulation of brain RAS components and attenuates Ang II-induced hypertension. 24419904: Antagonist of C5aR prevents cardiac remodeling in angiotensin II-induced hypertension. METHODS: Hypertension was induced by angiotensin II (Ang II) subcutaneously infused at a dose of 1500 ng/kg/min for 7 days. CONCLUSIONS: Our data suggest that inhibition of C5aR could be a potential therapeutic strategy in preventing organ damage in Ang II-induced hypertension. BACKGROUND: Inflammatory responses mediate the development of perivascular fibrosis and heart dysfunction induced by hypertension. 26630215: AIMS: T-regulatory lymphocyte (Treg) adoptive transfer prevented angiotensin (Ang) II-induced hypertension and microvascular injury. 26922123: These results demonstrate that renal medullary interstitial blockade of HO-1 exacerbates Ang II-induced hypertension via a mechanism that is dependent on enhanced superoxide generation and highlight the important antioxidant function of HO-1 in the renal medulla. The present study was designed to test the hypothesis that increased renal medullary superoxide production contributes to the increase in blood pressure in response to blockade of renal medullary HO-1 in Ang II-induced hypertension. 27141060: Interleukin-17A Regulates Renal Sodium Transporters and Renal Injury in Angiotensin II-Induced Hypertension. Angiotensin II-induced hypertension is associated with an increase in T-cell production of interleukin-17A (IL-17A). 27146402: The present study examined how curcumin regulates AT1R expression in vascular smooth muscle cells and investigated the physiological significance of this regulation in angiotensin (Ang) II-induced hypertension. 28330983: We aimed to determine whether angiotensin (Ang) II caused kinetic changes in gammadelta T cells; deficiency in gammadelta T cells blunted Ang II-induced hypertension, vascular injury, and T-cell activation; and gammadelta T cells are associated with human hypertension. gammadelta T Cells Mediate Angiotensin II-Induced Hypertension and Vascular Injury. 28587989: In this study, we evaluated the effect of Ang II-induced hypertension on basilar artery responsiveness to BK in the Microminipig (MMPig). 30658013: 1,2,3,4,6-Penta-O-galloyl-beta-d-glucose modulates perivascular inflammation and prevents vascular dysfunction in angiotensin II-induced hypertension. 30664704: The objective of this study is to investigate the effect of metformin on angiotensin II (Ang II)-induced hypertension and cardiovascular diseases. 31507536: The goal of the current study was to assess the impact of GPER deletion on sex differences in Ang II-induced hypertension and oxidative stress. 9323082: Angiotensin II-induced hypertension increases heme oxygenase-1 expression in rat aorta. Treatment with either losartan (25 mg x kg(-1) x d(-1)) or hydralazine (15 mg x kg(-1) x d(-1)), both of which prevented the Ang II-induced hypertension, blocked HO-1 mRNA upregulation. BACKGROUND: We investigated the in vivo effects of angiotensin (Ang) II-induced hypertension on heme oxygenase (HO) mRNA and protein expression, activity, and localization in rat aortas. 11215107: [Pathophysiological roles of angiotensin in the pathogenesis of hypertension and cardiovascular remodeling]. Here, we review recent advances in the roles of AT1 and AT2 receptors in the pathogenesis of hypertension and the cardiovascular remodeling. 1192615: Animal studies show that the amount of excess body water and salt required to cause hypertension is exceedingly small, and that the hypertensive effect of the excess water and salt may not develop for days or weeks. When vascular constriciton occurs simultaneously, as occurs in the presence of large quantities of angiotensin, the blood volume may be less than normal, but even in these circumstances the fluid volume is relatively increased and is responsible for the hypertension because the vascular constrictont has decreased the capacity of the circulation to a greater extent than the decrease in blood volume. 1209480: Current evidence suggests that angiotensin can produce hypertension by a direct effect on peripheral blood vessels in malignant hypertension and in renin-secreting renal tumors and by an intrarenal mechanism influencing intrarenal distribution of blood flow, and, thereby, sodium resorption in chronic renovascular hypertension. 12468106: The predominant role of brain angiotensinogen and angiotensin in environmentally induced hypertension. 1363433: CONCLUSIONS: The results show that SHR have increased kininase and angiotensin converting activity compared with NWR, and that kinins as well as angiotensin may contribute to the pathogenesis of hypertension. 13919621: Neurogenic factors and angiotensin in etiology of hypertension. 15702613: Moreover, we also have observed an increased production of superoxide anion in the aorta of rats made hypertensive according to the SHR, glucose or angiotensin-induced and DOCA-salt models during the development of hypertension. 16946584: The AHA angiotensin system is also responsible for hypertension induced by emotional stress and central Na(+) increases. 20448215: Treatment of mice in vivo with mitoTEMPO attenuated hypertension when given at the onset of Ang II infusion and decreased blood pressure by 30 mm Hg following establishment of both Ang II-induced and DOCA salt hypertension, whereas a similar dose of nontargeted TEMPOL was not effective. 20956897: In Bangladesh we are doing more conservative kidney preserving surgery for PUJO, but need long term follow up of the patients undergoing surgery for PUJO in childhood for potential of developing renin-angiotensin induced hypertension in later life. 25855778: Inappropriate activation of the type 1A angiotensin (AT1A) receptor contributes to the pathogenesis of hypertension and its associated complications. 2849951: The angiotensin converting enzyme (ACE)-inhibitor enalapril caused a complete reduction of the angiotensin induced hypertension. 29228345: Mechanisms and mediators of hypertension induced by erythropoietin and related molecules. Animal studies show the primary importance of chronic kidney disease in the genesis of EPO-induced hypertension. EPO-induced hypertension, at least in part, appears to be independent of an increase in hemoglobin, because experiments show that hemoglobin may be increased by EPO without an increase in blood pressure (BP) by simply treating the animals with EPO-binding protein and that treatment with EPO in the setting of iron deficiency may not increase hemoglobin but may still increase BP. Preclinical studies show deranged regulation of the nitric oxide, endothelins and porstanoids and the sympathoadrenal and renin-angiotensin pathways as causes of EPO-induced hypertension. Human studies suggest that EPO administration is also associated with increased responsiveness to catecholamines and angiotensin II on vascular tissue; in addition, hypoxia-induced vasodilation may be impaired in those with EPO-induced hypertension. However, experimental data are not consistent across studies and better mechanistic designs are needed, especially in patients with chronic kidney disease, to dissect the precise mechanism of EPO-induced hypertension. The purpose and focus of this review is to critically evaluate the mechanisms of EPO-induced hypertension. 29309677: We also examined sleep/wake behaviors in an animal model of preeclampsia, pregnancy-associated hypertensive (PAH) mice, in which increased angiotensin causes hypertension. 31551925: Together with altered vascular reactivity to Ang peptides, the iRAS causes hypertension, renal damage and secondary changes in the neurohumoral control of the maternal circulation and fluid and electrolyte balance, which contribute to the pathophysiology of preeclampsia. Experimental studies in animals have shown that placental renin, when released into the maternal circulation, can cause hypertension. 3306150: It is likely that the compensatory hemodynamic changes in response to reduction in renal mass in the glomeruli of clip-ablation rats make them more vulnerable to injury when exposed to a renin-angiotensin induced hypertension. 33091308: Ginseng also reduced abnormalities in left ventricular function as well as the angiotensin-induced increased blood pressure. 38281923: Therefore, we aimed to test the hypothesis that UCPPS patients have dysregulated angiotensin signaling, resulting in increased hypertension compared to controls. 4304221: Utilization of phentolamine (Regitine) test in essential, renal and angiotensin induced hypertension. 43064: Acute hypertension was induced by adrenaline, noradrenaline or angiotensin in awake unrestrained rats with chronic indwelling catheters in a jugular vein and in the aorta. Blood-brain barrier to albumin in awake rats in acute hypertension induced by adrenaline, noradrenaline or angiotensin. 4377512: Dynamic functions of angiotensin in hypertension: renal effects as the basic cause of chronic hypertension. 6204129: The data indicate that hypertension in the 2K1C model is due to the high angiotensin levels in these animals. 6365370: In the SHR both the salt appetite and the hypertension may be induced by angiotensin acting via central mechanisms. 6723887: Reversibility of blood-brain barrier dysfunction in acute hypertension induced by angiotensin. 7016597: Humoral agents discussed include angiotensin and vasopressin and the participation of their central and peripheral actions in the pathogenesis of hypertension. 7223903: Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. 7379899: Pathomorphological reactions of myocardium and intramural vessels of rats in the course of hypertension induced by depot angiotensin. 7398346: Although angiotensin II has powerful vasoconstrictor properties, it is doubtful that any substance can produce sustained hypertension solely by increasing total peripheral resistance. The results of these studies clearly demonstrate that angiotensin has a powerful direct antinatriuretic effect, the magnitude of which is sufficient to cause marked hypertension at angiotensin concentrations well within the pathophysiological range. 830813: Conversely, in angiotensin-induced systemic arterial hypertension, CSF pressure and its pulse amplitude increased. 879924: The data implicate a renin angiotensin mechanism as probable cause of hypertension in radiation nephritis. 9260993: As interactions between the renin-angiotensin and sympathetic nervous systems have been suggested in the pathogenesis of hypertension, we wanted to investigate the effect of chronic renin-angiotensin blockade with losartan and enalaprilat on the sympathetic reactivity to hypotension and on the cardiac beta-adrenergic-coupled adenylyl cyclase pathway in 12-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). 9809187: The second hypothesis suggests that chronic angiotensin produces hypertension by increasing Na+ reabsorption leading to volume expansion and hypertension. 10505492: Selection of antihypertensive agents in the overweight patient should take into account the mechanisms leading to hypertension and the metabolic abnormalities that characterize the obese patient. Hyperinsulinemia, which is characteristic of obesity, can contribute to the probability of developing hypertension by activating the sympathetic nervous system (SNS) and by causing sodium retention. 14483867: The significance of disturbances of the metabolic anti-hypertensive function of the kidney in the pathogenesis of hypertension. 15499025: Clinically, these channels form the target of antianginal and antihypertensive drugs, and their genetic disruption leads to hypertension and sudden cardiac death through coronary vasospasm. 2757809: The effects of antihypertensive drugs on the cock (kidney) seemed essential in their hypotensive action, similarly as abnormality of the renal function curve is essential in the genesis of hypertension. 27873231: The hypertension is considered a secondary form and can even be resistant to multiple antihypertensives. 29022534: BACKGROUND: Non-adherence to antihypertensives is a cause of 'pseudo-treatment-resistant' hypertension. 30014548: Non-adherence to antihypertensives is a leading cause of apparent treatment-resistant hypertension (aTRH). 31352698: Learning Points: In a young patient with concurrent hypokalemia and uncontrolled hypertension on multiple antihypertensive agents, secondary causes of hypertension should be evaluated.?? 35703879: BACKGROUND: Vascular dysfunction, an independent risk factor for cardiovascular disease, often persists in patients with hypertension, despite improvements in blood pressure control induced by antihypertensive medications. 36084087: Non-adherence to antihypertensive medications is a major cause of uncontrolled hypertension, leading to cardiovascular morbidity and mortality. 36606165: Introduction: Non-adherence to antihypertensive medications is a leading cause of uncontrolled hypertension and its complications. 38569838: Therefore, we aimed to investigate the use of antihypertensive drugs in domestic cats with hypertension in Japan, the causes of hypertension, and the vital prognosis of these patients. 7203608: This study investigated whether the riboflavin analogs, 7,8-dimethyl-10-formylmethyl isoalloxazine (FMI) and 7,8-dimethyl-10-(2'-hydroxyethyl) isoalloxazine (HEI), are effective antihypertensive agents in mineralocorticoid-induced or deoxycorticosterone acetate (DOCA)-salt hypertension. 10904027: The effects of BSO were mitigated by concomitant antioxidant therapy despite GSH depletion, which supports the notion that oxidative stress was involved in the pathogenesis of hypertension in this model. Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. 17954371: ACTH- but not Dex-induced hypertension was partially reversed by aspirin. The aim of the present study was to investigate the effects of aspirin, a potent antioxidant, on adrenocorticotropic hormone (ACTH) and dexamethasone (Dex)-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with increased oxidative stress. Aspirin prevented the development of hypertension caused by ACTH (P' < .01) and tended to prevent Dex-induced hypertension (P' = .07). 1836520: [The role of pro-oxidation and antioxidation in the etiology of arterial hypertension]. 18568695: However, the use of antioxidants in the clinical setting induced only limited effects on human hypertension or cardiovascular endpoints. 1930920: Although obesity and alcohol intake as well as dietary sodium, potassium and magnesium are the major non-genetic determinants of blood pressure levels, interest has recently been stimulated in the function of fatty acids and antioxidants in the aetiology of hypertension. 19765471: Since reactive oxygen species are implicated in the induction of hypertension, antioxidants have been used to reduce blood pressure and renal impairment in animal models and in human hypertension. 19807685: Oxidative stress resulting from imbalance between reactive oxygen species (ROS) generation and antioxidant mechanisms is important in the pathogenesis of cardiovascular diseases such as atherosclerosis, ischemic heart disease, heart failure, stroke, hypertension and diabetes. 22125211: Imbalance of antioxidants and reactive oxygen species contributes to endothelium damage and leads to hypertension. 23533693: The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. CONCLUSION: Glucocorticoid-induced hypertension in rats is prevented by alpha-lipoic acid via mechanisms other than mitochondrial superoxide reduction. AIMS: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition. 24047403: Oxidative stress resultant from imbalance between ROS generation and antioxidant defense mechanisms is important in pathogenesis of cardiovascular diseases, such as hypertension, heart failure, atherosclerosis, diabetes, and cardiac hypertrophy. 27747859: Curcumin can inhibit diabetes, heavy metal and stress-induced hypertension with its antioxidant, chelating and inhibitory effects on the pathways that lead to hypertension. 28189851: We tested the hypothesis that salt-sensitive hypertension is caused by renal oxidative stress by measuring the blood pressure and reactive oxygen species-related proteins in the kidneys of human G protein-coupled receptor kinase 4gamma (hGRK4gamma) 486V transgenic mice and non-transgenic (Non-T) littermates on normal and high salt diets. Thus, hGRK4gamma486V causes salt-sensitive hypertension due, in part, to defective renal antioxidant mechanisms. 30847157: In general, the aqueous extract of A. mongolicum Regel has the potential to be used as a functional food or nutraceutical in prevention and treatment of obesity and hypertension due to the high antioxidant and sound inhibitory potential against vital enzymes relevant to obesity and hypertension. 3189209: The marked elevation of blood pressure at the lowest levels of plasma ascorbic acid and serum Se concentrations supports the hypothesis that antioxidants play a role in the etiology of hypertension. 31902320: High concentrations of antioxidants could prevent H 2 O 2 production in renal proximal tubules, which would result in sodium retention and increased blood pressure. 32388270: We investigated the association of IDH2 between the development of prolonged high-fat diet (HFD)-induced hypertension. These results indicate that prolonged HFD intake disrupts the IDH2-NADPH-GSH-associated antioxidant system and activates the renin-angiotensin system in the kidney, leading to increased BP, suggesting that IDH2 is a critical enzyme in the development of hypertension and that the IDH2-associated antioxidant system could serve as a potential hypertension treatment target. 34202966: It is also used in traditional medicine for many human disorders including fever, gastrointestinal complications, arthritis, rheumatism, hypertension, and various infectious diseases due to its anti-inflammatory, antioxidant, antimicrobial, and antiemetic properties. 3481820: The marked elevation of blood pressure at the lowest levels of plasma vitamin C concentration supports the hypothesis of the role of antioxidants in the aetiology of hypertension. 36544300: The current study suggests that disturbed homeostasis, a consequence of altered interaction between antioxidant system and inflammatory events raises the oxidative stress levels which eventually leads to hypertension and associated complications. 38129126: The present study demonstrates that a new melatonin derivative, ITH13001, prevents hypertension development and the associated cardiovascular alterations, due to its antioxidant and anti-inflammatory properties, making this compound a potential candidate for treatment of resistant hypertension patients. 16311508: Strong evidence indicates oxidative stress in the pathogenesis of Alzheimer's disease (AD). Deregulation of GRX1 and TRX1 antioxidant systems could be important events in AD pathogenesis. 21166677: Recent findings suggest that 'aged garlic extract' (AGE) may be a therapeutic agent for AD because of its antioxidant and Abeta lowering properties. 22042981: BACKGROUND: Serum plasmalogens (Pls) have gained interest in several clinical symptoms such as metabolic syndrome/atherosclerosis or Alzheimer's disease possibly because of their antioxidant properties. 23645386: Curcumin, a dietary polyphenol, has shown a potential to act on the symptoms of neurodegenerative disorders, including Alzheimer's and Parkinson's diseases, as a consequence of its antioxidant, anti-inflammatory and anti-protein aggregation properties. 24426241: In Conclusion, melatonin significantly ameliorates the neurodegeneration characteristic of AD in experimental animal model due to its antioxidant, antiapoptotic, neurotrophic and anti-amyloidogenic activities. 28049401: Many dietary components, including different types of fruits, vegetables, spices, and marine products as well as a Mediterranean diet, are a good source of antioxidants and have anti-inflammatory properties, with many showing substantial potential against AD pathogenesis. 30021335: In conclusion, 4-PSQ protected against learning and memory impairment and anxiety in a mouse model of AD induced by Abeta, and anticholinesterase and antioxidant actions are involved in the pharmacological effect of the compound. 30596810: Objectives: In order to infer whether long-term circulating antioxidant exposure plays a role in AD etiology, we tested the hypothesis that AD risk would be lower in individuals with lifelong, genetically predicted increases in concentrations of 4 circulating antioxidants that are modifiable by diet. 31561062: Trans-crocin 4 (TC4) is an important carotenoid constituent of saffron showing potential activity against Alzheimer's Disease (AD) due to its antioxidant and antiamyloidogenic properties. 31778363: They are new promising compounds against AD due to their antioxidant, anti-inflammatory and acetylcholinesterase inhibitory activities in the neural system. 32391472: Effects of alpha-Mangostin Derivatives on the Alzheimer's Disease Model of Rats and Their Mechanism: A Combination of Experimental Study and Computational Systems Pharmacology Analysis.alpha-Mangostin (alpha-M) is a natural xanthone from the pericarp of fruit Garcinia mangostana and possesses versatile biological activities. alpha-M has a therapeutic potential to treat Alzheimer's disease (AD) because of its anti-inflammatory, antioxidative, and neuroprotective activities. 33384986: The findings in this review suggest that probiotics, prebiotics or synbiotics have potential as novel biological prophylactics in treatment of AD, due to their anti-inflammatory and antioxidant properties, their ability to improve cognition and metabolic activity, as well as their capacity of producing essential metabolites for gut and brain barrier permeability. 33399852: Human apolipoprotein-D (apoD) is a glycosylated lipocalin that plays a protective role in Alzheimer's disease due to its antioxidant function. 33971493: METHODS: Aluminum chloride (70 mg/kg, I.P for 5 weeks) was used to induce AD in rats that either normally fed or socially isolated and protein malnourished (SI&PM). Natural antioxidants enhance the power of physical and mental activities versus risk factors inducing progression of Alzheimer's disease in rats. 34553117: Conclusion: According to our results, we suggested that insufficient apelin-13 and TAS levels may contribute to the pathogenesis of AD. 35327563: This review highlights the neuroinflammatory and neuroprotective role of epigallocatechin-3-gallate (EGCG): the medicinal component of green tea, a known nutraceutical that has shown promise in modulating AD progression due to its antioxidant, anti-inflammatory, and anti-aging abilities. Using Alzheimer's disease (AD) as the archetype, the pathological findings include the aggregation of Amyloid Beta (Abeta) peptides, mitochondrial dysfunction, synaptic degradation caused by inflammation, elevated reactive oxygen species (ROS), and cerebrovascular dysregulation. 35412308: Furthermore, two-photon microscopic imaging of various regions in Alzheimer's disease (AD) mice brains revealed a down-regulated Msrs levels compared with that in normal brains, especially in the cornuammonis of the hippocampus region, which may in turn lead to an aggravation of AD pathogenesis due to the weakened antioxidant and self-repair capability of neurons. 36143299: The results of the studies showed that the use of phytochemicals against AD has gained relevance due to their antioxidant, anti-neuroinflammatory, anti-amyloid, and anti-hyperphosphorylation properties of Tau protein. 36277497: Mesenchymal stem/stromal cells (MSCs) could be a potential therapeutic option for treating AD due to their immunomodulatory, anti-inflammatory, regenerative, antioxidant, anti-apoptotic, and neuroprotective effects. 37659206: In recent years, natural compounds sourced from diverse origins have garnered considerable attention as potential therapeutic agents for AD, owing to their anti-inflammatory, antioxidant, and neuroprotective properties. 37877008: Recently, natural medicines, especially Chinese herbal medicines, have gained attention in the treatment of AD due to their antioxidant, anti-inflammatory, and neuroprotective effects. 37927255: These phytocompounds are widely available and a multitude of holistic therapeutic efficiencies for treating AD owing to their antioxidant, anti-inflammatory, and biological activities. 38151890: Consuming hazelnut may attenuate the risk of neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and Huntington's disease due to its anti-inflammatory and anti-oxidant qualities. 1037841: Aortic nascent histamine in neurogenic and aortic coarctation induced hypertension: effect on arterial permeability. 10744358: These data suggest contribution of lipoxygenase-derived products to mechanisms underlying aortic smooth muscle basal tone and elevated blood pressure in rats with aortic coarctation-induced hypertension. This study was designed to examine the contribution of lipoxygenase products to mechanisms of vascular contraction and elevated blood pressure in rats with aortic coarctation-induced hypertension. 11247816: We investigated the effect of intraluminal pressure or stretch on the development of tone in the descending thoracic aorta from rats with aortic coarctation-induced hypertension of 7-14 days duration. 11532103: Enhanced nitric oxide inactivation in aortic coarctation-induced hypertension. 11566933: Hypertension was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 9 days (4 control and 5 experimental days). 12541097: These results indicate that the involvement of cGMP-independent K(Ca) channels in nitroglycerin-mediated relaxation disappeared after the development of hypertension produced by aortic coarctation. 1425979: We investigated the role of prostanoids in the constrictor effect of calcium ionophore A23187, endothelin-1 and vasopressin in rings of thoracic aorta obtained from normotensive rats and rats with aortic coarctation-induced hypertension. 15078384: Perioperative hypertension due to undiagnosed aortic coarctation: are current standards of care adequate? 15117596: Aortic coarctation is an unusual cause of hypertension in pregnancy. 15132297: Treatment with Tempo did not affect the arterial pressure of un-operated normotensive rats but promptly decreased the arterial pressure of rats with aortic coarctation-induced hypertension (from 178 +/- 2 to 125 +/- 6 mmHg). Prostaglandin I2 does not contribute to the hypotensive effect of the superoxide dismutase mimetic Tempo in rats with aortic coarctation-induced hypertension. 15223269: In this study we have employed in situ hybridization to analyze changes in mRNA expression of NPY receptor subtypes Y1 and Y2 in the nucleus tractus solitarii (NTS), paraventricular nucleus of the hypothalamus (PVN) and petrosal and nodose ganglions 2 h, 3 and 7 days after aortic coarctation induced hypertension. The data suggest that NPY Y1 and Y2 receptors might participate in the mechanisms involved in the establishment/maintenance of hypertension induced by aortic coarctation. 15275958: In this study, we have employed in situ hybridization to analyse changes in mRNA expression of alpha CGRP and GAL in the nucleus tractus solitarii (NTS), hypothalamic paraventricular nucleus (PVN) as well as petrosal and nodose ganglia after aortic coarctation-induced hypertension in rats. Data suggest that alpha CGRP and GAL may participate in the mechanisms involved in the establishment/maintenance of hypertension induced by aortic coarctation. 15777385: Hypertension was the most common presentation (77%) and was usually a consequence of renal artery stenosis or aortic coarctation. 15814300: Aorta coarctation results in hypertension (HTN) in the arterial tree proximal to stenosis and, as such, provides an ideal model to discern the effects of different levels of blood pressure on the vascular tissue in the same animal. Compelling evidence has emerged supporting the role of oxidative stress as a cause of HTN. 16079792: Our results show that hypertension acutely induced by aortic coarctation induces a breaking of the blood-brain barrier (BBB) and reactive astrocytosis through hyperperfusion, and evokes trigger factors of neurodegeneration such as oxidative stress and inflammation, similar to that observed in cerebral hypoperfusion. 16280280: Hypertension induced by aortic coarctation above the renal arteries is associated with immune cell infiltration of the kidneys. 16381310: Emergency stage of hypertension was induced by an experimental aortal coarctation. 17562191: We analyzed here the levels of FGF-2 immunoreactivity in the nucleus tractus solitarii (NTS) of Wistar Kyoto rats in response to alterations of neuronal activity promoted by the stimulation of the baroreceptor reflex following an aortic coarctation-induced-hypertension. 17646033: Increased hypothalamic angiotensin-(1-7) levels in rats with aortic coarctation-induced hypertension. 188343: Aortic coarctation produced severe hypertension (MAP greater than 150 mmHg) and plasma renin activity values (radioimmunoassay) at least 10 times normal within 2-6 days after surgery. 1885220: To assess the effect of hypertension on diet-induced coronary artery plaques after a return to a nonatherogenic diet, 10 cynomolgus monkeys were fed an induction regimen containing 2% cholesterol and 25% peanut oil for 6 months and then were subjected to midthoracic aortic coarctation to induce hypertension. 1885223: The comparisons were made in rings of aorta taken from normotensive rats and from rats with aortic coarctation-induced hypertension at 12 days and 90-113 days after coarctation. These data suggest that a prostanoid-mediated and endothelium-dependent mechanism of vasoconstriction contributes to the constrictor effect of angiotensin II in aortic rings of rats in the early phase of aortic coarctation-induced hypertension. 2013478: Intravenous administration of a blocker of thromboxane A2/prostaglandin endoperoxide receptors, SQ29548 (2 mg/kg bolus injection plus 2 mg/kg/hr for 3 hours), reduced from 162 +/- 4 to 144 +/- 5 mm Hg (p less than 0.05) the blood pressure of rats with aortic coarctation-induced hypertension at 7-14 days after coarctation when plasma renin activity is greatly increased. Accordingly, the blood pressure of rats with aortic coarctation-induced hypertension is influenced by the interplay of prostanoid-mediated pressor and vasodepressor mechanisms. Also prostanoid-mediated vasodepressor mechanisms are operational in the early phase of aortic coarctation-induced hypertension since the blood pressure of rats pretreated with SQ29548 was increased by the subsequent administration of indomethacin. The blood pressure-lowering effect of SQ29548 in the early phase of aortic coarctation-induced hypertension was positively correlated with the prevailing plasma renin activity and could not be demonstrated in hypertensive rats pretreated with indomethacin. In contrast, treatment with SQ29548 was without effect on the blood pressure of either normotensive or hypertensive rats (i.e., aortic coarctation-induced hypertension at 90-113 days after coarctation, deoxycorticosterone-salt-induced hypertension) having normal or depressed values of plasma renin activity. 20304663: OBJECTIVE: Primary adult aortic coarctation (PAAC) is an unusual cause of hypertension. 20362505: Subsequent workup demonstrated severe proximal hypertension due to congenital aortic coarctation as the cause of this event. 21098870: The aims of this study were to identify the effect of clofibrate administration in the development of high blood pressure secondary to aortic coarctation (AoCo) and to assess its effect on vascular reactivity. Effect of clofibrate on vascular reactivity in a model of high blood pressure secondary to aortic coarctation. 21538288: [Hypertension due to aortic coarctation--a missed clinical diagnosis]. 22511530: Aortic coarctation is an unusual cause of hypertension during pregnancy and its management is not clarified. 22542661: Both can contribute to high blood pressure attenuation in hypertension secondary to AoCo. 24093067: The aim of this report is taking attention to CoA as a cause of systemic hypertension and is also emphasizing the differences of diagnostic approach for hypertension in children from adults. 25001168: With this case we aim to draw attention to aortic coarctation and interrupted aortic arch as potential causes of hypertension and to highlight the importance of the physical examination in the diagnosis of secondary causes of hypertension. 25084549: We discuss the evidence supporting the use of ob/ob mice, high-fructose diets, aortic coarctation-induced hypertension and Octodon degus, which spontaneously develops beta-amyloid deposits and metabolic derangements, as suitable animal models to address the relationships between MS and AD. 25634191: We report the first case of late presentation of familial aortic coarctation, a rare cause of hypertension. 25861324: A 26-year-old male with resistant hypertension due to a CoA diagnosed by computed tomography angiography referred to our center for an attempted stent implantation. 27091737: Medical therapy for hypertension due to CoA parallels treatment of essential hypertension with beta blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers as first-line agents. 30264739: Fundus examination helps in differentiating hypertension due to CoA from other causes of juvenile hypertension, as corkscrewing of retinal arterioles is seen only in CoA but not in other conditions. 32547662: Coarctation of the aorta (CoA) was definitively diagnosed and was the cause of the upper limb hypertension and headache. 34902023: Similar presentations in the postsubclavian aorta may result in acquired atheromatous aortic coarctation leading to systemic hypertension and heart failure. 3566562: [Arterial hypertension caused by aortic coarctation in dogs. Renal hemodynamics and pressure natriuresis]. 37961634: Coarctation of the aorta (CoA) often leads to hypertension (HTN) post-treatment. 38501250: BACKGROUND: Coarctation of the aorta (CoA) often leads to hypertension) posttreatment. 4053303: Hyperplastic growth response of vascular smooth muscle cells following induction of acute hypertension in rats by aortic coarctation. This study examines the growth response of vascular smooth muscle cells following induction of acute hypertension in rats by partial ligation of the abdominal aorta between the renal arteries. It is suggested that a non-denuding form of endothelial \injury\ may play an important role in the proliferative growth response of smooth muscle cells following induction of coarctation hypertension. 553866: Thus, in normotensive vascular beds of rats with chronic hypertension caused by aortic coarctation, resistance is elevated. 6322257: Thus, aorta-coarctation induced hypertension is not associated with any alterations in cardiac alpha-adrenoceptors, which is different from reports in other models of experimental hypertension. 6340859: UNLABELLED: To investigate the role of the renin-angiotensin-aldosterone system in hypertension due to coarctation of the aorta (COA), upright mean arterial pressure (MAP), plasma renin activity (PRA) and plasma aldosterone (Aldo) were determined before and 90 minutes after a single oral dose of captopril (25 mg) in eight patients with COA and in fourteen with essential hypertension (EH). 662602: [Action of beta blockaders in hypertension caused by isthmic aortic coarctation: a new proof in favor of renin-angiotensin system]. 6797108: Systemic hypertension (secondary to aortic coarctation) produces in monkeys, multifocal brain lesions where capillaries show increased diameter, endothelial degeneration and deposition of collagen and other substances in the basement membrane. 690267: Histological studies including electron microscopy were performed on the carotid sinuses of dogs with renal hypertension of 17 to 82 days duration or hypertension of two years secondary to aortic coarctation. 7616384: Similar relaxations to L-arginine were seen in rings of thoracic and abdominal aorta from rats made hypertensive by infusion of angiotensin II for 7 to 8 days but not in rings of thoracic aorta from rats with aortic coarctation-induced hypertension of 28 to 42 days. 7721428: We conclude that aortic rings from rats with aortic coarctation-induced hypertension display calcium-dependent, protein kinase C-mediated tone in the absence of exogenous vasoconstrictors. We examined the regulatory influence of nitric oxide on development of calcium- and protein kinase C-dependent basal tone in rings of thoracic aortas from rats with aortic coarctation-induced hypertension and from normotensive controls. 8206572: That pressor and aortic constrictor responsiveness to L-NAME are increased after aortic coarctation suggests that a mechanism of vasodilation, mediated by nitric oxide, is preferentially manifested in rats with aortic coarctation-induced hypertension. NG-Nitro-L-arginine methyl ester (L-NAME) (3 x 10(-4) mol/L) increased tension (82 +/- 11% of the response to 120 mmol/L potassium chloride) in rings of thoracic aorta taken from hypertensive rats 7 to 14 days after aortic coarctation, whereas rings of abdominal aorta from below the coarctation were unresponsive, as were rings of thoracic aorta from rats with deoxycorticosterone-salt-induced hypertension and from the corresponding normotensive controls of either model of hypertension. 8268825: Effect of bilateral nephrectomy on hypertension produced by acute aortic coarctation. 8293559: We tested the hypothesis that a prostanoid-mediated mechanism of vascular contraction is expressed in rats with aortic coarctation-induced hypertension. 8591882: Pretreatment with NG-nitro-L-arginine methyl ester did not interfere with the vasodepressor effect of sodium nitroprusside or prazosin in rats with aortic coarctation-induced hypertension or with the blood pressure reduction caused by discontinuation of an infusion of phenylephrine in rats made hypertensive by long-term administration of this drug. 8815261: A 10-year-old boy was admitted to our hospital with severe hypertension due to unusual aortic coarctation at the level of the diaphragm without renal artery stenosis. 8874951: We present a 72-year-old man with long-standing moderate hypertension, due to an aortic coarctation, who presented with a myocardial infarction. 8922345: In conclusion, suprarenal aortic coarctation leads to progressive hypertension resulting in LVH, progressive increases in plasma ANP and BNP and, in most cases, death from heart failure. 9336310: Contribution of constrictor prostanoids to the calcium-dependent basal tone in the aorta from rats with aortic coarctation-induced hypertension: relationship to nitric oxide. 9535423: CH was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 8 days (4 control and 4 experimental days). 9797182: OBJECTIVE: To evaluate the contribution of nitric oxide to the regulation of angiotensin II-induced renal vasoconstriction in normotensive rats and in rats with aortic coarctation-induced hypertension. 9817609: This study was designed to investigate involvement of potassium channels in the action of nitric oxide facilitating reduction of basal tone by thromboxane A2/prostaglandin H2 receptor blockade with ifetroban in rings of thoracic aorta taken from rats with aortic coarctation-induced hypertension. These observations suggest that a mechanism involving nitric oxide and potassium channels facilitates the reduction in basal tone produced by ifetroban in aortic rings of rats with aortic coarctation-induced hypertension. 9931125: DOCA-salt (volume expansion) or aortic coarctation (renin-dependent) induced similar hypertension and left ventricular hypertrophy (LVH) in 129/SvEvTac and B2-KO mice, suggesting that kinins do not play an essential role in the development of DOCA-salt- or aortic coarctation-induced hypertension. Effect of ACE inhibitor on DOCA-salt- and aortic coarctation-induced hypertension in mice: do kinin B2 receptors play a role? Using normal 129/SvEvTac mice and mice lacking the bradykinin B2 receptor gene (B2-KO), we investigated whether (1) the hypertensinogenic effect of DOCA-salt or aortic coarctation is enhanced in B2-KO mice and (2) the chronic antihypertensive and antihypertrophic effects of an ACEi (ramipril, 4 mg. kg-1. d-1) are mediated by B2 receptors in aortic coarctation (6 weeks)- and DOCA-salt (4 weeks)-induced hypertension. Thus, in mice, kinins acting via B2 receptors do not participate in (1) maintenance of normal basal blood pressure, (2) establishment and maintenance of hypertension induced by DOCA-salt or aortic coarctation, and (3) chronic antihypertensive and cardiac antihypertrophic effects of ACEi in DOCA-salt and aortic coarctation hypertension. 32163130: This suggests that structural vulnerability in neuronal networks associated with APOE-epsilon4 may be an early event in AD pathogenesis, possibly upstream of amyloid deposition. 32308396: Conclusions: Our findings suggested that APOE epsilon4 might affect CSF VILIP-1 level in preclinical AD, indicating an important role of APOE epsilon4 in neuron injury leading to AD. 32986665: OBJECTIVE: This study aimed to investigate the interactive role of androgen decline and APOEE4 genotype in the pathogenesis of amnestic mild cognitive impairment (aMCI) and AD. 33331110: In addition, apolipoprotein E epsilon4 status promotes them to result in the pathogenesis of AD. AIM: Heredity plays an important role in the pathogenesis of Alzheimer's disease (AD) especially for single-nucleotide polymorphism (SNPs) of susceptible genes, which is one of the significant factors in the pathogenesis of AD. 33748578: Apolipoprotein E4 (ApoE4) is the main genetic risk factor for Alzheimer's disease (AD), but the exact way in which it causes AD remains unclear. 34743630: Congruence across language and episodic memory results as well as hippocampal and inferior lateral ventricle volume findings suggest that APOE -epsilon4 may interact with cerebral oxygen metabolism in the pathogenesis of Alzheimer's disease and related neurodegeneration. 35088039: Several studies suggests that APOE E 4 causes AD via different processes like neurofibrillary tangle formation by amyloid-beta accumulation, exacerbated neuroinflammation, cerebrovascular disease, and synaptic loss. 36396603: DISCUSSION: Since HLA-DRB1 and APOE are expressed in the BBB, blood MCP-1 released in the peripheral inflammatory cascade may function as a mediator of the effects of HLA-DRB1 rs9271192-AC/CC and APOE epsilon4 genotypes on AD pathogenesis in the brain via the BBB pathways. 37018391: Our results support that the APOE epsilon4 genotype exerts Abeta-independent effects on AD pathogenesis by activating microglia in brain regions associated with early tau deposition. 37947590: Detrimental Effects of ApoE epsilon4 on Blood-Brain Barrier Integrity and Their Potential Implications on the Pathogenesis of Alzheimer's Disease. 38014339: Despite strong evidence supporting the involvement of both apolipoprotein E4 (APOE4) and microglia in Alzheimer's Disease (AD) pathogenesis, the effects of microglia on neuronal APOE4-driven AD pathogenesis remain elusive. These findings highlight the concerted roles of neuronal APOE, especially APOE4, and microglia in AD pathogenesis. 10420066: More specifically, it seems undisputed that the APOE*4 allele plays an important role in the pathogenesis of AD. 10655544: Our human apoE4 knock-in mice will be useful in clarifying the role of apoE in the etiologies of AD and cardiovascular diseases in relation to cholesterol and lipid metabolism. 10775884: Apolipoprotein E (protein: apo E; gene: APOE) plays an important role in the multifactorial etiology of both Alzheimer's disease (AD) and lipid level concentrations. 10818522: Our data suggest that ApoE modulates the outcome following cerebral ischemia via molecular events in common with AD pathogenesis. We propose that ischemic-reperfusion processes in brain are the fountain-head of a cycle of molecular and cellular events that have neurodegenerative consequences which finally lead to AD. 10899434: This review summarizes part of an experimental approach to identify biological pathways influenced by the different APOE polymorphisms that are relevant to the pathogenesis of AD. 11005255: While the relevance of these proposed functions to the etiology of AD remains a mystery, these and other hypotheses will be tested as the field of apoE neurobiology grows, adding relevant new data to the functions of apoE in health and in the pathogenic mechanisms leading to AD. 11145984: To further investigate the potential interaction between apoE and A beta in the pathogenesis of AD, we have determined the effect of apoE isoforms on the neurotoxicity of non-fibrillar A beta peptides. 11165374: Apolipoprotein E (apoE) is a lipid transport molecule, which has been linked to the pathogenesis of Alzheimer's disease. 11212354: However, no clear explanation of the pathogenesis of apoE-induced AD has been provided. 11980062: Hypotheses about apolipoprotein E function that may lead to Alzheimer's disease are also discussed. 12214015: Since inheritance of different alleles of the apolipoprotein (apo) E gene is a risk factor for AD and apoE is the major lipoprotein trafficking molecule in brain, we hypothesized that apoE may modify the pathogenesis of AD by directing the delivery of oxidized CSF lipoproteins to neurons. 12355988: First, the three genes in which mutations are known to result in early onset autosomal dominant familial AD (presenilins 1 and 2, and amyloid beta protein precursor [APP]): well characterized but that account for only a small proportion of AD cases. Many of these are controversial and studies have shown conflicting results, but apoE polymorphism seems to be only one of the possible genetic factors suggested to play a role in the multifactoral pathogenesis of AD. 12573540: Recent evidence strongly suggests a role for cholesterol and apolipoprotein E in the etiology of Alzheimer's disease. 12661900: Understanding how apoE participates in the formation of senile plaques is necessary to clarify the pathogenesis of AD; however, the mechanism remains unknown. 14511323: Consequently, NSAID-induced increases in apoE protein may enhance apoE-mediated immunosuppression and compensatory synaptic plasticity, potentially resulting in decreased AD risk and delay of disease onset. 14757931: These results suggest that apoE and transferrin may be part of a complex mechanism in the pathogenesis of Alzheimer's disease. 15159602: In particular, polymorphisms within the ApoE and alpha1-ACT gene have been implicated in the aetiology of AD and s-IBM. 15634227: Accumulating evidence suggests that genetic factors such as apolipoprotein E (APOE), can act in different ways in the pathogenesis of cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD). 15716586: This review examines the current evidence for diet, lipid homeostasis, and apoE in the pathogenesis of AD. 16198584: The mechanism of action of APOE in the etiology of AD remains unclear. 16641890: Presenilins and apolipoprotein E are other neurotoxic agents involved in the pathogenesis of AD. 17166269: Since apoE is important in the pathogenesis of Alzheimer's disease (AD), we tested whether apoE treatment of neurons affected molecules important to phosphorylation of tau, such as GSK 3beta, P35, and CDK5, and the phosphorylation of tau itself. 17854398: Apolipoprotein E (ApoE), encoded by the apolipoprotein E gene (APOE), plays an important role in the pathogenesis of Alzheimer's disease (AD). 18205697: This large body of evidence suggest that apoE is a key player in the pathogenesis of AD. 18430993: Further investigation of the genetic influence of these loci on apoE expression levels in the central nervous system is likely to provide new insight into apoE regulation as well as AD pathogenesis. 18580587: These findings suggest that small HC limits educational attainment only among individuals who have greater risk of AD owing to their APOE genotype or who are destined to develop this illness later in life. 19116777: However, exactly how apoE functions in the pathogenesis of AD remains to be fully determined. These studies show that the lipid binding capacity of apoE is a major mechanism of its function in the pathogenesis of AD, and suggest that increasing apoE lipidation may be of therapeutic importance for this devastating disease. 19472365: Although apolipoprotein E (apoE) is the most common genetic risk factor for Alzheimer's Disease (AD), how apoE participates in AD pathogenesis remains incompletely understood. 20348021: Research in genetics, pathology, epidemiology, biochemistry, and cell biology, as well as in animal models, suggests that cholesterol, its transporter in the brain, apolipoprotein E, amyloid precursor protein, and amyloid-beta all interact in AD pathogenesis. 20538374: The findings suggest that abnormally high levels of ApoE may play a causative role in the pathological events of AD, particularly those involving the early cholinergic deficit in the AD brain, through modulation of cholinesterases activities, hence disturbing the acetylcholine-dependent activity of neurons and nonexcitable cells such as glial cells. 21676498: Despite the considerable converging evidence that implicates ApoE and LRP in the pathogenesis of AD, the precise mechanism by which ApoE and LRP modulate the risk for AD remains elusive. 22482075: Three genes, SORL1, APP, and APOE, are suspected to cause Alzheimer's whereas the other 21 genes are related to other diseases but may also be found to be associated with Alzheimer's, and these are TMEM59, CCT4, IGF2R, SFPQ, PRDX3, RNF14, IDS, SSBP1, SYNE2, TXNL4A, STXBP3, SMARCB1, ULK2, AGTPBP1, FABP7, CALB1, H2AFY, COPA, SAP18, ATIC and SYNCRIP. 22502767: This 'double whammy' result opens up a new direction for studies aimed at elucidating the relevant neurobiological activities of APOE isoforms in the pathogenesis of AD. 22883744: While apoE isoforms differentially interact with amyloid beta (Abeta), a pleiotropic neurotoxin key to AD etiology, more recent work has focused on immune regulation in AD pathogenesis and on the mechanisms of innate immunomodulatory effects associated with inheritance of different APOE alleles. 23541982: Analysis of side chain oxysterols in the CSF is likely to provided useful information about cholesterol metabolism and ApoE function in the pathogenesis of AD. 24154541: To directly determine the effects of APOE genotype on intraneuronal accumulation of Abeta1-42 at the onset of AD pathogenesis, we introduced lentiviral Abeta1-42 into the cortex of APOE targeted replacement (TR) mice at the age of 8-9 months. 24894353: Here, we review ApoE-lipid interactions, as well as the roles that lipids may play in the pathogenesis of AD. Evidence suggests that the ApoE protein, a major lipid transporter, plays a key role in the pathogenesis of AD, and its role in both normal and aberrant lipid metabolism warrants further extensive investigation. 24971061: In this review we will summarize the evidence supporting a role for metals in the function of ApoE and its consequent role in the pathogenesis of AD. 26401939: BACKGROUND/OBJECTIVE: Apolipoprotein E (ApoE) has an active part in the pathogenesis of Alzheimer's disease (AD). 26413387: Here, we will further discuss the linkage between elevated levels of LDL cholesterol and AD pathogenesis, and explore the underlying mechanisms whereby elevated levels of plasma LDL cholesterol promote amyloidogenesis. Among those factors, altered circulating cholesterol homeostasis, independent of the APOE genotype, continues to be implicated in brain deposition of amyloid beta protein (Abeta) and the pathogenesis of AD. 26582899: Apolipoprotein E (ApoE) is an important modifier of Alzheimer's disease (AD) pathogenesis, and its abundance has been linked to the clearance of beta-amyloid (Abeta) in the brain. 27104063: The Role of Upregulated APOE in Alzheimer's Disease Etiology. 27922847: The objective of this article is to review the recent findings about the metabolism of apolipoprotein E (ApoE) and amyloid beta and other possible mechanisms by which ApoE contributes to the pathogenesis of Alzheimer's disease. 28218653: The role of different genotypes of apolipoprotein E (apoE) in the etiology of Alzheimer's disease is widely recognized. 29376871: This suggests a vicious cycle between inflammation, RA signaling, and ApoE homeostasis in AD pathogenesis. 30032423: Regardless of widespread indispensable studies, the appropriate function of APOE in AD etiology stays ambiguous. This review also highlighted utmost ApoE targeting therapeutic tactics that are crucial for controlling Alzheimer's pathogenesis. Existing proof recommends that the disparate outcomes of ApoE isoforms on Abeta accretion and clearance have a distinct function in AD pathogenesis. 30140051: Here, we review the rapidly growing literature on the role of disease-associated microglia, TREM2 and APOE in the pathogenesis of Alzheimer disease and present an integrated view of innate immune function in Alzheimer disease. 30194628: Herein, (1) we identified the aggregation prone sequence in Abeta40 and Abeta42 as 'HHQKLVFFAE' and 'SGYEVHHQKLVFFAEDVG/KGAIIGLMVGGV' respectively with critical lysine (K) at 16 and 28 for stabilizing the aggregates; (2) elucidated the interaction pattern of AbetaPP with other Alzheimer's related proteins BACE1, APOE, SNCA, APBB1, CASP8, NAE1, ADAM10, and PSEN1 to describe the pathophysiology; (3) found APOE as commonly interacting factor between amyloid beta and Tau for governing AD pathogenesis; (4) reported K224, K351, K363, K377, K601, K662, K751, and K763 as potential putative lysine for facilitating AbetaPP clearance through ubiquitination thereby arresting Abeta formation; and (5) observed conserved glutamine (Q), glutamic acid (E), and alpha-helical conformation as few crucial factors for lysine selectivity in the ubiquitination of AbetaPP. 30804776: APOE in the brain is primarily expressed by astrocytes and microglia, cell types that are now widely appreciated to play key roles in the pathogenesis of AD; thus, a picture is emerging wherein APOE4 disrupts normal glial cell biology, intersecting with changes that occur during normal aging to ultimately cause neurodegeneration and cognitive dysfunction. 31062326: The Roles of Apolipoprotein E, Lipids, and Glucose in the Pathogenesis of Alzheimer's Disease. In this chapter, we discuss the roles of ApoE, lipids, and glucose in the pathogenesis of AD by considering their potential interactions. 31623648: However, the specific contributions of different apoE pools to AD pathogenesis remain unknown. 32027932: Here we review the critical role of APOE in the pathogenesis of AD and some of the most promising therapeutic approaches that focus on the APOE-Abeta interaction. 35639372: However, the mechanisms linking APOE to AD-particularly the apoE protein's role in AD pathogenesis and how this is affected by APOE variants-remain poorly understood. 7615568: These findings, together with the strong genetic association between late onset AD and the E4 allele of apoE, have strengthened the hypothesis that apoE may have a central role in the pathogenesis of AD by modulating A beta cerebral accumulation. 7619525: Thus, we conclude that A beta-apoE complexes are principal components of AD-associated brain amyloid and that the data presented here support a role for apoE in the pathogenesis of AD. 7695621: These findings suggest that the interaction of ApoE with tau and amyloid-beta proteins in AD could play a important role in the formation of NFT and SP, respectively, contributing to the pathogenesis of AD. In this study we sought to understand the role that ApoE protein could play in the pathogenesis of AD. 7761390: These and other isoform-specific interactions of apoE give rise to testable hypotheses for the mechanism(s) of pathogenesis of Alzheimer disease. 8809843: We suggest that microglia might be one of the sources of apoE in the brain, and that apoE synthesized in microglia might be closely related to the pathogenesis of AD. 8813351: However, apoE levels vary in different brain regions, and local factors related to the synthesis and metabolism of apoE may be crucial in the pathogenesis of AD. 8832646: Apolipoprotein E (Apo E), one of the major structural and functional apolipoproteins, has recently been implicated in the pathogenesis of Alzheimer's disease (AD). 9073026: To evaluate the usefulness of apoE concentration in pathogenesis of AD, we measured the cerebrospinal fluid (CSF) levels of apoE. 9307253: In the 162 patients for whom autopsy and ApoE genotype data were available, the clinical diagnosis of AD was verified as the primary cause of dementia in 139 cases (139 of 162, or 86%). 9326451: Apolipoprotein E (apoE) and certain peptides derived from it have been shown to exert neurotoxic effects in vitro, and apoE has been linked to the etiology of Alzheimer's disease. 9523562: To further investigate the potential interaction of apoE and A beta in the pathogenesis of AD, we have determined the binding, internalization, and degradation of human apoE isoforms in the presence and absence of A beta peptides to rat primary hippocampal neurons. 9700208: These data indicate that in addition to the qualitative effect of the APOE epsilon2/epsilon3/epsilon4 polymorphisms on the AD occurrence, the quantitative variation of expression of these alleles due to functional APOE promoter mutations, is a key determinant of AD development. 9740234: ApoE might play an important part in the etiology of Alzheimer's disease by functioning as a \pathologic chaperone\ to promote the formation of amyloid filaments. 9751198: In parallel, we determined the concentrations of apolipoprotein E (apoE), another apolipoprotein also implicated in nerve regeneration and in the etiology of AD. 9844032: This patient group was thought to be separable from those with Alzheimer's disease based on the results of ApoE allele analysis in addition to the substantial absence of amyloid beta deposits and has been designated as senile dementia of the tangle type (SDT). 10413059: Moreover, whereas the systemic delivery of N(G)-monomethyl-L-arginine (L-NMMA), a NOS inhibitor, results in sinus bradycardia and arterial hypertension, its intracoronary administration has little effect on sinus heart rate. 11243210: In addition, hypertension and tachycardia were produced by icv L-arginine and the dipeptide Arg-Arg. 11811381: Long-term administration of L-arginine derivatives, mainly NG-nitro-L-arginine methylester (L-NAME), resulted in hypertension, intrarenal vascular, tubular and glomerular lesions and reduction in renal function. 12035872: In NNA-induced AH, the number of newly formed vessels and the ingrowth of vascularized connective tissue into the wound chamber decreased as compared to controls. 12736168: Reduced NO production may also result from reduced cellular uptake of l-arginine in the medullary tissue, resulting in hypertension. 14512271: Previous work demonstrated that l-arginine, the substrate for nitric oxide (NO) synthase, is carried into inner medullary collecting duct (IMCD) cells via system y+, that the major system y+ gene product in IMCD is the cationic amino acid transporter 1 (CAT1), and that blockade of l-arginine uptake in the renal medulla decreases NO and leads to systemic hypertension. 1516948: In a separate group of rats, nitro-L-arginine administered for 1 week induced hypertension that was partially reversed by acute L-arginine, but not D-arginine or L-glycine, infusions. 15750285: Feeding WKY with N(G)-nitro-L-arginine resulted in hypertension followed by enhanced acidic pH-induced increase in perfusion pressure. 22477579: Cysteine, glutathione (a tripeptide), glutamate and arginine attenuate and prevent alterations that cause hypertension including insulin resistance, decreased nitric oxide bioavailability, altered renin angiotensin system function, increased oxidative stress and formation of advanced glycation end products. 7532526: Enhanced vascular responsiveness to Bay K 8644 in mineralocorticoid- and N-nitro arginine-induced hypertension. The present study evaluates the response to the L-type voltage gated calcium channel agonist Bay K 8644 in two forms of experimental hypertension (mineralocorticoid- and hypertension induced by the nitric oxide synthase inhibitor N omega-nitro-L-arginine (N-Nitro arginine)) and under conditions of acute stretch. 7678190: L-NAME alone and L-NAME with D-arginine produced hypertension and increased sphincter of Oddi and duodenal motilities. 7777724: The characterization of endothelin and the nitric oxide (NO)-arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. 7802675: Deficiency of endogenous arginine synthesis provokes hypertension by exhausting substrate arginine for nitric oxide synthesis. 7843755: In the present studies, we produced chronic nitric oxide blockade by oral administration of the L-arginine analogue NG-nitro-L-arginine methyl ester, which produced sustained hypertension and increased renal vascular resistance in conscious rats. These findings indicate the following: (1) Hypertension induced by chronic nitric oxide blockade due to substituted L-arginine analogue cannot be acutely reversed with excess L-arginine, suggesting that the maintenance of the hypertension is not solely caused by competitive inhibition of nitric oxide production; (2) in contrast, the kidney remains responsive to L-arginine whereas the renal vasodilator response to glycine is abolished in this model of hypertension. 8478045: Sustained hypertension induced by orally administered nitro-L-arginine. 10074798: Using recent advances in brain physiological, neurohistochemical, and molecular biological techniques, it could be demonstrated that the central action of vasopressin (VP) is important in cardiovascular regulation and in the pathogenesis of hypertension. 10795926: Third, medullary blood flow does not remain reduced in the face of sustained elevations of plasma vasopressin concentration, which appears to be related to the inability of vasopressin to produce a sustained hypertension. 11016871: The aim of the study was to investigate the effect of two various atherogenic stimuli (vasopressin-induced hypertension or hypercholesterolemia) on the collagen and glycosaminoglycan (GAG) content in the internal or external part of both thoracic and abdominal aorta, which are differently susceptible to atherosclerosis. 11681404: The physiology of VP, both as ADH and as a pressor peptide, is reviewed, and recent evidence suggesting that VP has a role in the maintenance of blood pressure and possibly in the pathogenesis of hypertension is presented. 18436696: Percent change of PAR (%DeltaPAR) and percent change of SimR (%DeltaSimR) in response to vasopressin-induced acute hypertension were computed and compared. To evaluate pressure reactivity, vasopressin-induced acute hypertension was administered to normocapnic and hypercapnic (N = 12) piglets equipped with closed cranial windows. 18464746: Increased circulating vasopressin may account for ethanol-induced hypertension in rats. 18599033: V(1A) receptor-mediated inhibitory activity was assessed in vivo in a vasopressin-induced hypertension model and in normotensive rats and in two hypertensive rat models. RWJ-676070 inhibited AVP-induced hypertension in rats but had no effect on arterial pressure in normotensive and spontaneously hypertensive rats but did decrease arterial pressure in Dahl, salt-sensitive hypertensive rats. 2274751: The increase in serum osmolality and hypersecretion of AVP during light and moderate exercise may be important in the pathogenesis of hypertension in this group of patients. 2420968: MGTA potentiated the hypertension due to angiotensin I, angiotensin II and vasopressin, but it did not affect the response to phenylephrine. 2434778: Taken together, our results suggest a link between vasopressin, the locus coeruleus, and the sympathetic nervous system in normal cardiovascular regulation as well as in the pathogenesis of DOCA-salt hypertension. Our data further suggests that vasopressin may participate in the pathogenesis of DOCA-salt hypertension by inducing stimulation of the sympathetic nervous system at the region of the locus coeruleus in this model. 2632718: The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. 30015755: Increased excitatory regulation of the hypothalamic paraventricular nucleus and circulating vasopressin results in the hypertension observed in polycystic kidney disease. 30950978: Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. 3515969: Further, the failure of AVP to produce prominent hypertension, even when pronounced systemic vasoconstrictor effects are manifested, may be a result of its inability to promote significant renal vasoconstriction and antinatriuresis. 3536587: Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. 3599806: Activation of the central vasopressin system: a potential factor in the etiology of hypertension. 3763434: It is concluded that both intrathecal and intracerebroventricular vasopressin-induced hypertension appears to be mediated by the sympathetic system and that the spinal cord is more sensitive than the supraspinal sites to vasopressin in regulating autonomic functions. Intrathecal injection of arginine vasopressin in rats at a dose as small as 10 ng produced dose-dependent hypertension and tachycardia. New evidence for neuronal function of vasopressin: sympathetic mediation of intrathecal vasopressin-induced hypertension. Intracerebroventricular injection of arginine vasopressin also induced hypertension and tachycardia, but 600 ng was needed. 3835382: [Role of vasopressin in the regulation of arterial blood pressure and in the pathogenesis of arterial hypertension]. 4021224: A sufficient dose of vasopressin-antagonist given to each rat shortly before determination of cerebral blood flow, prevented vasopressin-induced hypertension from stimulating the medulla. 4080618: These include assessment of cardiovascular regulation in Brattleboro rats, cardiovascular responses to central nervous system injections of vasopressin, and changes in central nervous system vasopressin content in spontaneous and induced hypertension. 4238633: [Does hypertension induced by vasopressin require a sympathomimetic factor? Research on dogs and rabbits]. 6124043: When A1 noradrenergic neurons in the caudal ventrolateral medulla of rabbits are destroyed electrolytically or by local injection of the neurotoxin kainic acid, the concentration of vasopressin in plasma increases, causing hypertension. 6396982: The importance of plasma vasopressin and aldosterone in the pathogenesis of hypertension seems to be probable but not yet unanimously proved. 6697549: A number of experiments were performed in order to investigate the possible importance of vasopressin (AVP) in the pathogenesis of high blood pressure in spontaneously hypertensive rats of the stroke prone strain (SHRSP). 6958400: In unanaesthetized sheep, transitory hypertension caused by intravenous angiotensin II and angiotensin III is not associated with a progressive increase in pulse interval, while hypertension caused by intravenous vasopressin produces a progressive increase in pulse interval. 7016597: Humoral agents discussed include angiotensin and vasopressin and the participation of their central and peripheral actions in the pathogenesis of hypertension. 7068203: AV3V lesion in DI rats completely prevented VP-induced DOCA/salt hypertension and enhanced vascular responsiveness. 7977848: In an earlier study, we reported that chronic intravenous administration of the V1 agonist [Phe2,Ile3,Orn8]vasopressin (V1AG) results in sustained hypertension. 8258666: OBJECTIVE: To determine the roles of vasopressin, the renin-angiotensin system and sex in the pathogenesis of salt-sensitive hypertension in the Dahl rat. 8737453: RESULTS: Arg (100, 200, and 400 ng) injected into the LSN produced a dose-dependent hypertension and tachycardia. 9794722: That brain CNP has an inhibitory effect on release of vasopressin in acute experiments indicates that the impairment of this inhibitory effect of brain CNP on secretion of vasopressin could be involved in the pathogenesis of DOCA-salt hypertension in rats. 11230329: We conclude that small, normally subpressor elevations of plasma AVP can produce chronic hypertension in SS/Mcw rats and that this phenomenon is related to the reduced medullary NOS enzyme activity, which in turn reduces the AVP-stimulated NO synthesis. Evidence that reduced renal medullary nitric oxide synthase activity of dahl s rats enables small elevations of arginine vasopressin to produce sustained hypertension. 11984003: Further molecular analysis was done to identify putative AngII/AVP receptor molecular variants that could account for the AngII/ AVP receptor involvement in salt-sensitive hypertension pathogenesis. 14695824: A variety of novel heterocyclic compounds having thienoazepine, pyrroloazepine, furoazepine, and thienodiazepine skeletons were synthesized, most of which exhibited potent antagonism of [(3)H]-AVP specific binding in assays using rat liver (V1), rat kidney (V2), human platelet plasma membranes, and recombinant human CHO cells (V2), as well as antagonizing AVP-induced hypertension in rats (V1, intravenous) and showing a diuretic effect in rats (V2, oral). 1562384: There were no significant changes in CSF AVP by induced hypertension for 80 minutes (Group C). 18599033: V(1A) receptor-mediated inhibitory activity was assessed in vivo in a vasopressin-induced hypertension model and in normotensive rats and in two hypertensive rat models. RWJ-676070 inhibited AVP-induced hypertension in rats but had no effect on arterial pressure in normotensive and spontaneously hypertensive rats but did decrease arterial pressure in Dahl, salt-sensitive hypertensive rats. 2859221: An activation of the sympathetic nervous system and increased AVP activity appeared to be responsible for the hypertension in rats maintained on normal and high sodium intake. 30282823: AVP infusion into pregnant C57BL/6J mice resulted in hypertension, renal glomerular endotheliosis, intrauterine growth restriction, decreased placental growth factor (PGF), altered placental morphology, placental oxidative stress, and placental gene expression consistent with human PE. 3415808: It is concluded that the enhanced activity of both SNS and AVP system responsible for DOCA-salt hypertension may be attributed to the mechanism(s) unrelated to the increased CSF Na concentration. 3518603: Many studies implicate AVP in the pathogenesis of hypertension, but the actual mechanism and relative importance of vasopressin's role remain a matter of intense investigation. 3763434: It is concluded that both intrathecal and intracerebroventricular vasopressin-induced hypertension appears to be mediated by the sympathetic system and that the spinal cord is more sensitive than the supraspinal sites to vasopressin in regulating autonomic functions. Intrathecal injection of arginine vasopressin in rats at a dose as small as 10 ng produced dose-dependent hypertension and tachycardia. New evidence for neuronal function of vasopressin: sympathetic mediation of intrathecal vasopressin-induced hypertension. Intracerebroventricular injection of arginine vasopressin also induced hypertension and tachycardia, but 600 ng was needed. 7505732: [The role of arginine-vasopressin and substance P in the pathogenesis of hypertension and their interrelation]. 7977537: CONCLUSION: These findings suggest that neural modulation of arginine vasopressin-induced hypertension is altered during pregnancy and are consistent with a reduction in intrinsic vascular sensitivity to arginine vasopressin during gestation. 8067431: Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. 9705577: The neuropeptides arginine vasopressin (AVP) and oxytocin (OT) have been implicated in the genesis of hypertension due to deoxycorticosterone acetate (DOCA)-salt treatment of uninephrectomized rats. 10559023: Thus hypertension and endothelial dysfunction observed in 7.5-month-old Apoe(-/-) mice may be due mainly to atherosclerosis. 10720962: Cyclosporine-induced hypertension is a particular problem and has variously been attributed to increased sympathetic nerve activity, salt and water retention, and increased circulating endothelin levels. This may predispose patients to atherosclerosis and may be involved in the etiology of post-transplant hypertension. 11173993: Nitric oxide, peroxynitrite and cGMP in atherosclerosis-induced hypertension in rabbits: beneficial effects of cicletanine. 12817309: Endothelial function is thought to play a central role in the process of atherosclerosis, and in the pathogenesis of arterial hypertension and chronic heart failure. 12847196: MATERIALS AND METHODS: In this prospective cohort study, serum creatinine, NO, SOD, catalase, plasma MDA, urinary microalbumin, and NO levels, and blood pressure were determined in 21 patients with hypertension and unilateral renal artery stenosis caused by atherosclerosis at entry and after 24 hours, 2 weeks, and 6 weeks of endovascular treatment. 18318068: Vasorenal hypertension occurs approximately in 5% of patients, suffering arterial hypertension and in majority of them constitutes the consequence of the renal arteries stenosing atherosclerosis. 1883592: Renal artery occlusive disease, from either atherosclerosis or fibrous dysplasia, may cause hypertension or renal insufficiency. 20092994: This is the first report showing that ABA prevents or ameliorates atherosclerosis-induced hypertension, immune cell recruitment into the aortic root wall and up-regulates aortic eNOS expression in ApoE(-/-) mice. 23575736: Although many of the cardiovascular sequelae of chronic hypertension are due to large artery atherosclerosis, an equal number are due to small artery dysfunction. 27894808: Atherosclerosis, a chronic and progressive disease, is a leading cause of endothelial dysfunction, diabetes mellitus, hypertension, and hypercholesterolemia. 30206000: Admission presentation of imbalance, African-American race, history of hypertension, diabetes mellitus, hypercholesterolemia, tobacco use, atrial fibrillation, and prior AIS due to extracranial artery atherosclerosis were each positively associated with an AIS diagnosis independently. 30307448: Atherosclerosis and hypertension are the most common causes of CVD, and multiple factors confer the susceptibility. 3072442: Atherosclerosis, aorto-arteritis and fibromuscular dysplasia are the most common causes of vasorenal hypertension. 3099694: These cases are three young women (20, 40 and 42 years old) with severe hypertension secondary to atherosclerosis with stenosis of renal arteries, one or both sided, and in association in one case with diffuse arterial stenosis. [Essential thrombocythemia and hypertension as a result of stenosis of the renal artery]. 37047559: Cocaine abuse increases the risk of atherosclerotic cardiovascular disease (CVD) and causes acute coronary syndromes (ACS) and hypertension (HTN). 6112936: Secondary complications are frequently affecting the brain in CVD; they are mainly sequels of systemic atherosclerosis, hypertension, thromboemboli from SLE endocarditis, cardiac, hepatic or renal dysfunctions, or infections and should be clinically differentiated from primary brain involvement in CVD to ensure the appropriate therapeutic measures. 6460424: Percutaneous transluminal angioplasty was performed in 7 patients with hypertension and renal artery stenosis, caused by atherosclerosis in 3 patients and fibromuscular disease in 4. 7812826: To determine if endothelial and ROS-induced changes in hypertension, atherosclerosis, ischemia/reperfusion etc. are the primary cause of specific diseases or merely secondary effects remains to be clarified in several areas from inflammatory processes to cardiovascular diseases. 11105461: Atherosclerotic renal artery stenosis is the most common secondary cause of hypertension and can cause hypertension to be difficult to control. 11322912: Atherosclerotic renal artery stenosis (RAS) is the most common secondary cause of hypertension, and often results in hypertension that is difficult to control. 15153815: Atherosclerotic renal artery stenosis (ARAS) may cause hypertension, progressive renal failure, and recurrent pulmonary edema. 15374808: Atherosclerotic renal artery stenosis (RAS) is an underdiagnosed disorder and a treatable etiology of hypertension and renal insufficiency. 15735947: Atherosclerotic renal artery stenosis is a significant cause of poorly controlled hypertension and progressive renal dysfunction leading to ischemic nephropathy and other end-organ damage. 17274464: [Determinants of therapeutical success of percutaneous transluminal renal angioplasty in patients with hypertension caused by atherosclerotic renal artery stenosis]. 17341996: Atherosclerotic renal artery stenosis is the most common disease of the renal arteries and may lead to ischemic renal disease and hypertension. 17673882: Atherosclerotic renal artery stenosis may result in hypertension and ischemic nephropathy. 22097232: BACKGROUND: Percutaneous angioplasty (PTA) and stenting is an established procedure for the treatment of hypertension caused by atherosclerotic renal artery stenosis. 22279335: Atherosclerotic renal artery stenosis (ARAS) is a common condition that causes hypertension and reduction in the glomerular filtration rate and is an independent risk factor for death. 22511402: BACKGROUND: Atherosclerotic renal artery stenosis (ARAS) causes hypertension (HTN) and threatens renal function (RF). 22581488: BACKGROUND: Atherosclerotic RAS can cause hypertension and ischemic nephropathy. 23657871: Atherosclerotic renal artery stenosis is a frequent cause of arterial hypertension and/or allograft dysfunction after kidney transplantation and is usually located at the iliac artery anastomosis. 24333404: Atherosclerotic renal artery stenosis (ARAS) is a common and complicated disease, which can result in high blood pressure and loss of kidney function. 24531663: Atherosclerotic renal artery stenosis as a cause for hypertension in an adolescent patient. 24744282: Atherosclerotic renal artery stenosis can cause ischaemic nephropathy and arterial hypertension. 25450992: Atherosclerotic renal artery stenosis can cause ischaemic nephropathy and arterial hypertension. 30533129: Atherosclerotic renal artery stenosis (ARAS) can cause resistant hypertension, progressive renal failure and/or cardiorenal syndrome. 38594599: BACKGROUND AND OBJECTIVES: Atherosclerotic renal artery stenosis may cause hypertension, chronic kidney disease and heart failure, but large randomized control trials to date have shown no major additional benefit of renal revascularization over optimal medical management. 432770: In addition, two patients underwent hepatorenal bypass with a saphenous vein graft as surgical treatment for azotemia and hypertension caused by atherosclerotic right renal artery stenosis. 8472097: Atherosclerotic renal artery stenosis is a relatively common cause of hypertension and renal impairment in the elderly. 12919717: Reduced coherence between central and temporal cortex is discussed in light of a neurological model of AD that hypothesizes reduced electrocortical efficiency and a breakdown of neural network communication to temporal lobes possibly resulting from temporal lobe atrophy. 14745078: White matter lesions (WML) and hippocampal atrophy (HA) on MRI commonly co-occur in Alzheimer's disease (AD) and are thought to play a role in the etiology of AD. 15377431: BACKGROUND: Neurone atrophy and loss are major causes of chronic neurodegenerative disorders such as Alzheimer's disease. 18646617: Atrophy of the hippocampus can lead to Alzheimer disease. 19596405: Hippocampal atrophy is the key marker in the pathogenesis of Alzheimer's disease (AD), which is associated with white matter (WM) disruption. 20371138: Present findings suggest that most DTI-derived changes in AD and a-MCI are largely secondary to gray matter atrophy. 21174483: Indeed, the available evidence suggests that hippocampal atrophy is the starting point of the pathogenesis of Alzheimer's disease and a significant number of patients with hippocampal atrophy will develop Alzheimer's disease. 21391278: BACKGROUND: Cerebral small vessel disease (SVD) and hippocampal atrophy are related to verbal memory failures and may ultimately result in Alzheimer's disease. 29984299: Introduction: Current models posit a sequence of amyloid beta (Abeta), tau, atrophy, and cognitive change leading to Alzheimer's disease, but ambiguities remain. 37009529: It often starts with abnormal aggregation and deposition of beta amyloid and tau, followed by neuronal damage such as atrophy of the hippocampi, leading to Alzheimers Disease (AD). 10832009: Catecholamine samples were collected before, during and 1 h after AD induced hypertension with colorectal distension. 10933032: Severe hypertension occurred probably due to autonomic hyperreflexia (AH) during both operations. 19896908: Colorectal distension, used to trigger autonomic dysreflexia, caused episodic hypertension and bradycardia. 2051183: Autonomic dysreflexia is an emergency condition resulting in sudden severe hypertension that can occur in spinal cord injury (SCI) patients above the T-5-6 level. 27073353: AD is characterized by an episodic, massive sympathetic discharge that causes severe hypertension associated with bradycardia. 28003699: Autonomic dysreflexia was suspected with stimulus arising from distended rectum as all other causes of hypertension were ruled out. 28486884: He presented with an intermittent headache and severe hypertension because of persistent autonomic dysreflexia. 3735644: Severe hypertension due to autonomic dysreflexia. 7574437: Hypertension in a patient with acute spinal cord injury is commonly caused by autonomic dysreflexia, which is a syndrome of paroxysmal hypertension associated with headaches, relative bradycardia and vasomotor instability secondary to sympathetic overactivity. 7702001: In one patient, hypertension and bradycardia due to autonomic hyperreflexia were observed during ESWL, and the treatment was discontinued, but the stone was successfully disintegrated and the fragments were voided. 7771558: Episodic hypertension due to autonomic dysreflexia in acute and chronic spinal cord-injured rats. 11401413: Hypertension in the rats was produced by aortic banding and the responses in the abdominal and thoracic aortic rings were studied 2 and 8 weeks after aortic banding. 12124218: Aortic banding produced sustained hypertension and gradually developing LVH. 12619877: Aortic banding produced sustained hypertension and gradually developing LVH that progressed to diastolic heart failure over time. 1324047: The present data show for the first time that the beneficial effects of an ACE-inhibitor on LVH in rats with hypertension caused by aortic banding can be prevented by a specific B2-receptor antagonist. 15128700: It was found, however, after induction of hypertension by suprarenal aortic banding, that the degree of cardiac hypertrophy in transgenic rats was significantly higher than that of banded control rats. 15710719: Measurements were taken both at normal aortic pressures and during hypertension induced by banding of the distal thoracic aorta in 14 pigs and by intravenous administration of phenylephrine in 10 pigs. 19644389: In rats with hypertension induced by abdominal aortic banding, H(2)S generation and CSE protein expression were significantly increased in PAT but not aortic tissues. 23736127: After surgery, the AAB-induced hypertension (AABIH) rats were treated with losartan 40 mg/kg/day, candesartan 10 mg/kg/day, irbesartan 10 mg/kg/day per os for 16 weeks. 33568793: Second, using murine models of pressure overload, including Ang II infusion and aortic banding, we mimicked the clinical conditions of Ang II- and mechanical stress-induced hypertension, respectively. 8899887: In spontaneously hypertensive rats (SHR) but not in Wistar rats with nephrogenic hypertension due to aortic banding (WIab), the Ang II-induced expression of c-Fos, and c-Jun was enhanced in all four areas when compared to normotensive Wistar Kyoto (WKY)- and Wistar (WI) rats. 9040444: in Wistar rats with nephrogenic hypertension induced by aortic banding, and in normotensive Wistar-Kyoto and Wistar rats immunohistochemically. 9124502: Single LV myocytes were isolated from normotensive control rats and from rats with hypertension, which was induced by abdominal aortic banding (for approximately 4 mo). 9336396: We investigated the effects of aortic banding-induced hypertension on the endothelium-dependent vasodilator responses in the aorta and coronary circulation of Sprague-Dawley rats. These findings indicate that in hypertension induced by aortic banding, an enhanced O2- production alone is not sufficient to produce endothelial dysfunction. 12025924: He had renal insufficiency and severe hypertension secondary to bilateral atherosclerotic renal artery stenosis. 15863593: CASE: In this report we describe a 36-year-old woman with severe hypertension caused by bilateral renal artery stenosis due to fibromuscular dysplasia. 18070585: This case reports a young child having uncontrolled hypertension, resulting from bilateral renal artery stenosis due to fibromuscular dysplasia presenting with abdominal pain, headache and visual disturbance. 18971178: METHODS: Bilateral renal artery stenosis was conducted to induce hypertension in rats, which were randomly divided into hypertensive model group (n = 10), sham-operated group (n = 8), high-dose drug group (n = 11) and low-dose drug group (n = 11), with 8 normal untreated rats as the normal control group. 2061803: Experience with bilateral renal artery stenosis as a cause of hypertension in childhood. Since 1981, eight children have been treated at this hospital for hypertension due to bilateral renal artery stenosis (RAS). 20673603: Imaging showed midaortic syndrome with bilateral renal artery stenosis as the cause of her hypertension, and further investigations showed neurofibromatosis type 1 as the underlying disorder. 21720804: We describe a 5-year-old boy with conjunctival lipodermoid, cervical and facial sebaceous nevi who presented at 3 years of age with hypertension due to bilateral renal artery stenosis together with multiple vascular anomalies (aorta, celiac trunk, superior mesenteric artery) as shown by magnetic resonance angiography. 24610892: Short stature, successfully treated with growth hormone, and hypertension secondary to bilateral renal artery stenosis expand the phenotype. 25574348: We present a 7-year-old child with uncontrolled hypertension caused by bilateral renal artery stenosis. 26783006: His resistant hypertension was considered to be a consequence of bilateral renal artery stenosis and he subsequently underwent sequential stenting of his renal arteries leading to improvement in blood pressure and reduction in the number of antihypertensive medications. 2900930: Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. 29984004: The CHB in this case is thought to be caused by hypertensive cardiomyopathy due to ongoing uncontrolled hypertension, which is caused by bilateral renal artery stenosis. 30560138: The clinical phenotype was secondary to resistant hypertension due to bilateral renal artery stenosis, and her blood pressure and heart failure resolved after successful renal artery angioplasty. In this article, we describe a case of resistant hypertension in a 63-year-old woman leading to heart failure and marked morbidity. Resistant hypertension remains an important cause of heart failure. 34062947: We report a 10-year-old girl with LNSS who had concomitant cystic kidney disease and diffuse aortopathy with bilateral renal artery stenosis, leading to hypertension requiring oral anti-hypertensive medications. 34210635: Pickering's syndrome is a clinical entity described in 1988 that consists of the presentation of recurrent and predominantly nocturnal acute flash pulmonary oedema and arterial hypertension secondary to bilateral renal artery stenosis or unilateral in single-kidney patients. 6990838: The role of the liver in the metabolism of renin was evaluated in dogs with high plasma renin and hypertension due to experimental bilateral renal artery stenosis. 794516: The second was used in the treatment of hypertension due to bilateral atheromatous renal artery stenosis with a lesion at the main bifurcation of the artery. 10862644: The aim of this study was to determine the sensitivity of ABPM in revealing hypertension in potential renal transplant donors, and to measure the correlation between ABPM results and target organ damage. 14994253: The severity of hypertension was graded according to the results of ambulatory blood pressure monitoring as white coat, borderline, or proven hypertension. 15241644: Subjects with white-coat normotension (WCNT) or masked hypertension, i. e. a normal office blood pressure (BP) reading but elevated ambulatory blood pressure monitoring (ABPM) results, have not been extensively studied. 16368325: Eighty patients (59%) had hypertension on the basis of the results of the ambulatory blood pressure monitoring (mean daytime blood pressure > or = 135/85 mm Hg). 23636009: Threshold BP values for hypertension based on 24-h ABPM results have been established, including daytime and night-time averages. 24389604: RESULTS: Twenty-nine patients were included in the study, including 13 patients with newly diagnosed untreated HT according to the results of ambulatory blood pressure monitoring (ABPM). 26717222: The diagnosis of hypertension was based on ambulatory blood pressure monitoring results. 27133905: OBJECTIVE: This study aimed to evaluate the prevalence of masked hypertension using the results of office blood pressure measurement compared with the results of ambulatory blood pressure monitoring. 30451702: OBJECTIVE: Evaluation of the tolerability to ABPM in 232 adolescent participants (median age: 15.7 years, 64% white, 16% Hispanic, 53% male) in the Study of Hypertension In Pediatrics Adult Hypertension Onset in Youth and its potential effects on ABPM results. 32723189: The patients were assigned to dipper hypertension (n = 41) and non-dipper hypertension (n = 47) groups based on the ambulatory blood pressure monitoring results according to the presence of >= a 10% decrease in nighttime blood pressure values or not. 10652986: Brain regional oxidative damage is thought to be a central mechanism in the pathogenesis of Alzheimer's disease (AD). 11404403: Because LPO precedes amyloid plaque formation in Tg2576 mice, this suggests that brain oxidative damage contributes to AD pathogenesis before Abeta accumulation in the AD brain. 12202836: Finally, different hypotheses link the origin of Alzheimer's disease to that of progressive cerebrovascular dementia caused by cerebral microcirculation damage. 12574667: Finally, different hypotheses link the origin of Alzheimer's disease to that of progressive cerebrovascular dementia caused by cerebral microcirculation damage. 1461171: Beta amyloid protein appears to be the principal active constituent of senile plaques thought to be a probable cause of brain damage resulting in AD. 28926722: There is now an unprecedented opportunity to improve the care of the over 5 million people who are living with Alzheimer's disease and related dementias and many more with cognitive impairment due to brain injury, systemic diseases, and other causes. 29843241: It proposed that the brain damage leading to Alzheimer's disease (AD) was instigated by soluble, ligand-like AbetaOs. 33292860: Since the brain is a sterile organ, neuroinflammation in Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) is triggered by cerebral cellular damage or the abnormal accumulation of inflammatogenic molecules in CNS tissue through the activation of innate and acquired immunity. 37712394: In astrocytes, dysregulation of P2X7Rs has been associated with neurodegenerative illnesses such as Alzheimer's disease (AD), as well as the consequences of cerebral ischemic injury and status epilepticus (SE). 37714710: SIGNIFICANCE STATEMENT Alzheimer's disease (AD)-associated cognitive dysfunction is hypothesized to be a consequence of brain network damage. 32965360: Previous studies have noted hypertension is associated with increased mortality due to COVID-19; however, it is not clear whether the increased risk is due to hypertension itself or antihypertensive agents. 33284825: Appropriately addressing the modifiable risk factors such as smoking, hypertension, and diabetes could reduce morbidity and mortality due to COVID-19; public messaging can be accordingly adapted. 33458761: We therefore sought to identify novel mechanisms of interaction by identifying genes with altered expression in SARS-CoV-$2$ infection that are relevant to the pathogenesis of cardiovascular disease and hypertension. 34080261: PURPOSE: Considering the anti-inflammatory effect of atorvastatin and the role of medical comorbidities such as hypertension and coronary artery disease on the prognosis of the COVID-19 patients, we aimed to assess the effect of atorvastatin add-on therapy on mortality due to COVID-19. 34889662: These findings suggest that COVID-19 increases systolic and diastolic BP and may cause new onset hypertension. 34995147: Targeting obesity, hyperglycemia, dyslipidemia, and hypertension could address modifiable risk factors to reduce mortality due to COVID-19. Background: Hypertension, diabetes, and obesity are common comorbidities that portend worse outcomes due to coronavirus disease 2019 (COVID-19). 35144453: BACKGROUND: Non-communicable diseases (NCDs), including type-2 diabetes and hypertension, have been associated with increased morbidity and mortality rates because of coronavirus disease 2019 (COVID-19). 35251646: A 50-year-old man with a medical history of diabetes mellitus and hypertension was admitted to a university hospital for severe respiratory insufficiency caused by SARS-CoV-2 infection. 35639214: COVID-19-induced silent myocarditis and newly developed hypertension in a 3-year-old boy. 35726121: This can either be associated with hypertension caused by the COVID-19 infection, more frequent diagnosis of hypertension among people with COVID-19 since they consult healthcare, or residual confounding factors not adjusted for in the study. 36016170: Specifically, several medical, economic factors, and sociodemographic characteristics are more prevalent in vaccine-hesitant groups, such as asthma, hypertension, mental health problems, financial strain due to COVID-19, gender, lack of health insurance plans, and limited test availability. 36027060: We assessed the impact of hypertension on in-hospital mortality in patients hospitalized due to COVID-19. OBJECTIVE: Cardiovascular diseases including hypertension are common comorbidities in patients hospitalized due to COVID-19. 36067796: The other nine maternal deaths had causality C, that is, without causal relationship with the vaccine, and most were due to complications inherent to pregnancy, such as pregnancy-specific hypertensive disorder (PSHD) in 4 cases and 3 due to COVID-19. 36082666: BACKGROUND: Cardiovascular diseases including arterial hypertension are common comorbidities among patients hospitalized due to COVID-19. 36411156: In the pooled analysis, pre-existing hypertension was significantly associated with mortality due to SARS-CoV-2 infection, both in unadjusted and adjusted models (HR: 1.55; 95% CI: 1.22 to 1.97). METHODS: A systematic search of the on-line databases available up to 31 March 2022 was conducted, including peer-reviewed original articles, involving the adult population, where the role of hypertension on mortality due to SARS-CoV-2 infection was determined by Cox-proportional hazard models. 37597321: SARS-CoV-2 infection can cause hypertension, and endothelial damage, which can lead to intravascular thrombosis. 37864346: Does COVID-19 Cause Non-Dipper Hypertension? 151509: These data indicate that genetic differences influence the pathogenesis of cadmium-induced hypertension. Dahl hypertension-resistant (R) and hypertension-sensitive (S) rats were used to determine whether cadmium-induced hypertension is dependent on genetic predisposition. Genetic influence on cadmium-induced hypertension. Also, the development of salt-induced hypertension was accelerated in cadmium-fed (1 and 2.5 mg/liter) S rats. 16938374: In conclusion, the underlying mechanism of the myocardial hypertrophy may be related to hypertension due to inhibition of NO production in the vessels, and CAPE has a protective effect on Cd-induced hypertension mediated cardiac impairment in the rats. 18155860: Cadmium (Cd) has been reported to induce hypertension in both humans and animals; however, its mechanism has not been clearly elucidated. 18197299: INTRODUCTION: Cadmium induces hypertension in animal models. 1893157: [Morphofunctional characteristics of cadmium-induced arterial hypertension]. In the rehabilitation period (9 weeks) a relatively quick fall in the blood pressure is observed, as well as morphological features of myocardial and renal function recovery, suggesting the nonpersistent nature of cadmium-induced hypertension. 20399841: It was found that Cd-induced hypertension and markedly blunted vascular responses to vasoactive agents, including acetylcholine, phenylephrine and sodium nitroprusside. 20872046: The findings in this study provide the first evidence in pharmacological effects of ascorbic acid on alleviation of oxidative damage and improvement of vascular function in a mouse model of Cd-induced hypertension and vascular dysfunction. 21787712: The aims of the study were to investigate (i) the effects of environmental cadmium (Cd) on hypertension, biological markers of renal dysfunction and renal cytochrome P450-mediated arachidonate metabolism; and (ii) the association between genetic polymorphism of heme oxygenase-1 (HO-1) and hypertension and Cd-induced renal injury in the exposed Thai population. 23193898: BACKGROUND: Cadmium (Cd) is a metal, which induces hypertension in animals. 23703608: Inhibition of NADPH oxidase activity may be a useful strategy for prevention and treatment of cadmium-induced hypertension. 23857371: OBJECTIVES: In the general population, cadmium seems to be responsible for hypertension, atherosclerosis and an increase in acute coronary events. 24662163: These findings suggest that curcumin, due to its antioxidant and chelating properties, is a promising protective agent against hypertension and vascular dysfunction induced by Cd. Cd induced hypertension and impaired vascular responses to phenylephrine, acetylcholine and sodium nitroprusside. This study investigated the protective effect of curcumin on a mouse model of cadmium (Cd)-induced hypertension, vascular dysfunction and oxidative stress. 25502771: In this study, we investigated the protective effect of THU against Cd-induced hypertension, raised arterial stiffness and vascular remodeling in mice. 2652377: Neither dose of cadmium was able to induce significant hypertension in the treated animals. 2755962: Cadmium-induced hypertension in rats. 2795699: Reversal of cadmium-induced hypertension by D-myo-inositol-1,2,6-trisphosphate. 2944489: [Molecular bases of arterial hypertension induced by cadmium]. In order to establish at subcellular level the biochemical role of cadmium in the etiology of arterial hypertension, we studied the effect of this metal on some mitochondrial functions. 29446707: Arsenic, cadmium, and mercury-induced hypertension: mechanisms and epidemiological findings. 2977116: These results demonstrate that the ingestion of drinking water contaminated with Cd can cause hypertension and an increase in left ventricular mass over a short time period in rabbits. 3412202: Preferentially bound to melanin, cadmium, lead, and copper have implications not only in the etiology of black hypertension, but in the etiology of all hypertension. 3415787: These trace metals could pose health hazards to the public such as lead poisoning, dementia, and hypertension due to cadmium. 3415793: Cadmium can induce persistent hypertension in rats, yet, studies involving humans have been limited by the lack of controlling for confounding variables. 3945873: Neurobehavioural effects in rats fed low doses of cadmium and lead to induce hypertension. 422935: Young female rats were given a regimen of intraperitoneal cadmium treatments reported to cause hypertension reliably within a month. The suggestion that cadmium-induced hypertension in rats might be due to renal sodium retention, known to result from Cd treatment, was examined. 4353877: Elevated circulating renin activity in rats following doses of cadmium known to induce hypertension. 488039: Exposure to another metal along with cadmium can markedly alter the ability of cadmium to induce hypertension. In contrast, lead, which like cadmium, can also induce hypertension, augments rather than inhibits cadmium-induced hypertension; thus, lead and cadmium together can induce an average increase in systolic pressure in excess of 40 mm Hg, at least twice as large as is usually induced by either metal alone. Cadmium-induced hypertension is not limited to females or to a particular strain. Large excesses of both zinc and copper have also inhibited the induction of hypertension by cadmium. 488040: Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. 522184: Having no known essential bodily functions and possibly altering the action of various other trace metals, eg, lead and zinc, cadmium has been suspect as a causative factor in certain pathological alterations, such as hypertension. 5406990: [Morphological signs of hyperactivity of the renin-aldosterone system in experimental cadmium-induced hypertension]. 6113136: Cadmium (Cd) produces injurious effects on reproductive function and has been implicated in the pathogeneses of hypertension. 625192: A possible mechanism for cadmium-induced hypertension in rats. 6344213: Thus, chronically fed cadmium can induce hypertension in rats, but conditions are important. Additional observations on cadmium-induced hypertension indicate that: (1) concentrations from 0.1 to 5 ppm cadmium in water are pressor; (2) sex, strain, and age of animals are apparently not limiting factors; (3) there is associated sodium retention; (4) there is a concomitant decrease in the high energy phosphate content of tissues. Using Schroeder's food and water, but a slightly less cadmium-free environment, we repeatedly induced mild hypertension with 5 ppm cadmium, mild because control pressures were higher not because cadmium-fed animals had lower pressures. Rats with cadmium-induced hypertension have renal cadmium concentrations which bracket those of the average environmentally exposed American or European. 6385135: Chronic environmental exposure of cadmium produces hypertension in experimental animals. 6788563: The aim of this study was to investigate the possible involvement of cadmium in the aetiology of hypertension at the chronic low levels of environmental exposure. 6908749: Heart rate, however, was lowered, suggesting that the hypertension in these rates may be due to an increase of the total peripheral resistance, possibly involving a central nervous system (CNS) component in Cd-induced hypertension. 6947240: The results indicate that (i) lead and cadmium induced aortic atherosclerosis and hypertension, and (ii) calcium protects against the cardiovascular effects of cadmium. 7044111: Cadmium has been shown to cause hypertension in animals; however, it is unclear whether it is capable of causing similar effects in exposed human populations. 7097810: Effects of cadmium on the tension of isolated rat aorta (a possible mechanism for cadmium-induced hypertension). 7336200: Sodium retention in rats with cadmium-induced hypertension. All four cadmium challenges induced sodium retention and also induced hypertension. 7367855: Inhibition of cadmium-induced hypertension in rats. 7462901: Cadmium enhanced the rate and the degree of salt-induced hypertension development. These data indicate that differences in genetic background influence the development of cadmium-induced hypertension in weanling rats, and that cadmium exacerbates the severity of salt-induced hypertension. 775217: (2) Long-term exposure to low levels of cadmium has reproducibly caused mild hypertension in animals. 8684536: In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 micrograms/ml cadmium for 30 days, and the results were compared with those of 30 controls. 8822235: Cadmium, which has been implicated in the etiology of hypertension was used as the hypertensive agent and the classical blocker of voltage-operated calcium channels nifedipine was used to treat hypertension. 9246924: Effect of verapamil on cadmium induced hypertension in rats. 9441733: Cadmium-induced hypertension cannot be obviously accounted for on its basis of augmented plasma or tissue renin angiotensin involvement. 11152234: Calcineurin inhibitors and corticosteroids induce hypertension in renal, cardiac, liver, bone marrow, and lung transplant recipients. 12352326: In patients with cyclosporine-induced hypertension, upregulation of the nitric oxide system and oxidative stress were shown, which could induce hypertension, remodeling, and chronic rejection by increasing nitric oxide catabolism. Oxidative stress in kidney transplant patients with calcineurin inhibitor-induced hypertension: effect of ramipril. 15839366: A significant number of transplant recipients suffer from posttransplant hypertension in part because of corticosteroid and calcineurin inhibitor use. 21963515: Together, these findings indicate that tacrolimus-induced chronic hypertension is mediated largely by NCC activation, and suggest that inexpensive and well-tolerated thiazide diuretics may be especially effective in preventing the complications of CNI treatment. In wild-type mice, the CNI tacrolimus caused salt-sensitive hypertension and increased the abundance of phosphorylated NCC and the NCC-regulatory kinases WNK3, WNK4 and SPAK. Moreover, hydrochlorothiazide, an NCC-blocking drug, reversed tacrolimus-induced hypertension. We hypothesized that CNIs induce hypertension by stimulating NCC. 22172729: How calcineurin inhibitors cause hypertension. 22573529: Here, we review the pertinent literature on the hypertensinogenic effects of calcineurin inhibitors, including neural, vascular and renal effects, and we propose an integrated model of calcineurin inhibitor-induced hypertension. This article reviews the current understanding of the mechanisms of calcineurin inhibitor-induced hypertension. Pathogenesis of calcineurin inhibitor-induced hypertension. 26687832: Calcineurin inhibitors induce hypertension by a mechanism related to the imbalance of vasoactive substances endothelin and nitric oxide, and probably by causing overactivity of thiazide-sensitive sodium-chloride-cotransporter. 27496479: The aim of this retrospective clinical study was to estimate the prevalence of arterial hypertension among patients after successful liver transplantation and the role of immunosuppressive drugs in the pathogenesis of hypertension in these patients. CONCLUSIONS: Based on study findings, the following conclusions were drawn: arterial hypertension occurs in more than 50% of patients after liver transplantation (significantly higher frequency than in the general population); calcineurin inhibitors may participate in the pathogenesis of arterial hypertension in patients after successful liver transplantation; and the clinical importance of these findings and the influence on cardiovascular outcome of the liver transplant recipients need further investigation. 27982677: Pathophysiological mechanisms of calcineurin inhibitor-induced nephrotoxicity and arterial hypertension. 28250402: The term CAI, sometimes referred to as chronic allograft nephropathy (CAN), describes the deterioration of renal allograft function and structure as a result of immunological processes (chronic antibody-mediated rejection), and other non-immunological factors such as calcineurin inhibitor (CNI) induced nephrotoxicity, hypertension and infection. 28584011: Regulatory T-Cell Augmentation or Interleukin-17 Inhibition Prevents Calcineurin Inhibitor-Induced Hypertension in Mice. The immunosuppressive calcineurin inhibitors cyclosporine A and tacrolimus alter T-cell subsets and can cause hypertension, vascular dysfunction, and renal toxicity. Daily treatment of mice with cyclosporine A or tacrolimus for 1 week significantly decreased CD4+/FoxP3+ regulatory T cells in the spleen and lymph nodes, as well as induced hypertension, vascular injury and dysfunction, and glomerular mesangial expansion in mice. 29031357: These sensing mechanisms can be interrupted by drugs, such as the calcineurin inhibitors to cause both hypertension and hyperkalemia in kidney transplant patients, or can be inherited as familial hypertensive hyperkalemia. 29131070: Clarification of how the biochemical and molecular mechanisms that regulate the processes involved in CNIs induced post transplant hypertension work and interact, would provide further insights not only into the comprehension of the pathophysiology of CNIs induced post transplant hypertension but could also have a positive impact on the clinical ground through the identification of significant targets. We examined literature data including those coming from our group regarding the role of oxidative stress and sodium retention in CNIs induced hypertension and their involvement in cardiovascular-renal remodeling. A common pathway between oxidative stress and hypertension induced by CNIs may be identified in the involvement of the activation of RhoA/Rho kinase pathway, key for the induction of hypertension and cardiovascular-renal remodeling, of the oxidative stress mediated increased nitric oxide (NO) metabolism and increased renal sodium retention via increased activity of thiazide-sensitive sodium chloride cotransporter (NCC) in the distal tubule. The demonstration that in kidney transplanted patients with CNIs induced post-transplanted hypertension, the treatment of hypertension with different antihypertensive drugs inducing a comparable blood pressure reduction but different effects for example on oxidative stress and oxidative stress related proteins and/or Rho kinase and sodium retention, could be helpful for the choice of the antihypertensive treatment in these patients which takes advantage from effects of these drugs beyond blood pressure reduction. 11452650: [The role of mitochondrial calcium overload and energy deficiency in pathogenesis of arterial hypertension]. 11551369: The DASH trials implicate dysfunction in calcium regulation in the pathogenesis of human hypertension. 12111752: This review focuses its attention on sodium, potassium, calcium, and magnesium ions in order to investigate whether these electrolytes play a role in the pathogenesis of arterial hypertension and its treatment. 1283581: Arterial hypertension and arteriosclerosis are dramatic consequences of vascular calcium overload. 136891: This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. 27885057: Further research is needed to confirm these findings and help unravel the mechanistic pathways of calcium in the pathogenesis of hypertension. 3003794: Water hardness may have some effect in reducing hypertension incidence, and any effectiveness would probably result from calcium and magnesium in the drinking water. 30446179: Alterations in metabolic pathways associated with the sensitivity of sodium, potassium, magnesium and calcium may lead to obesity, hypertension, and insulin resistance. 3537234: Sodium and calcium appear to be the electrolytes most closely implicated in the pathogenesis of hypertension but potassium, magnesium and chloride should not be neglected. 8206565: Recent studies from our laboratory in fasting pregnant ewes with twin gestation have implicated low serum calcium concentration in the etiology of hypertension in pregnancy. 12420190: Hypertension confers cardiovascular risk by causing target-organ damage that includes retinopathy in addition to heart disease, stroke, renal insufficiency and peripheral vascular disease. 1361506: To address the issue whether the SA gene is one of the genes responsible for the hypertension of SHR, a genetic cosegregation analysis of the blood pressure values with the genotypes in an F2 rat population was undertaken in this study. Identification of a candidate gene responsible for the high blood pressure of spontaneously hypertensive rats. 14697241: To identify candidate genes responsible for hypertension in Dahl salt-sensitive rats (Dahl-S), an oligonucleotide microarray analysis was performed to find differentially expressed genes in kidneys of Dahl-S and Lewis rats. The present study provided evidence that Pnpo is a candidate gene responsible for hypertension in Dahl-S rats. Pyridoxine 5'-phosphate oxidase is a candidate gene responsible for hypertension in Dahl-S rats. 14769432: We describe approaches others and we have undertaken to investigate gene expression profiles in hypertensive models in order to identify genes that contribute to the pathogenesis of hypertension. The combination of gene expression profiling and the phenotypic characterization of in vitro and in vivo loss or gain of function experiments for candidate genes have the potential to identify genes involved in the pathogenesis of hypertension and may present novel targets for therapy. 16289097: Adducin is a candidate gene in the pathogenesis of hypertension. 19620519: Candidate genes identified in these studies merit further investigation as potentially causative hypertension genes in SHR and human hypertension. 23346037: In this study, ROS-hypertension-related genes were collected by the biological literature-mining tools, such as SciMiner and gene2pubmed, in order to identify the genes that would cause hypertension through ROS. This study demonstrates that a text mining approach combined with association analysis may be useful to identify the candidate genes that cause hypertension through ROS or oxidative stress. 24452243: Thus, in this study, we analyzed gene expression profiles in the brains of SHR in order to identify the genes responsible for causing hypertension and stroke, as well as those involved in ADHD. Analysis of genes causing hypertension and stroke in spontaneously hypertensive rats: gene expression profiles in the brain. The IPA of SHR-specific genes revealed that prostaglandin E receptor 4 (Ptger4) is one of the candidate genes responsible for causing hypertension in SHR, and that albumin (Alb) and chymase 1 (Cma1) are also responsible for causing hypertension in SHR in the presence of angiotensinogen (Agt). 25707311: Candidate genes in quantitative trait loci associated with absolute and relative kidney weight in rats with Inherited Stress Induced Arterial Hypertension. 8750215: Two groups of candidate genes have so far been of particular interest: those implicated in the aetiology of hypertension, and those involved in the metabolism of glomerular basement membrane proteins. 9774362: The position of tyrosine hydroxylase (TH) as the rate-limiting enzyme in catecholamine biosynthesis renders it a candidate gene for the etiology of hypertension. 11016804: Endothelin-1 (ET-1), one of the endogenous pathological humoral factors of cardiovascular diseases such as hypertension and heart failure, has a strong vasoconstrictive action and could induce hypertension and cardiac hypertrophy. Benidipine could thus be a useful tool for preventing cardiac hypertrophy due to hypertension. 11733803: CONCLUSION: Socioeconomic indicators (family heading and vehicle ownership) may be added to well stabilished medical factors (diabete mellitus and hypertension to select target groups for programs intended to reduce deaths due to cardiovascular diseases in elderly people. 16386203: Hypertension affects 20% to 60% of all diabetics, contributing to up to 75% of deaths due to cardiovascular disease. 18006585: Possibly, the relative influence of the prenatal environment on cardiovascular disease is determined in part by genetic factors that predispose individuals to the development of environmentally induced hypertension. 18433913: CONCLUSIONS: In this population, hypertension is more aggressively monitored and treated among diabetic than non-diabetic patients, but largely due to their CVD and not to the level recommended in guidelines. 18938721: Inflammatory status is involved in the pathophysiology of several cardiovascular disorders and in the genesis of high blood pressure. C reactive protein participates during inflammation activating the first component of complement with disorganization of the phospholipidic array of the endothelial sarcolemmal membrane and the consequent endothelial dysfunction related to the genesis of high blood pressure. 19731113: Sleep apnea may be present and is usually investigated in these patients; however, the prevalence of restless legs syndrome (RLS), which is high in dialysis patients and which has been associated with increased risk for cardiovascular disease in the general population, could also play a role in the pathogenesis of sleep-time hypertension in renal patients. 23614041: BACKGROUND: Prevention and control of hypertension are critical in reducing morbidity and mortality attributable to cardiovascular diseases. 24861467: CONCLUSIONS: Hypertensive postmenopausal women with low risk for cardiovascular diseases have increased levels of prolactin, suggesting a possible role in the pathogenesis of hypertension. 26264814: INTRODUCTION: Prehypertension is considered a precursor of systemic arterial hypertension and a predictor of morbidity-mortality due to cardiovascular diseases, which are the main causes of death in Brazil and the world. 2679012: Diuretic-based treatment regimens for hypertension have consistently reduced blood pressure and the morbidity and mortality due to stroke and overall cardiovascular disease. 26975032: OBJECTIVES: To examine the prevalence, diagnosis, treatment, and control of hypertension and to assess the CVD mortality attributable to hypertension in China. Uncontrolled hypertension was associated with relative risks for CVD mortality of 4.1 (95% CI, 3.7-4.6), 2.6 (95% CI, 2.4-2.9) and 1.9 (95% CI, 1.8-2.0) at ages 35 to 59, 60 to 69, and 70 to 79 years, respectively, and accounted for about one-third of deaths due to CVD (approximately 750 000) at 35 to 79 years of age in 2010. IMPORTANCE: Hypertension is a leading cause of premature death in China, but limited evidence is available on the prevalence and management of hypertension and its effect on mortality from cardiovascular disease (CVD). 27121332: Prehypertension is not categorized as a disease currently; however, individuals with untreated prehypertension are known to be at increased risk of progression to hypertension and mortality caused by cardiovascular disease. 29699875: We found that the main risk factor for CVD events was hypertension with about 50% of population attributable fraction; prehypertension (22.24%) only acts at rural older females; the efficiency of low- and moderate-level physical activities were higher in males (over 20%) than females (under 20%); ever smoked contributed to CVDs in rural older populations (males, 19.25%; females, 5.57%) and urban younger males (54.52%); while as for high body mass index, overweight (12.59%) only made contribution to rural males over 60 years. 29803897: Most epidemiological studies but not all of them suggested the existence of an association between elevated serum UA level and CVD, including coronary heart disease (CHD), stroke, congestive heart failure, arterial hypertension and atrial fibrillation as well as an increased risk for mortality due to CVD in general population and subjects with confirmed CHD. 31242835: AHT received 6324 persons (61.1% of those with AH); according to American recommendations, the onset of AHT was indicated to additional 620 persons with 1-st degree AH because of high CVD risk. 31472952: Thus, hypertension could be both a cause and a consequence of cardiovascular disease. 32102826: Hypertension (defined by systolic BP (SBP)/diastolic BP (DBP) >=140/90 mm Hg) was significantly associated with mortality due to CVDs (HR=2.49, 95% CI=1.77 to 3.50) among people aged 35-59 years rather than people aged >=60 years. 32756946: The population-attributable fraction for premature mortality due to cardiovascular disease associated with stage 1 and 2 hypertension among Japanese.BACKGROUND: Our aim was to assess how the population-attributable fraction (PAF) for premature mortality due to cardiovascular disease (CVD) associated with hypertension changes if blood pressure (BP) thresholds for hypertension were lowered from systolic /diastolic BP >=140/90 mm Hg to >=130/80 mm Hg, as defined using the 2017 American College of Cardiology/American Heart Association blood pressure guideline. 32930786: The latter are ideally suited to learn about immune-mediated mechanisms in cardiovascular disease leading to high blood pressure. 33846799: Central AT1R is involved in almost all types of hypertension, including spontaneous hypertension, salt-sensitive hypertension, obesity-induced hypertension, renovascular hypertension, diabetic hypertension, L-NAME-induced hypertension, stress-induced hypertension, angiotensin II-induced hypertension and aldosterone-induced hypertension. Present in more than one billion adults, hypertension is the most significant modifiable risk factor for mortality resulting from cardiovascular disease. 34054307: Background: Hypertension (HTN) is the leading risk factor for mortality due to cardiovascular diseases, it accounts for 7% of global disability adjusted life years. 35628307: It is characterized by the association of obesity, hypertension, and atherogenic dyslipidemia, which lead to premature morbidity and mortality due to cardiovascular disease (CVD). 36794581: This study aimed to determine if chemogenetic activation of hypothalamic OXT neurons in animals with existing obstructive sleep apnea-induced hypertension would reverse or blunt the progression of autonomic and cardiovascular dysfunction. Hypothalamic OXT (Oxytocin) Neuron Activation Attenuates Intermittent Hypoxia-Induced Hypertension and Cardiac Dysfunction in an Animal Model of Sleep Apnea. BACKGROUND: Obstructive sleep apnea is a prevalent and poorly treated cardiovascular disease that leads to hypertension and autonomic imbalance. METHODS: Two groups of rats were exposed to chronic intermittent hypoxia (CIH), a model of obstructive sleep apnea, for 4 weeks to induce hypertension. 37671571: Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. 7997817: The efficacy of health actions, related to arterial hypertension and used as a strategy to decrease morbimortality due to cardiovascular diseases, in accordance with the \risk approach\ and carried out in a Primary Health Care Clinic is assessed. 8417402: Although cardiovascular disease is an uncommon cause of hypertension, the number one cardiovascular cause of hypertension, coarctation of the aorta, is easy to diagnose and treat. 8737194: Long-term costs of uncontrolled hypertension include those resulting from other cardiovascular diseases for which hypertension is a significant risk factor, involving the brain, kidneys and arterial system. 9047418: [Hypertension secondary to cardiovascular disease]. 10694184: BACKGROUND: Attenuated vasodilator responses to endogenous catecholamines may contribute to the aetiology of hypertension. 12025908: The patient was diagnosed with catecholamine induced hypertension, which was caused by paraganglionoma. 1334353: Kallikrein-kinin,enkephalin, renin-aldosterone and catecholamine systems in the vanadate (as vanadyl)-induced arterial hypertension. 1415603: We conclude that toxic concentrations of catecholamines are responsible for SNS-induced LV dysfunction and that hypertension, most likely because of its ability to increase myocardial energy demand, is one of the important events that leads to depressed cardiac function. 14597643: We therefore analyzed the biosynthetic pathways of catecholamines in peripheral nervous system structures involved in the pathogenesis of intermittent hypoxia-induced hypertension, namely, carotid bodies, superior cervical ganglia, and adrenal glands. Chronic intermittent hypoxia, a characteristic feature of sleep-disordered breathing, induces hypertension through augmented sympathetic nerve activity and requires the presence of functional carotid body arterial chemoreceptors. 16227066: The complications associated with stimulant abuse are thought to be primarily mediated through excess catecholamines, resulting in acute arterial hypertension, vasospasm, thrombosis, and accelerated atherosclerosis. 1813878: Participation of catecholamines and renin in the pathogenesis of hypertension in KTP is not dominant. 19232942: Preoperative alpha- and beta-adrenergic receptor block with phenoxybenzamine and labetalol, the intraoperative course of a 4-month-old infant with neuroblastoma and elevated catecholamines causing sweating, hypertension, and tachycardia, are presented. 1973879: The intraoperative vasodilator requirement for the treatment of catecholamine induced hypertension during tumor manipulation was significantly less for group II: total nitroprusside administration averaged 8.7 mg in group I and 0.8 mg in group II (P less than 0.0005). 21565668: High circulating levels of catecholamines can lead to severe hypertension and can have devastating effects on multiple body systems (eg, cardiovascular, cerebrovascular), and can lead to death if untreated. 22346144: Hypertension was confirmed to result from both excess catecholamine production and hyperreninemia of left kidney. 23566412: TCCS was performed during the initiation phase of catecholamine-induced controlled hypertension. 23919200: Hypertension was confirmed biochemically to result from excess catecholamine production. 23933152: Pheochromocytoma also causes hyper-secretion of catecholamines that cause severe hypertension. 2399038: The level of catecholamines in the brain of rats with inherited stress-induced arterial hypertension (ISTAH) was studied. 24794965: Isoprenaline induced low blood pressure and predominantly apical dysfunction whereas the other catecholamines induced high blood pressure and basal dysfunction. 25304108: Importantly, catecholamine-induced endothelial dysfunction and hypertension may not only be due to catecholamine production by neuroendocrine tumors, as vascular endothelial cells have now been demonstrated to synthesize and secrete catecholamines. 25819736: CONTEXT: Overproduction of catecholamine induces not only hypertension but also glucose intolerance and hyperlipidemia. 27396805: The resultant increased sympathetic activity and elevated serum concentrations of catecholamines may adversely affect the cardiovascular system, resulting in cardiovascular instability (hypertension, tachycardia, and arrhythmia), morbidity (myocardial ischemia, myocardial infarction, and stroke), and mortality (cardiac death and fatal stroke), particularly in patients at an elevated cardiovascular risk and with reduced cardiovascular reserve. 29359806: The ensuing CB chemosensory reflex activates the sympathetic nervous system and increased secretion of catecholamines by the adrenal medulla, resulting in hypertension and breathing abnormalities. 29409060: PCCs secrete catecholamines, which cause hypertension and have adverse cardiovascular consequences as a result of catecholamine excess. 30625773: We have experienced catecholamine-induced cardiovascular crisis, with severe hypertension, tachycardia, and acute pulmonary edema, after subcutaneous infiltration with a 2% lidocaine and 1:200,000 epinephrine solution. 31493938: These tumors produce most often catecholamines in excess, causing hypertension and sometimes severe acute cardiovascular complications. 33542830: Pheochromocytoma is a tumor arising from the adrenal medulla, most frequent benign and, due to the excretion of catecholamines, a rare cause of hypertension. 35847796: In total, 35-50% of CPGL lesions secrete catecholamines, causing hypertension, excessive sweating, palpitations, headache, and other symptoms. 37376729: Massive secretion of catecholamines in pheochromocytoma/paraganglioma causes hypertension and cerebrocardiovascular disease due to rapid blood pressure fluctuation. 38130863: Paragangliomas are catecholamine-secreting neuroendocrine tumours outside the adrenal gland that can cause palpitations, hypertension, and rarely cardiomyopathy. 38222164: Catecholamine production by the tumors leads to high blood pressure. 38572182: Pheochromocytoma and paraganglioma (PPGL) are chromaffin cell tumors that produce, store, and secrete catecholamines, leading to HT and other adrenergic manifestations. Even though primary HT, obesity, and preeclampsia are the main causes of HT in this period, other less familiar conditions must be considered during the investigation. 3952474: Recent progress in the diagnostic work-up of secondary forms of arterial hypertension caused by mineralocorticoids or catecholamines excess is briefly reviewed. 441101: Arterial hypertension and pulmonary edema induced by catecholamines in unanesthetized rats. 5622808: [Paroxysmal catecholamine-induced high blood pressure without pheochromocytoma]. 6095720: This paper reports a case of a patient who suffered a cerebral vascular accident due to hypertension resulting from a catecholamine-secreting infratemporal fossa paraganglioma. 6098975: Since catechol estrogens are potent competitive inhibitors of catechol-O-methyl transferase (COMT), it has been suggested that they may prolong the half-life of catecholamines which in turn can cause hypertension. 6428358: A case of severe systemic hypertension due to catecholamines discharge after ligation of a large patent ductus arteriosus in an 8 months old child is reported. 7131785: The role of adrenal catecholamines (CAs) was investigated with regard to the etiology of hypertension and cerebral stroke in the spontaneously hypertensive rats-stroke prone (SHRSP). 8804229: In general, these pheochromocytomas produce catecholamines that result in hypertension. Hypertension attributable to pheochromocytoma is a very attractive model for the elucidation of the pathogenesis of hypertension. 9651733: Changes in SNS activity measured as catecholamines in plasma or organ spillover have been implicated in the pathogenesis of hypertension. 11004129: Several mutations in the amyloid precursor protein (APP) gene may lead to either Alzheimer's disease or cerebral haemorrhage due to congophilic amyloid angiopathy (CAA). Further insight into the relationship between CAA and Alzheimer's disease may provide clues about the aetiology of Alzheimer's disease. 19822028: In this review we focus on the pathology and pathogenesis of CAA, its role in the aetiology of AD and its impact on immunotherapy for AD. 20359779: Epidemiologic evidence and postmortem studies of cerebral amyloid angiopathy suggest that vascular dysfunction may play an important role in the pathogenesis of Alzheimer's disease (AD). 21037967: Cerebral amyloid angiopathy (CAA) is increasingly recognized as a major contributor of Alzheimer's disease (AD) pathogenesis. 21239853: The accumulation of amyloid-beta (Abeta) peptides as toxic oligomers, amyloid plaques, and cerebral amyloid angiopathy (CAA) is critical in the pathogenesis of Alzheimer's disease (AD). 21760540: The relevance of cerebral amyloid angiopathy (CAA) to the pathogenesis of Alzheimer disease (AD) and dementia in general emphasizes the importance of developing novel targeting approaches for detecting and treating cerebrovascular amyloid (CVA) deposits. 29620941: Cerebral amyloid angiopathy (CAA) is a major contributor to Alzheimer's disease (AD) pathogenesis. 29770843: In this study, we have compared the severity of amyloid plaque formation and cerebral amyloid angiopathy (CAA), and the subtype pattern of CAA pathology itself, between APP genetic causes of AD (APPdup, APP mutations), older individuals with Down syndrome (DS) showing the pathology of Alzheimer's disease (AD) and individuals with sporadic (early and late onset) AD (sEOAD and sLOAD, respectively). 31727169: Alzheimer's disease (AD)-related amyloid beta-peptide (Abeta) pathology in the form of amyloid plaques and cerebral amyloid angiopathy (CAA) spreads in its topographical distribution, increases in quantity, and undergoes qualitative changes in its composition of modified Abeta species throughout the pathogenesis of AD. 33590547: VSI and mVD increased in Tg mice; these findings indicated microvascular disruption in the brain that could be related to damage to the neurovascular unit in AD caused by cerebral amyloid angiopathy. 35367207: Compared with the pathology of CAA in humans, the pathology in most mouse models of AD is not as evident, making it difficult to examine the contribution of CAA to the pathogenesis of AD. 7780697: Deposits of beta A4 amyloid in a form of amyloid (senile) plaques, diffuse amyloid deposits and congophilic angiopathy is central to the pathogenesis of AD. 11255453: BACKGROUND: Brain glucose metabolic rates measured by positron emission tomography can be more affected by partial volume effects in Alzheimer disease (AD) than in healthy aging because of disease-associated brain atrophy. 15110003: In eight patients with probable AD and eight age-matched normal control subjects, the IPCA was comparable to the established but partly manual digital subtraction (DS) method in characterizing annual rates of whole-brain atrophy: resulting rates were correlated (Spearman rank correlation = 0.94, P < 0.0005) and comparable in distinguishing probable AD from normal aging (IPCA-detected atrophy rates: 2.17 +/- 0.52% per year in the patients vs. 15345807: There was a 25% increase (not statistically significant) in vessel density in mm/mm2 in AD subjects (AD = 11.88 +/- 0.87; control = 9.53 +/- 0.78; p = 0.06), presumably due to brain atrophy in the white matter. 22011258: Abstract Posterior cortical atrophy (PCA) is a visual-cognitive syndrome caused by Creutzfeldt-Jakob disease (CJD), Alzheimer's disease (AD), or subcortical gliosis. Clinical manifestations of PCA caused by AD included visual agnosia, cortical blindness, optic apraxla, delusions, hallucinations, agitation, depression, amnestic deficit, Wernicke's aphasia, acalculia, and left/right disorientation. Posterior cortical atrophy produced by AD can be demonstrated on magnetic resonance imaging, positron emission tomography, and electroencephalography; determination of the etiology requires tissue examination. 23634965: Specifically, since MCI coincides with the onset of clinical symptoms and brain atrophy, and LC pathology is already present at this early stage of AD pathogenesis, MCI may offer a critical window of time to initiate novel noradrenergic-based therapies aimed at the secondary wave of events that lead to progressive neurodegeneration. 26222866: Nevertheless, mild DAT in illiterate participants seems to be due to brain atrophy.In this study, we compared the impact of brain metabolism efficiency in healthy participants and less-educated patients with mild DAT using 2-fluoro-2-deoxy-D-glucose (F-FDG-PET) positron emission tomography. 27879212: Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease causing neural cell degeneration and brain atrophy and is considered to be the most common form of dementia. 30582529: Structural magnetic resonance imaging (sMRI) has been widely used for computer-aided diagnosis of neurodegenerative disorders, e.g., Alzheimer's disease (AD), due to its sensitivity to morphological changes caused by brain atrophy. 32183332: Alzheimer's disease is an age-related disease characterized by the progressive loss of memory and cognitive function, caused by the unstoppable neurodegeneration and brain atrophy. 33327913: RESULTS: These data highlight the importance of the role of olfactory cortical atrophy in the pathogenesis of AD and the interplay between the olfactory deficits and degeneration of olfactory regions in the brain. 36294870: Alzheimer's disease (AD) is a neurologic disorder causing brain atrophy and the death of brain cells. 38102439: The deposition of Abeta is believed to initiate a detrimental cascade, including cerebral hypometabolism, accelerated brain atrophy, and cognitive problems-ultimately resulting in AD. 12218644: Cerebrospinal fluid (CSF) contains proteins known to be involved in the pathogenesis of Alzheimer disease (AD), including amyloid-related proteins, tau protein and apolipoprotein E. 15288699: Upregulation of MCP-1 may occur in the brain of subjects affected by Alzheimer's disease (AD) and MCP-1 levels in plasma and cerebrospinal fluid have been proposed as biological markers for the inflammatory process that accompanies AD pathogenesis. 19026494: Stasis of cerebrospinal fluid (CSF) has been previously suggested to be a factor in the etiology of AD, but it has generated little attention among researchers. 19363993: In cerebro-spinal fluid (CSF), it is the second most abundant protein, and is considered as an important protein in the pathogenesis of Alzheimer's disease, depression, and lead intoxication. 20727007: We here analysed adiponectin, one of the most important adipocytokines, in plasma and cerebrospinal fluid (CSF) from cognitive normal controls (NC), mild cognitive impairment (MCI) subjects, and patients with Alzheimer's disease (AD) and discussed if/how adiponectin could relate to the pathogenesis of AD. 21880396: Furthermore, continuous sampling of CSF proved to be a useful and robust method, which may also be used to investigate AD pathogenesis and to evaluate pharmacotherapeutic interventions. 23186986: Diagnoses of AD and other dementias were established by multidisciplinary expert teams, based on neuropsychological exams and structural brain imaging, blinded from CSF results. 24311739: Zinc (Zn) is an essential element for normal brain function; an abnormal Zn homeostasis in brain and the cerebrospinal fluid (CSF) has been implied in the etiology of Alzheimer's disease (AD). 25079796: Vitamin D binding protein (VDBP), a multifunctional protein, has been found to be elevated in the cerebrospinal fluid (CSF) of neurodegenerative disorder cases, implicating it in the pathogenesis of Alzheimer's disease (AD). 25946191: The current study indicates that reduction in water influx into the CSF may disturb the clearance rate of beta-amyloid, and therefore be linked to the pathogenesis of AD. 30297997: The parameters other than CSF results were included to study the difference between high- and low-AD-risk subjects in NC or MCI groups, based on CSF results. 32225073: Importantly, there is also clinical evidence supporting their potential use as biomarker candidates for AD, due to reduced serum and CSF levels that correlate with amyloid burden in AD patients compared with controls. Although the exact etiology of the disease remains elusive, accumulating evidence highlights the key role of lipid rafts, as well as the endocytic pathways in amyloidogenic amyloid precursor protein (APP) processing and AD pathogenesis. 35344967: Demographics, cognitive measurements, AD phenotypes, apolipoprotein E status, and results from cerebrospinal fluid and amyloid positron emission tomography analyses were included as explanatory variables of the hippocampal subtypes. 36171657: In this regard, the search for new protein markers and studies of proteomic changes in CSF and blood plasma are of particular interest and may consequentially identify particular pathways involved in the pathogenesis of AD. 37355215: Recently, it was suggested that dysregulated microRNA-485-3p (miRNA-485-3p) in the brain and cerebrospinal fluid is closely related to pathogenesis of AD. 38043012: CONCLUSIONS: Our comprehensive analyses identified the cells in cerebrospinal fluid from AD patients are expanded TEMRA or TEM cells and the TEMRA cells communicating with other immune cells is weakened, which may be an important immune feature that leads to AD. 9086466: Hence, it is concluded that increases in cerebrospinal fluid (CSF) levels of apoE are not involved in the pathogenesis of Alzheimer's disease and that measurement of CSF apoE levels does not seem to be useful as a diagnostic procedure. 11131274: However, death in the early stages of hypertension was due almost entirely to sudden death or stroke. 1291169: A 61-year-old man with history of mild hypertension and diabetes mellitus was admitted to our department because of recurrent minor stroke. 19195933: Parasympathetic nerves from the pterygopalatine ganglia may participate in development of cluster headaches, in vascular responses to hypertension and in modulation of damage due to stroke. 2103653: [Treatment of hypertension and the decline of mortality caused by cerebrovascular accidents]. 21512881: Their comorbidities included arterial hypertension, n = 12 (24%); atrial fibrillation, n = 4 (8%); cerebral stroke sequels, n = 4 (8%); diabetes mellitus, n = 6 (12%); chronic coronary ischemic disease, n = 20 (40%); and obstructive bronchitis, n = 4 (8%). 22588364: Arterial hypertension is one of the leading causes of overall mortality and is responsible for a high proportion of deaths due to stroke as well as coronary heart disease. 22879113: To avoid long working hours, stress management and treatment of hypertension, diabetes, and hyperlipidemia are key issues in preventing karoshi caused by stroke. 23591024: Existing epidemiologic and clinical trial data suggest that the blood pressure in patients with hypertension at high risk for cardiovascular events because of coronary artery disease, diabetes mellitus, chronic kidney disease, stroke, or heart failure should be reduced to <140/90 mm Hg in patients younger than 80 years and the systolic blood pressure be reduced to 140-145 mm Hg if tolerated in patients aged 80 years and older. 24582530: BACKGROUND: It is often assumed that blood pressure increases acutely after major stroke, resulting in so-called post-stroke hypertension. 24662339: 29 patients with acute carotid and vertebrobasilar stroke caused by combination of atherosclerosis and arterial hypertension were examined, of them 8 patients were diagnosed as having type II diabetes mellitus. 2595731: Hypertension was present in 58.24% of the cases, while strokes due to valvular heart disease and puerperium-related strokes were most common in the young. 2679012: Diuretic-based treatment regimens for hypertension have consistently reduced blood pressure and the morbidity and mortality due to stroke and overall cardiovascular disease. 27841110: (R) * Rapidly correcting pre-operative hypertension with beta blockade appears to cause higher mortality due to stroke and hypotension and should not be used. 30458665: Anger appears to be explained by prestroke variables such as age, hypertension, and the profile of anger, stroke itself as a sudden and potentially disabling condition, the environment, and the psychological and functional consequences of stroke. 31645472: CONCLUSION: Among patients with noncardioembolic stroke who were ineligible for revascularization therapy and those with progressive stroke, phenylephrine-induced hypertension was safe and resulted in early neurologic improvement and long-term functional independence. After adjustment for age and initial stroke severity, induced hypertension increased the occurrence of the primary (odds ratio 2.49, 95% confidence interval [CI] 1.25-4.96, p = 0.010) and secondary (odds ratio 2.97, 95% CI 1.32-6.68, p = 0.009) efficacy endpoints. 33473056: AIM: Stroke is well known to lead to hypertension; nevertheless, the role of vascular function in hypertension remains unclear. 36986445: The prognosis of hypertension leads to organ damage by causing nephropathy, stroke, retinopathy, and cardiomegaly. 37245670: 1 A 56-year-old man with history of hypertension, hyperlipidemia, and diabetes mellitus presented to the clinic with right hemiparesis due to previous left cerebral hemispheric stroke. 37843942: Treatment of hypertension reduces morbidity and mortality due to coronary artery disease, myocardial infarction, heart failure, stroke, and chronic kidney disease. 6689709: In this unanesthetized primate model of moderate experimental stroke, induced hypertension had beneficial effects on neurological status, local CBF, and infarct size without causing hemorrhagic infarction. 8421827: RESULTS: In the control group, severe hypertension developed, and all rats died within 12 weeks because of stroke. 8622152: To identify technical and patient-specific risk factors for perioperative stroke, the authors examined a series of patients in whom induced hypertension and mild hypothermia and intravenous mannitol administration were used as protection during temporary vessel occlusion for aneurysm clipping. 12515903: Previous studies employing the cholesterol-fed rabbit model of AD demonstrated that induction of AD-like Abeta accumulation in brain could be reversed by co-administration of cholesterol lowering drugs or removing cholesterol, prompted initiation of an AD Cholesterol-Lowering (Statin) Treatment Trial. 12573540: Recent evidence strongly suggests a role for cholesterol and apolipoprotein E in the etiology of Alzheimer's disease. 12668899: Since apoE is a regulator of lipid metabolism, it is reasonable to assume that lipids such as cholesterol are involved in the pathogenesis of AD. 12737522: Use of in vivo models to study the role of cholesterol in the etiology of Alzheimer's disease. 12843267: Epidemiology, in vitro, and in vivo studies strongly implicate a role for cholesterol in the pathogenesis of Alzheimer's disease (AD). 12920183: Despite the crucial role played by cholesterol and copper in nutrition and normal brain function, recent evidence indicates that they may both be important factors in the etiology of Alzheimer's disease (AD). 15212822: This review focuses on the newly recognized importance of cholesterol and its oxygenated metabolites in the pathogenesis of ischemic stroke and AD. 15270198: Although early studies recognized the loss of cholesterol and other lipids in the brain, these findings have been poorly connected with AD pathogenesis, despite the identification of the epsilon4 allele of APOE as a major risk factor in AD. 15351438: Epidemiological and biochemical studies strongly implicate a role for cholesterol in the pathogenesis of Alzheimer's disease (AD). 15844755: AD is a complex multifactorial disorder that involves numerous susceptibility genes, but the exact pathogenesis and biochemical basis of AD is not well understood Cholesterol is receiving a great deal of attention as a potentially crucial factor in the etiology of AD. 16096813: Cholesterol regulates the production of amyloid beta (Abeta), which is central to the pathogenesis of Alzheimer's disease (AD), with high cellular cholesterol promoting and low cellular cholesterol reducing Abeta in vitro and in vivo. 16786033: ApoE has roles in cholesterol metabolism and Abeta clearance, both of which are thought to be significant in AD pathogenesis. It can be seen that abnormal lipid, cholesterol and glucose metabolism are consistently indicated as central in the pathophysiology, and possibly the pathogenesis of AD. 18387175: High levels of serum cholesterol and disruptions of the blood brain barrier (BBB) have all been implicated as underlying mechanisms in the pathogenesis of Alzheimer's disease. 19239689: Growing evidence suggests an important function for cholesterol in the pathogenesis of AD, particularly in APP metabolism and production of A beta peptides. 19293239: In conclusion, long-term, low-level cholesterol feeding was sufficient to promote the formation of extracellular beta-amyloid plaque formation in rabbits, supporting the integral role of cholesterol in the aetiology of Alzheimer's disease. 19297055: A growing body of evidence implicates low membrane cholesterol in the pathogenesis of Alzheimer's disease (AD). 19996111: Significantly, LXR activation has been found to reduce the symptoms of Alzheimer disease (Fan, J., Donkin, J., and Wellington C. (2009) Biofactors 35, 239-248); thus, cholesterol metabolites may play an important role in the etiology of Alzheimer disease. 20138836: It has been suggested that cholesterol may modulate amyloid-beta (Abeta) formation, a causative factor of Alzheimer's disease (AD), by regulating distribution of the three key proteins in the pathogenesis of AD (beta-amyloid precursor protein (APP), beta-secretase (BACE1) and/or presenilin 1 (PS1)) within lipid rafts. 20157255: Our results suggest that cholesterol-enriched diets and cholesterol metabolites induce AD-like pathology by altering leptin signaling. 20304094: Many preclinical and clinical studies have implied a role for cholesterol in the pathogenesis of Alzheimer's disease (AD). 20638472: However, the effects of caffeine on cholesterol-induced sporadic AD pathology have not been determined. 21091943: High-fat diabetogenic diets, cholesterol, and the omega-6 fatty acid arachidonate and its prostaglandin metabolites have all been implicated in promoting the pathogenesis of Alzheimer's disease. 21590435: Additionally, excess brain cholesterol has been associated with increased formation and deposition of amyloid-beta peptide from amyloid precursor protein which may contribute to the risk and pathogenesis of AD. 21605030: Apo E is the major component of lipoprotein particles in the brain that mediate transport of cholesterol and other lipids between neurons and glial cells, indicating an implication of cerebral lipid metabolism in the pathogenesis of AD. Importantly, mutations in the genes of APP and the two homologous PS proteins are a major cause of familial early onset AD, indicating that the metabolism of APP and generation of Abeta play critical roles in the initiation of the disease. 21741455: Cholesterol seems to be intimately linked with the generation of amyloid plaques, which is central to the pathogenesis of AD. In this review, we aim to provide a background on AD and the contribution of cholesterol in the etiology of Alzheimer's. 21851605: Epidemiological studies correlated high plasma cholesterol levels with high incidence of AD, and feeding rabbits with a diet rich in cholesterol has been shown to induce AD-like pathology in rabbit brain. 21965313: The aim of this review is to summarize the findings of epidemiological and cell biological studies to elucidate the role of cholesterol in AD etiology. The role of cholesterol in the etiology of Alzheimer's disease (AD) is still controversial. 22046282: We have previously shown that the cholesterol oxidized metabolite 27-hydroxycholesterol (27-OHC) triggers AD-like pathology in organotypic slices. 22108168: Cholesterol in the plasma membrane plays an important role in the pathogenesis of Alzheimer's disease, but the exact function of cholesterol in the regulation of amyloid-beta (Abeta) generation, aggregation, and toxicity remains elusive. 22367100: This review summarizes the current state of our knowledge of the influence of cholesterol and lipid pathways in AD pathogenesis in vitro and in vivo. 22580286: Endolysosome involvement in LDL cholesterol-induced Alzheimer's disease-like pathology in primary cultured neurons. 24155031: Here, we first provide a brief overview of cholesterol-protein interactions and then offer our perspective on how and why binding of cholesterol to APP and its C99 domain (beta-CTF) promotes the amyloidogenic pathway, which is closely related to the etiology of Alzheimer's disease. 24329875: Cholesterol as a causative factor in Alzheimer's disease: a debatable hypothesis. 24754001: The significant up regulation of miR-26b is consistent with the decrease of leptin levels in the brains of cholesterol fed rabbit model for AD, confirming that miR-26b is indeed regulated by leptin and that both leptin and miR-26b may be involved in cholesterol induced AD-like pathology. 25859562: Role of endolysosomes and cholesterol in the pathogenesis of Alzheimer's disease: Insights into why statins might not provide clinical benefit. 26413387: Here, we will further discuss the linkage between elevated levels of LDL cholesterol and AD pathogenesis, and explore the underlying mechanisms whereby elevated levels of plasma LDL cholesterol promote amyloidogenesis. Among those factors, altered circulating cholesterol homeostasis, independent of the APOE genotype, continues to be implicated in brain deposition of amyloid beta protein (Abeta) and the pathogenesis of AD. 26944571: Although numerous studies have shown the important function of cholesterol in AD pathogenesis and development, the underlying mechanism remains unclear. 27687218: A significant body of evidence indicates that oxidized cholesterol, in the form of oxysterols, is one of the main triggers of AD. 28461971: Cholesterol in the Pathogenesis of Alzheimer's, Parkinson's Diseases and Autism: Link to Synaptic Dysfunction. 29736006: Although increasing evidence implicates cholesterol in the pathogenesis of Alzheimer's disease, the detailed mechanistic link between this lipid molecule and the disease process remains to be fully established. 30684043: Accumulating evidence suggests that cholesterol may play a role in the pathogenesis of Alzheimer's disease since abnormal deposits of cholesterol surrounding senile plaques have been described in animal transgenic models and patients with Alzheimer's disease. 30689571: Epidemiologic and experimental evidence also suggests that cholesterol (CH) contributes to the pathogenesis of AD, particularly the formation of amyloid plaques. 31950579: Presumed chronic kidney disease (80%) was the most common cause of systemic hypertension with eye disease, followed by hyperthyroidism (20%). 32016622: Mechanisms of Synergistic Interactions of Diabetes and Hypertension in Chronic Kidney Disease: Role of Mitochondrial Dysfunction and ER Stress.PURPOSE OF REVIEW: To discuss the importance of synergistic interactions of diabetes mellitus (DM) and hypertension (HT) in causing chronic kidney disease and the potential molecular mechanisms involved. 32059997: Thus, salt-sensitive hypertension is induced in CKD via activation of the renal WNK1- SPAK-NCC phosphorylation cascade by TNF-alpha, reflecting a link with the immune system. Although chronic kidney disease (CKD) is a common cause of salt-sensitive hypertension, the involvement of the WNK phosphorylation cascade is unknown. Moreover, a high-salt diet did not adequately suppress activation of the WNK1-SPAK-NCC phosphorylation cascade in this model, leading to salt-sensitive hypertension. 32127862: The other factors that work in concert with hypertension to cause CKD are yet to be clearly elucidated. Introduction: Hypertension is a cause and consequence of chronic kidney disease globally. 32604820: We found maternal CKD induced hypertension in adult offspring, which tryptophan supplementation prevented. The protective effect of tryptophan supplementation against maternal CKD-induced programmed hypertension is relevant to alterations to several tryptophan-metabolizing microbes and AHR signaling pathway. 32765290: CKD causes hypertension and cardiovascular disease; and hypertension causes CKD. 32985236: Chronic kidney disease (CKD) causes salt-sensitive hypertension that is often resistant to treatment and contributes to the progression of kidney injury and cardiovascular disease. 33008046: Additionally, maternal adenine-induced CKD caused hypertension and renal hypertrophy in adult male offspring. 33230698: In CKD, enhanced tubular sodium reabsorption is a leading cause of HTN due to augmented extracellular fluid volume expansion. 35052587: CKD-induced hypertension is associated with an altered gut microbiota profile, dysregulated renal short chain fatty acid (SCFA) receptor expression, activation of the aryl hydrocarbon receptor (AhR) signaling pathway, and reduced nitric oxide bioavailability. 35052651: Our data suggest that the oral administration of STS improves hypertension in an adenine-induced CKD model, which brings us closer to the clinical translation of H 2 S-targeting therapy in CKD-induced hypertension. 36014941: We examined whether perinatal propionate supplementation can prevent offspring hypertension induced by maternal CKD. 36364887: Maternal CKD leads to hypertension in adult rat progeny, which was linked to disruption of the gut microbiota. This study validated the benefits of perinatal garlic oil supplementation against offspring hypertension induced by maternal CKD via modulation of H 2 S signaling, nitric oxide (NO), and the gut microbiota. 36613730: CKD is both a common cause of uncontrolled hypertension and a risk factor for altered sequelae. 36771342: The CKD-induced hypertension coincided with: decreased nitric oxide (NO) bioavailability; augmented renal protein expression of a (pro)renin receptor and angiotensin II type 1 receptor; and increased oxidative stress damage. 37428459: The swelling was caused by the antihypertensive amlodipine, which he used because of arterial hypertension due to a chronic kidney disease. 37843942: Treatment of hypertension reduces morbidity and mortality due to coronary artery disease, myocardial infarction, heart failure, stroke, and chronic kidney disease. 38238510: CKD-induced systemic arterial hypertension (SAH) and vascular dysfunction by reducing the vasorelaxant response of angiotensin 1-7 and increasing the contractile response to angiotensin II. 38338891: Our prior investigation showed that the administration of adenine to pregnant rats resulted in the development of CKD, ultimately causing hypertension in their adult offspring. 14174370: [ON A CASE OF NEPHROGENIC HYPERTENSION DUE TO UNILATERAL OBSTRUCTIVE ANGIOPATHY (STENOSIS OF THE RIGHT RENAL ARTERY) SECONDARY TO CHRONIC INFLAMMATION OF PERIARTERIAL CELLULAR TISSUE]. 23961783: HCV+ psoriatic patients were less obese, but still had a higher frequency of diabetes mellitus and hypertension, possibly due to chronic inflammation in the liver and other organs. 25774191: Experimental findings suggested that paradoxical brain discharge led to cardiac arrest instead of epileptic seizures; the insult was associated with chronic inflammation on the cerebral surface, which subsequently led to hypertension and poor blood circulation in focal cerebral areas. 26294657: RATIONALE: Chronic inflammation is a major contributor to the progressive pathology of hypertension, and T-cell activation is required for the genesis of hypertension. 27488663: We conclude that HHcy promotes TLR-4-driven chronic vascular inflammation and mitochondria-mediated cell death, inducing hypertension. 28326006: Background: Recent studies indicate the important role of chronic inflammation and oxidative stress in the pathogenesis of hypertension. 30332305: Recent evidence suggests hypertension may be secondary to chronic inflammation that results from hypoactive neuro-immune regulatory mechanisms. To further understand this association, we used systemic lupus erythematosus (SLE) as a model of inflammation-induced hypertension. 32692322: This review examines the potential of tropical foods to treat signs of metabolic syndrome, defined as a chronic low-grade inflammation leading to obesity, hypertension, impaired glucose tolerance, insulin resistance, dyslipidaemia and fatty liver. 32903041: CONCLUSIONS: Chronic allergen-induced airway inflammation results in systemic hypertension that is correlated to the degree of distal airway obstruction induced by the allergen. 36595776: The chronic inflammation caused by hyperuricemia maybe one of important pathogenesis of incident hypertension in patients with hyperuricemia. 36839212: Metabolic syndrome (MetS) is a cluster of metabolic disorders primarily caused by central obesity, which results in chronic inflammation leading to hypertension, diabetes and atherogenic dyslipidemia. 37975169: Purpose : The development of hypertension is shown to be triggered by chronic low-grade inflammation. 10446805: In addition, increasing data claim the importance of chronic inflammation in the pathogenesis of AD. 12189211: Similar observations in Alzheimer's disease (AD) have lead to the hypothesis that chronic localized inflammation is an important element of AD pathogenesis, with significant neurodegenerative consequences. 15931589: In conclusion, neurodegenerative diseases such as Alzheimer's disease, which is caused primarily by cell death due to chronic inflammation and cell stress, might be controlled by proper doses of non-toxic, natural Rg1 and Rb1. 15979880: Chronic inflammation is known to play an important role in the heterogeneous pathogenesis of Alzheimer's disease (AD). 19320056: Using novel engineered dominant negative TNF inhibitors (DN-TNFs) selective for soluble TNF (solTNF), we investigated whether blocking TNF signaling with chronic infusion of the recombinant DN-TNF XENP345 or a single injection of a lentivirus encoding DN-TNF prevented the acceleration of AD-like pathology induced by chronic systemic inflammation in 3xTgAD mice. 19946744: Glycated proteins can induce activation of microglia, which exacerbate the pathology of Alzheimer's disease by causing chronic inflammation. 20080314: CLU, CR1 and PICALM support existing hypotheses about the amyloid, lipid, chaperone and chronic inflammatory pathways in AD pathogenesis. 20629514: These susceptibility loci support existing hypotheses about the amyloid, lipid, chaperone and chronic inflammatory mechanisms in AD pathogenesis, and are therefore likely to provide the basis for the development of hypothesis-driven novel biomarker candidates. 28448946: INTRODUCTION: There is increasing evidence for the involvement of chronic inflammation and oxidative stress in the pathogenesis of Alzheimer's disease (AD). 29134678: Chronic inflammation represents a central component in the pathogenesis of Alzheimer's disease (AD). 30657587: OBJECTIVE: the role of microbes and chronic inflammation in the pathogenesis of Alzheimer' disease (AD) has been postulated by many authors. 31797529: In particular, chronic inflammation plays a central role in Alzheimer's disease (AD) etiology, and dysregulated LX production and activities have been reported in a variety of AD rodent models and clinical tissue samples, yet with complex and sometimes conflicting results. 32035419: Oxidative stress and chronic inflammation have been suggested as causes of AD. 33408815: Chronic inflammation is thought to contribute to the early pathogenesis of Alzheimer's disease (AD). 35717405: Microglia cells play a key role in the pathology of Alzheimer's disease by causing chronic inflammation. 35892582: Amyloid-beta (Abeta)-peptide production or deposition in the neuropathology of Alzheimer's disease (AD) was shown to be caused by chronic inflammation that may be induced by infection, but the role of pathogenic-bacteria-related AD-associated Abeta is not yet clearly understood. 37059510: The detrimental role that chronic inflammation plays in the pathogenesis of Alzheimer's disease is increasingly recognised; however, it is largely ascribed to the accumulation of amyloid beta, leaving the effect of chronic inflammation on tau pathology and neurofibrillary tangle-related pathways greatly overlooked. 38622351: This study hypothesized that chronic aseptic inflammation might lead to AD in KOA patients. 9790168: Chronic inflammatory reactions in the brain appear to be one of the primary etiological factors in the pathogenesis of Alzheimer's disease (AD). 1010180: It is concluded that propranolol might be the specific treatment for hypertension in those cases which are accompanied or caused by high plasma renin. 14171562: HYPERTENSIVE VASCULAR DISEASE PRODUCED BY HOMOLOGOUS RENIN. 19513415: Renin system of the kidney in ISIAH rats with inherited stress-induced arterial hypertension. 2100527: [Arterial hypertension caused by low renin: comparison of the calcium antagonist nifedipine and the ACE-inhibitor enalapril as to antihypertensive efficacy]. 21949629: Chronic activation of the renin system causes HTN and, ultimately, end-organ damage. 2656313: [Significance of brain renin for pathogenesis of hypertension: effect of antihypertensive drugs on active and inactive renins in the brain of spontaneously hypertensive rat]. 3070096: [Significance of brain renin in pathogenesis of hypertension: effect of diltiazem on active and inactive renins in the brain of spontaneously hypertensive rat]. 470018: A case is presented of a 1-year-old boy with hypertension resulting from abnormal renin production by the right kidney. 6355549: Arterial renin--partial characterization and its possible role in the pathogenesis of hypertension. 6986606: Eleven cases of hypertension secondary to a renal tumour secreting renin have been described in the literature between 1967 and 1978. [Hypertension secondary to a \renin tumor\. 6993568: [Another case of hypertension due to a tumour of the juxta-glomerular apparatus (author's transl)]. Eleven cases of hypertension secondary to a renal tumour secreting renin have been described in the literature between 1967 and 1978. 7016159: It is suggested that sustained high blood pressure due to the sustained high plasma renin concentration in bilaterally nephrectomized rat was responsible for the production by renin of lesions of the fibrinoid necrosis type in the arteries. 804756: The morphological characteristics of the hamartomatous abnormality are described and evidences are put forward which would suggest that the liver lesion might have been the site of the abnormal renin production which was responsible for the systemic arterial hypertension. 8613199: Thus, chronic human renin infusion resulted in severe hypertension with extreme plasma renin activity and plasma renin concentration. 8795440: The findings of slow fetal renal growth rate and associated high renin concentrations seen in small-for-gestational-age fetuses could be implicated in an irreversible reno-vascular pathology leading to adult hypertension. 14519445: Hypertension was induced using silver clip on renal artery by surgery. 17853043: MATERIAL AND METHODS: The right renal artery was constricted by a silver clip in 63 male Sprague-Dawley rats to induce hypertension, while a sham operation was performed in 17 control rats. Six months after the induction of hypertension, nephrectomy of the clipped kidney was performed. 21097645: Hypertension was induced by the two-kidney one-clip (2K1C) method. 27189349: OBJECTIVE: The present study has been structured to explore the effects of bosentan, an ET-1 antagonist on two-kidneyone- clip: 2K1C method induced hypertension provoked vascular dementia (VaD). 27966210: The Goldblatt model of two-kidneys, one clip (2K1C) was used to induce hypertension. 28158469: METHODS: Holtzman NT rats received a silver clip around the left renal artery to induce 2K1C hypertension. 30170073: Thus, we evaluated in rats the effect of hypertension induced by two-kidney one-clip (2K1C) model on the gastric motility, as well as the influence of exercise and RAS blockers treatment in such phenomenon. 3339954: We examined the interrelationships between the pressor response to the administration of norepinephrine and arginine vasopressin and baroreflex function in rats with hypertension of two days' duration induced by heminephrectomy and a clip placed on the right renal artery (2-day clipped rats). 35396697: This study investigates the role of ulinastatin (UTI) and quercetin alone as well as in combination in hypertension-induced endothelial dysfunction and vascular dementia (VaD). Therefore, the utility of these agents might be studied further to understand their full potential in hypertension-induced VaD. METHOD: Two-kidney one-clip (2K1C) renovascular model was set up to induce hypertension in the Albino Wistar rats (males). 37415906: The rats in RVH groups were subjected to the modified Goldblatt two-kidneys, one clip (2K1C) for induction of hypertension. 38613379: Male Wistar rats were divided into 2 groups; the 2K1C group in which a silver clip was placed around renal artery to induce hypertension, and the SO normotensive group. 6098234: In the rat model of hypertension induced by a clip on the right renal artery, sparing the left kidney, we compared the efficacity and the endocrine, renal and cardiac effects of classical therapy (CT) of hypertension (Clonidine 0.2 mg/kg and Dihydralazine 15 mg/kg in 2 daily subcutaneous injections and Furosemide 30 mg/kg/day in the drinking water), with inhibition of the angiotensin converting enzyme with a new drug, the S-9490-3 (0.5 mg/kg in one daily administration). 7270147: At 3-8 weeks after induction of hypertension, nodular lesions of mesenteric arteries were biopsied, and constricting clips were removed. 7582082: Enhancement of intrarenal angiotensin II levels in 2 kidney 1 clip and angiotensin II induced hypertension. 9707215: METHODS: The 1-kidney, 1 clip (1k1c); 2-kidney, 1 clip (2k1c); and 2-kidney, 2 clip (2k2c) methods were used to induce hypertension in male Sprague-Dawley rats with a ring-shaped silver clip. 9755128: In clipped kidneys of GH, which were not exposed to the hypertension because of the arterial clips, NHE3 was localized on the brush border as in normal SD. 10614985: 5.58 +/- 0.08 beats/min per mmHg in B2+/+, P < 0.01), as well as by an exaggerated tachycardic response to chronic hypertension induced by clipping of the left renal artery (60 +/- 3 vs. 15 +/- 3 beats/min in B2+/+, P < 0.01). In B2-/- mice, the presence of an alteration in baroreceptor regulation of HR was supported by a reduced gain in the HR responses to acute nitroprusside-induced hypotension or phenylephrine-induced hypertension (slope of the regression line: 0.82 +/- 0.07 vs. 2059900: Hypertension was effected by clipping the left renal artery of Wistar-Kyoto (WKY) rats, and diabetes was induced 2 weeks later by streptozotocin (STZ; 55 mg/kg i.v.). 25223948: BACKGROUND: The clipping of an artery supplying one of the two kidneys (2K1C) activates the renin-angiotensin (Ang) system (RAS), resulting in hypertension and endothelial dysfunction. 25740291: Hypertension was induced by clipping the right renal artery, and the following five groups were divided: SHAM operated; 2-kidney, 1-clip (2K1C); 2K1C plus ALSK; 2K1C plus L-ARG; and 2K1C plus ALSK+ L-ARG. 26877946: METHODS: The 2K1C hypertension was induced by clipping the left renal artery; age-matched rats receiving sham treatment served as controls. 26885474: METHODS: Hypertension was induced by clipping the left renal artery, and control age-matched rats were sham treated. 27383506: Hypertension was induced by clipping the left renal artery, and the following five groups were created: SHAM; two-kidney, 1-clip (2K1C); 2K1C plus ALSK (ALSK); 2K1C plus l-ARG (l-ARG); and 2K1C plus ALSK+l-ARG (ALSK+l-ARG). 29935157: Hypertension was induced by clipping the renal artery with a silver clip. 3346063: The left kidney was ablated by two thirds in 12 rats, and in 5, hypertension was induced by clipping the right renal artery. 6368102: Exchangeable sodium (NaE), plasma active renin concentration and blood pressure were measured in rats with a sole remaining kidney before and after the development of hypertension induced by clipping of the single renal artery and again after unclipping. 702944: We determined antihypertensive effect of L 6150 for 11 weeks in spontaneously hypertension due to clipping (CLIP). 7863781: Clipping the left renal artery induced marked hypertension and hypertrophy of the left ventricle in elderly (24-month-old) rats. m-Nifedipine (m-Nif, ig 20 mg.kg-1, qd x 9 wk) significantly decreased the systolic blood pressure and the weight of the left ventricle in the renovascular hypertensive rats (RVHR). 8060580: Denudation was accomplished by scraping the aortic lumen with a balloon catheter, and hypertension was induced by clipping the left renal artery. 8458534: Hypertension, whether induced by the clipping of one renal artery or genetically determined (spontaneously hypertensive rats), resulted in a similar elevation in type VI collagen (2.71 +/- 0.12 mg/g, p < 0.005 compared to normal rats). 13761140: In doses which significantly depressed the action of eserine bretylium did not inhibit the hypertension due to excitation of medullary centres induced by clamping the common carotid arteries. 17516307: The purpose of this study was to test whether delayed versus immediate cord clamping would result in higher blood pressure (BP) and hematocrit (Hct), and to assess its clinical effects on the neonatal course in premature neonates (< 35 weeks). 1893254: NMDA antagonists attenuate hypertension induced by carotid clamping in the rostral ventrolateral medulla of rats. 2189830: Hypertension was induced by unilateral renal artery clamping, while the contralateral kidney was left intact (2 KIC). 25298674: Hypertension was induced by clamping the renal artery with renal bulldog clamp for 4 h. 4134204: Blood-brain barrier dysfunction in acute arterial hypertension induced by clamping of the thoracic aorta. 699604: Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). 7627572: We previously reported that AP7 antagonizes NMDA and carotid clamping-induced hypertension. Thus, carotid clamping-induced hypertension may also involve NMDA receptors in the RVLM. In this study, we found that when locally applied to RVLM, AP5 antagonized hypertension evoked by clamping the carotid arteries in SHRs and WKYs. 8121174: Ablation of afferent nerves from the left hind limb (n = 4) eliminated the hypertension produced by left iliac artery clamping. 8613200: Induction of hypertension by renal artery clamping (two-kidney, one-clamp Goldblatt model) did not alter the pattern of expression observed in the SD rat. 10433872: Cocaine causes hypertension at least in part by stimulating the sympathetic nervous system, but it is not clear if this effect is centrally or peripherally mediated. Cocaine-induced hypertension: role of the peripheral sympathetic system. 11021182: The pathogenesis of cocaine-induced arterial hypertension as well as the differential diagnosis of increased urinary catecholamines will be discussed. The work-up revealed the diagnosis of cocaine-induced arterial hypertension. 11416624: Potential therapies for cocaine induced hypertension and vasoconstriction include nitroglycerin, alpha-blockade combined alpha-A -blockade, and calcium channel blockers. 1387505: Treatment of cardiovascular complications focuses on cocaine-induced ischemia, hypertension and arrhythmias. 1550283: Hydralazine does not restore uterine blood flow during cocaine-induced hypertension in the pregnant ewe. 1646895: Combined administration of benzodiazepine and an angiotensin converting enzyme inhibitor has also been reported to protect rats against cocaine-induced hypertension and to increase survival rates after a toxic dose of cocaine. 2091237: Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. 2213551: Propranolol (1 mg/kg i.a.) prolonged the duration of cocaine-induced hypertension and bradycardia. These results demonstrate that cocaine acts centrally to increase sympathetic outflow leading to hypertension and reflex bradycardia in conscious rats. 23283356: Cocaine-induced acute hypertension is mediated largely by increased central sympathetic nerve activity. Thus, in a low nonsedating dose, dexmedetomidine constitutes a putative new treatment for cocaine-induced acute hypertension but higher sedating doses can increase blood pressure unpredictably during acute-cocaine challenge and should be avoided. 27879921: The rationale for selecting this medication is: ketanserin (a) is an antihypertensive and cocaine and caffeine produce hypertension and (b) acts at 5-HT2A/2C receptors, prevalent in NAc and implicated in hypertension and cocaine addiction. 29545982: Aortic dissection is a rare and fatal complication of cocaine-induced hypertension. 3376742: The relationship between severe cocaine-induced hypertension, and the development of subarachnoid or intracerebral hemorrhages is noted, and apparently is related to sudden transient increases of blood pressure related to cocaine use. 3603597: Analysis of these cases suggests that the hypertension induced by cocaine secondary to sympathetic stimulation may be the common factor. 9247556: In contrast, nitroglycerin and verapamil reverse cocaine-induced hypertension and coronary arterial vasoconstriction; therefore, they are the agents of choice in treating patients with cocaine-associated chest pain. 9330917: We have proposed that this pattern of responses may reflect a predisposition in individual rats to cocaine-induced cardiomyopathies and hypertension. 9628710: Cocaine can cause hypertension, tachycardia, coronary vasospasm, arrhythmias, and increased core temperature. 9657630: Cocaine causes acute hypertension by blocking catecholamine reuptake. 101177: [Arterial hypertension and mortality due to cardiovascular complications in patients on chronic hemodialysis]. 11596949: Adult respiratory distress syndrome: a complication of induced hypertension after severe head injury. 12661740: Hypertension may develop secondary to thromboembolic complications of central lines, steroid use, or be a sign of an underlying renal or cardiac problem. 12714226: Stenosis, the most common vascular complication, occurs in 1-12% of transplanted renal arteries and represents a potentially curable cause of hypertension following transplantation and/or renal dysfunction. 19583065: Long-term complications involve the eyes, kidneys, nerves, and blood vessels, resulting in hypertension, cardiac ischemia, atherosclerosis, and renal failure, among other syndromes. 20601365: BACKGROUND: Transplant renal artery stenosis (TRAS) is a recognized complication resulting in post-transplant hypertension associated with allograft dysfunction. 20610351: Although hypertension is often perceived as asymptomatic, it is associated with impaired HRQOL because of complications or comorbidities, awareness of the diagnosis, and adverse effects from antihypertensive medications. 22064430: High blood pressure, or hypertension, is a very common disorder with a substantial impact on public health because of its associated complications. 23559180: We conclude that the association of chronic hypertension and pregnancy shows strong risk for maternal and perinatal complications, especially when associated with the severity and etiology of hypertension, showing no trend during the two decades studied on perinatal outcome. 24475427: BACKGROUND: Hypertension (HTN) is a very common disorder with a substantial impact on public health because of its complications. 24614724: Systemic complications of oxidative stress are involved in the pathogenesis of hypertension, endothelial dysfunction, shortened erythrocyte lifespan, deformability, and nitric oxide (NO) dysfunction. 26628389: Posterior Reversible Encephalopathy Syndrome as an Overlooked Complication of Induced Hypertension for Cerebral Vasospasm: Systematic Review and Illustrative Case. Furthermore, the electronic database MEDLINE was searched for additional data in published studies of PRES after induced hypertension. METHODS: We present an illustrative case of PRES in a patient with induced hypertension for SAH-related cerebral vasospasm and performed a systematic review. Posterior reversible encephalopathy syndrome (PRES) is a reversible intracranial complication that has rarely been reported in the setting of induced hypertension. Triple-H therapy, induced hypertension, hypervolemia, and hemodilution, is often used to treat cerebral vasospasm. 26915846: BACKGROUND: Transplant renal artery stenosis (TRAS), the most common vascular complication after transplant (Tx), leads to resistant hypertension, impaired renal function, and even loss of the graft. 27306087: Hypertension is a rising global burden, and low- and middle-income countries account for 80% of deaths due to complications of hypertension. 29889252: Commentary: Posterior Reversible Encephalopathy Syndrome as a Complication of Induced Hypertension in Subarachnoid Hemorrhage: A Case-Control Study. 29889274: Posterior Reversible Encephalopathy Syndrome as a Complication of Induced Hypertension in Subarachnoid Hemorrhage: A Case-Control Study. 29996172: Hypertension was induced by oral administration of nitric oxide synthase inhibitor, N-nitro L-arginine-methyl-ester (L-NAME), at 40 mg/kg body weight to the male Wistar rats for 14 consecutive days. There is a growing global interest in hypertension due to its associated complications including renal dysfunction in patients. 30010952: Commentary: Posterior Reversible Encephalopathy Syndrome as a Complication of Induced Hypertension in Subarachnoid Hemorrhage: A Case-Control Study. 3056211: They suggest early screening, especially for rheumatoid valvulopathies and hypertension, which cause major social problems because of their complications. 31424260: Morbidity and mortality associated with hypertension are caused by organ complications. 31775784: An early detection and/or identification of novel biomarkers of this phenotype could avoid the progression or future complications leading to arterial hypertension. 32806787: A proper concentration of these elements in the body of women during pregnancy reduces the risk of complications such as anemia, induced hypertension, low birth weight, preeclampsia, and postnatal complications. 33122940: BACKGROUND: Hypertension is a major health problem throughout the world which affects over one billion people due to severe complications and inadequate control. 33897189: Background: Worldwide, hypertension is considered as an important health issue due to its unbearable complication of cardiovascular, renal, and nervous system diseases. 34441010: Careful pregnancy monitoring in moderate-to-severe psoriasis vulgaris is required given the high risk of related complications in pregnancy, including pregnancy-induced hypertensive disorders, low birth weight for gestational age, and gestational diabetes. 34773425: BACKGROUND: Renal scarring is a significant complication in recurrent urinary tract infections (UTIs) in children that can lead to hypertension and end-stage renal disease. 35059979: To date, however, it is unclear whether these findings can be attributed solely to obesity or whether they are a consequence of cardiometabolic complications that often co-exist with obesity, such as low-grade systemic inflammation, hypertension, insulin resistance, or dyslipidemia. 35260962: Future tailored blood pressure management based on patient- and time-point-specific needs will hopefully better balance the neurological advantages versus the systemic complications of induced hypertension. 35983401: Given the history of uncontrolled hypertension, the right hemispheric infarction and edema were thought to be due to secondary complications of severe PRES. 3615226: Emergency department presentation of severe hypertension secondary to complications of umbilical artery catheterization. 9411585: Hypertensive cardiomyopathy is nowadays the most precious, prevalent and fatal condition of all cerebral, renal and arterial complications that leads to arterial hypertension. 9767934: In rare cases with obstructive complications alone an aneurysm may lead to acute hypertension either after dissection as in our case or after thrombus formation. 10203151: These findings support the hypothesis that brief hypertension due to DA compression impairs endothelium-dependent pulmonary vasodilation in the fetus, and that this may be due to decreased NO production. 10337336: CONCLUSION: This is undoubtedly the first case of metastatic cancer of the ovary revealed by hypertension; it can be added to the list of 49 other published cases of extrinsic compression of the renal artery by various causes leading to hypertension. Intrinsic stenosis is a common finding, but hypertension secondary to extrinsic compression of the renal artery is exceptional. 10353413: We present a 15-year-old boy who developed hypertension, seizures, and acute renal failure due to extrinsic compression of the bladder and ureters by a large retrovesical Burkitt lymphoma. 11273151: Renovascular hypertension is an important but not so common cause of hypertension. Rarely the extrinsic compression of renal arteries by retroperitoneal structures may be responsible for hypertension. 11281245: Hypertension due to perinephric compression: the \Page\ kidney. 11507171: Partial compression of the umbilical cord produced fetal hypertension, a reduction in femoral blood flow and, consequently, an increase in calculated fetal femoral vascular resistance for the duration of the challenge. 12627783: Abdominal pain and hypertension may occur as a result of renal vasculature compression; respiratory distress may be evident in thoracic tumors; and Homer's syndrome or heterochromia of the iris may manifest from neuroblastoma of the head and neck. 129836: Selected groups of rats were made hypertensive by means of a surgical compression of the renal capsule which produced systemic hypertension. The purpose of this investigation was to determine whether growth hormone was an important element in the cardiac hypertrophy induced by systemic hypertension. Growth hormone in cardiac hypertrophy induced by nephrogenous hypertension. 13161675: [Nephrogenous arterial hypertension caused by ganglionic compression]. 1331961: Several authors have reported on the association between arterial hypertension and nephroblastoma as being the result of hyperreninism due to hilar compression; however severe hypertension was uncommon. Within 48 h, cardiac failure secondary to systemic arterial hypertension occurred, requiring intensive care. 14368713: Hypertension due to renal compression resulting from subcapsular hematoma. 14384822: Hypertension due to renal compression resulting from subcapsular hematoma. 15912650: INTRODUCTION: [corrected] Left renal vein compression, causing retrograde hypertension, determines a syndrome characterized by the presence of hematuria, gonadal vein dilatation and varicocele. 16835981: RESULTS: Standard external cardiac massage of the cadavers generated BPs of 55 +/- 20/13 +/- 7 mmHg; however, external compression on the back of the cadavers generated higher BP of 79 +/- 20/17 +/- 10 mmHg (p = 0.028, Wilcoxon signed-rank analysis). 16924459: Hypertension caused by arterial compression of the rostral ventrolateral medulla is well described. 171793: The studies reported herein demonstrate that unilateral compression also fails to cause hypertension in the presence of a normal contralateral gland. 17572218: Hyper-reninemic hypertension as a result of renal compression is often referred to as a \Page\ kidney. 17715081: We propose this technique, which directly targets inhibition of overactivity of the diaphragmatic crus, for treatment of hypertension caused by diaphragmatic compression of the renal artery as an alternative to surgery and renal artery stenting. OBJECTIVE: Our objective was to describe the technique and outcome of CT-guided injection of botulinum toxin into the diaphragmatic crus in a patient with hypertension caused by left diaphragmatic crus compression of the left renal artery. 18099950: Plasma electrolytes in hypertension produced by renal compression. 18386812: The development of renal failure and hypertension due to extrinsic renal compression by hematoma in the subcapsular space is well-described and most commonly seen after blunt trauma. 18444936: The acute Page kidney phenomenon occurs as a consequence of external compression of the renal parenchyma leading to renal ischemia and hypertension. 20476671: IAH provokes the raising of the diaphragm, and vascular and visceral compressions which induce hypertension in the various spaces with compartmental characteristics. 20694451: Page kidney refers to a clinical picture characterized by acute onset of hypertension due to external compression of the kidneys from hematoma, tumor, lymphocele, or urinoma. 21516709: [Unstable hypertension due to renal artery compression by the developed diaphragm in a 17-year-old athlete: a case report]. 22540399: OBJECT: Pulsatile arterial compression (AC) of the ventrolateral medulla (VLM) is hypothesized to produce the hypertension in a subset of patients with essential hypertension. Further studies in which a concentric bipolar electrode is used to generate this type of vasomotor map should also increase understanding of the pathophysiological mechanisms of neurogenically mediated hypertension, and assist in the design of studies to prove the hypothesis that it is caused by pulsatile AC of the VLM. 22819752: Malformation of the inferior vena cava (IVC), although rare and frequently asymptomatic, may also result in left renal vein hypertension, with resultant hematuria when it is severely compressed. Left renal vein hypertension secondary to left renal vein compression has been described as a cause of persistent hematuria in nutcracker syndrome. 23985460: CONCLUSION: Page kidney is a cause of arterial hypertension due to external compression of renal parenchyma. 25032140: INTRODUCTION: The Page kidney is a rare phenomenon that refers to hypertension resulting from any external compression of a kidney by a hematoma, tumor, lymphocele, or urinoma. 26595895: When carrying out an excision of cerebellar hemangioblastomas in patients with intracranial hypertension complicated by abnormal hypertension due to pheochromocytoma whose blood pressure is not sufficiently controlled, tumor resection of the pheochromocytoma prior to cerebellar hemangioblastoma excision in the same surgery may prevent increased ICP and reduce perioperative risk. We were not able to perform an craniotomy because abdominal compression in the prone or sitting position resulted in severe hypertension. INTRODUCTION: This report describes a patient with Von Hippel-Lindau (VHL) syndrome and uncontrolled hypertension due to pheochromocytoma who underwent craniotomy for the excision of a cerebellar hemangioblastoma combined with a laparoscopic adrenalectomy. Craniotomy for cerebellar hemangioblastoma excision in a patient with von Hippel-Lindau disease complicated by uncontrolled hypertension due to pheochromocytoma. 27000252: We suggested that symptom severity in symptomatic patients with non-hydrocephalic PCs relates to venous compression causing central venous hypertension. 27790304: Page kidney refers to the occurrence of hypertension secondary to renal compression and is usually associated with a subcapsular or perinephric hematoma. 28246490: The complications are: bleeding, local pressure effects; infection; rupture (including post-traumatic); arterial hypertension due to renal vessels compression. 29854553: Page kidney, a rare phenomenon whereby external compression of renal parenchyma can induce hypertension, can be caused by subcapsular hematoma following renal transplant biopsy. 30271469: Hypertension in the clinical setting of posterior fossa tumors is a known entity and occurs due to medullary compression by the tumor. 3808850: [Arterial hypertension caused by extrinsic compression of the renal artery of tumor origin in a child]. 9200080: He had a dense fibrous pseudocapsule causing renal parenchymal compression, which lead to hypertension, a Page kidney. 12055772: The hypertension resulted from a complex malformation of the right renal artery and dysplasic stenosis of the left inferior polar artery treated successfully by simple angioplasty. 13595946: [Hypertension due to malformation of the renal artery]. 13815080: A case of serious arterial hypertension due to ureteral malformation and ascending pyelonephrytis associated with congenital alacrimia. 14358085: [Arterial hypertension caused by malformation of one kidney in a child; surgery]. 14452520: [Juvenile arterial hypertension caused by multiple aneurysmal malformations of the branches of the abdominal aorta]. 14749499: It may arise secondary to an insult, such as infarct or chronic hypertension, or may occur as a consequence of a genetic defect, such as in hypertrophic cardiomyopathy. 16028778: In cases of Chiari malformation and concomitant neurogenic arterial hypertension, careful preoperative clinical and neuroimaging assessments may reveal the cause of the arterial hypertension. 18078063: Genetic defects resulting in deficit of natriuretic peptides or their functionally active receptors in transgenic mice cause development of arterial hypertension, myocardial hypertrophy and increased mortality in early age. 18320238: However, secondary causes of hypertension such as renal parenchymal diseases, congenital abnormalities and renovascular disorders still remain the leading cause of pediatric hypertension, particularly in children under 12 years old. 2135192: The child has mid-face hypoplasia and it appeared that his posterior fossa hypertension was partially caused by anterior compression of the brain stem as a result of the malformation at the base of the skull. 22819752: Malformation of the inferior vena cava (IVC), although rare and frequently asymptomatic, may also result in left renal vein hypertension, with resultant hematuria when it is severely compressed. Left renal vein hypertension secondary to left renal vein compression has been described as a cause of persistent hematuria in nutcracker syndrome. 235123: [Persistent systemic arterial hypertension caused by congenital malformations of kidneys in children (author's transl)]. 28355742: Lumbosacral nerve bowstring disease was defined as axial hypertension of nerve root and spinal cord caused by congenital anomalies, which could be accompanied by other lesions as lumbar disc herniation, spinal cord stenosis or spondylolisthesis, or aggravated by iatrogenic lesions, resulting in neurological symptoms. 35840428: After the study, he was diagnosed with arterial hypertension secondary to malformation of the renal artery. 3793203: The possible role of catecholamines in the abnormal renal response to salt loading, a genetic defect resulting in hypertension in the salt-sensitive strain of Dahl rats, was investigated by measuring the adrenal synthesis of norepinephrine, epinephrine, and dopamine as well as their content in several tissues and the urinary excretion of these catecholamines as well as some of their metabolites at the height of salt-induced hypertension. 7943210: The rise of blood pressure in SHR is genetically based, but it is not clear that the genetic defects responsible for hypertension also produce the observed deficits in skeletal muscle function. 8009189: When symptomatic they can as other renal AV shunts and malformations cause hypertension, congestive heart failure and hematuria. 10052740: Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy. 10209558: OBJECTIVE: Primary aldosteronism (PA) is the most common endocrine cause of curable hypertension, but no single test unequivocally identifies it. 10378827: Coronary artery aneurysms, aortic dissection, and hypertension secondary to primary aldosteronism: a rare triad. Primary aldosteronism is a relatively uncommon etiology of hypertension. 10423672: Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. 10715768: It is likely that widespread use of this class of drugs contributes to under-diagnosis of Conn's syndrome as a curable cause of hypertension. 10739546: Pregnancy may conceal the clinical symptoms of primary aldosteronism that causes unexpected severe hypertension in the postpartum period. 10768828: Our group consisted of 9 patients with arterial hypertension caused by primary hyperaldosteronism. 10798779: BACKGROUND: Primary hyperaldosteronism is an uncommon cause of hypertension in the general population. 10994747: Primary aldosteronism (PAL) has been traditionally regarded as a rare cause of hypertension and not worth looking for in the absence of hypokalemia. 10999820: In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. 1101838: Apparently, the antihypertensive effect of spironolactone is not solely on patients with hypertension due to primary aldosteronism. 11287520: Primary hyperaldosteronism is a potential cause of hypertension. 12003705: Recent reports suggest that primary aldosteronism may be the most common secondary cause of hypertension. 12195418: Pheochromocytoma and primary hyperaldosteronism are well-known causes of hypertension. 12381542: Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. 12389555: Primary hyperaldosteronism as a cause of hypertension. 12442092: Pheochromocytoma, hypercorticism, primary aldosteronism or glucocorticoid-remediable aldosteronism can be present or diagnosed at any term and may cause severe hypertension. Hypertension may be pregnancy-induced, essential or secondary to endocrine disorders. 12463132: Primary hyperaldosteronism represents less tha 1% of all causes of hypertension. 12613148: Primary aldosteronism (PA) has been regarded for a long time as being a rare cause of arterial hypertension, but its prevalence has recently been reassessed as about 10%. 12798753: CONCLUSIONS: Primary hyperaldosteronism is a rare but important cause of hypertension. 14503982: Hyperaldosteronism represents one of the few treatable causes of hypertension and a systematic approach is therefore needed to ensure that the few patients with an aldosterone-secreting adrenal adenoma are identified. Primary hyperaldosteronism is an important cause of hypertension. 14655595: A 49-year-old female with a long history of untreated hypertension secondary to PA was admitted to our hospital for medical examinations on July 18th, 2000. 14761862: Primary aldosteronism causes severe hypertension in humans (Conn's syndrome) with cardiac hypertrophy, characterized by a fibrosis more severe than the one observed in patients with essential hypertension. 15171428: [Hypertension secondary to primary aldosteronism]. 15278465: Primary aldosteronism is one of the few causes of hypertension which is subject to total surgical treatment, but a hypertensive crisis can occur during the resection of the adrenal tumor. 15808808: Evidence is now compelling that inappropriate aldosterone for salt status can cause not only hypertension, but vascular inflammation and end-organ damage, preventable by mineralocorticoid receptor blockade. Primary aldosteronism was considered rare, but recent work beginning in 1992 suggests that it might be the most common curable cause of hypertension, worth screening for in every hypertensive. 15943104: Primary aldosteronism is a rare cause of hypertension. [Hypertension due to primary aldosteronism]. 16041202: Primary aldosteronism (PA) was initially thought to be a rare cause of hypertension. 16208147: CONCLUSIONS: Primary hyperaldosteronism is a frequently neglected cause of residual hypertension despite technically successful endovascular treatment of renal artery disease. 16256009: As such, PA has become the most common secondary cause of hypertension. 16291704: OBJECTIVE: The aim of our study was to assess the prevalence and the characteristics of the metabolic syndrome in a group of patients with hypertension due to primary aldosteronism compared with patients with essential hypertension. 16296225: Although primary aldosteronism is not a common cause of hypertension it is reasonable to screen for this disorder because complete cure can be provided in a large percentage of patients. 16669823: Primary hyperaldosteronism is a potentially curable cause of hypertension and should be considered in hypertensive patients who present with diuretic - induced hypokalaemia. 16685214: BACKGROUND: Primary aldosteronism is a cause of hypertension in up to 10% of hypertensive patients, but the mechanisms by which excess aldosterone raises arterial pressure remain unclear. 16858077: BACKGROUND: Measurements of aldosterone have become more common since the recognition that primary aldosteronism is a more frequent cause of hypertension than previously believed. 16980201: Surgically correctable hypertension caused by primary aldosteronism. 17179189: Aldosterone antagonists are the mainstay of therapy in patients with hypertension due to primary aldosteronism. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in hypertension due to primary aldosteronism: a case for exclusion. 17460380: Primary aldosteronism (PA) has been considered a rare cause of hypertension. 17490489: Among various factors, primary aldosteronism is an important cause of resistant hypertension and is now more commonly recognised. 17508690: In 3 patients, men aged 60, 55 and 60, respectively, with hypertension due to primary hyperaldosteronism, the aldosterone level in the adrenal veins was determined for the purpose of further diagnosis. 17685956: BACKGROUND: Primary hyperaldosteronism is a frequent cause of resistant hypertension and is amenable to surgical intervention when caused by a unilateral aldosterone-producing adenoma. The aim of this study was to investigate the long-term results of laparoscopic adrenalectomy in the control of hypertension caused by primary hyperaldosteronism. 17885557: OBJECTIVE: Primary aldosteronism (PA) is the most common secondary cause of hypertension and recently has been implicated as a cause of impaired glucose tolerance. 18072409: Primary hyperaldosteronism (PH), resulting in hypokalaemic hypertension, may be due to an aldosterone-producing adenoma (APA) or bilateral zona glomerulosa hyperplasia. 18476460: This choice is based on two facts; primary aldosteronism is believed to be the most common and the most commonly detected cause of symptomatic hypertension and pheochromocytoma is thought to have rapid progress and stormy clinical course. 18949169: Primary aldosteronism (PA) is a known cause of hypertension. 19022636: Primary aldosteronism is a rare but curable cause of hypertension in children. 19099278: The primary hyperaldosteronism (PHA) is the most prevalent form (8-10%) of secondary causes of hypertension among hypertensive subjects. 19135616: Contrary to the historical belief, recent studies indicate that primary aldosteronism is a common cause of hypertension with a prevalence of 5-10% among general hypertensive patients. 1932505: [Arterial hypertension secondary to primary hyperaldosteronism caused by an adrenal adenoma]. 19462261: We report an interesting morphological alteration in the adrenal of a 72-year-old woman suffering from severe hypertension due to primary hyperaldosteronism. 19565821: This literature review concerns diagnosis and differential diagnosis of primary hyperaldosteronism, a frequent cause of arterial hypertension. 19605974: UNLABELLED: Primary aldosteronism (PA) is the most common secondary cause of hypertension that has recently been implicated in alterations of the immune system and progression of cardiovascular disease. 19697002: Primary hyperaldosteronism is the most common curable cause of hypertension with a prevalence of up to 12% among patients with hypertension. 20104005: Primary aldosteronism causes hypertension, hypopotassiumemia, hyporeninemia, and hyperaldosteronemia via excessive secretion of aldosterone in the adrenal glands. 20392751: BACKGROUND: Primary aldosteronism (PA), the most common secondary cause of hypertension, can be screened for using the aldosterone/renin ratio. 20447545: BACKGROUND: The discussion on the relationship between aldosterone concentration and blood pressure has recently gone beyond the role of primary aldosteronism in the genesis of arterial hypertension. 20540920: Primary hyperaldosteronism has historically been underdiagnosed as a cause of hypertension, but recent reports highlight its ubiquitous nature with a prevalence of 5%-10% in screened hypertensive patients. 20665130: Primary aldosteronism (PA) is a common cause of arterial hypertension: in the PA Prevalence in Hypertensives (PAPY) Study, the prevalence of PA was 11.2% in consecutive referred hypertensive patients. 209543: Primary hyperaldosteronism usually causes moderate hypertension. 21286821: Primary aldosteronism is unquestionably the most common secondary cause of hypertension, and effective approaches to diagnosis and targeted treatments exist. 21423678: Drug-induced hypertension, obstructive sleep apnoea, primary aldosteronism, and chronic kidney disease represent the most common secondary causes of resistant hypertension. 21826023: Here we discuss recent evidence supporting a significant involvement of the immune system, especially adaptive immunity, in the genesis of hypertension and organ damage induced by primary aldosteronism. 21993610: Primary aldosteronism is one of several potentially reversible causes of resistant hypertension. 22665682: CONCLUSIONS: Primary hyperaldosteronism, which is potentially a surgically curable cause of hypertension, appeared to be underdiagnosed in our locality. 23153688: Hypertension caused by primary hyperaldosteronism: increased heart damage and cardiovascular risk. 23200178: Primary aldosteronism (PA), an underdiagnosed cause of hypertension, is associated with more significant cardiac remodeling and myocardial fibrosis than is essential hypertension (EH). 23402683: The growing realisation since the early 1990s that primary aldosteronism (PA) is a much more common cause of hypertension than previously thought, and that aldosterone excess has adverse effects that are at least partly independent of blood pressure, has been the main driving force for a renaissance in clinical and research interest in PA. 23471976: CONTEXT: Primary aldosteronism (PA) is an established cause of hypertension, whereas high-normal serum aldosterone levels have been linked to an increased risk for hypertension. 23648698: Primary aldosteronism (PA), a common cause of high blood pressure (BP), induces left ventricular (LV) hypertrophy and an excess rate of cardiovascular events. 23953804: The identification of primary aldosteronism as a common cause of resistant hypertension is a significant advance in our ability to care for patients with hypertension. 24104388: Contrary to what was believed before, PA may be the cause of resistant hypertension rather than mild hypertension, while 70% of the patients have normal serum potassium levels rather than hypokalemia (previously believed to be a classical PA symptom). 24285684: CONTEXT: The molecular mechanisms of primary aldosteronism, a common cause of human hypertension, are unknown, but alterations of K(+) channels can play a key role. 24459237: OBJECTIVE: As it is now known that primary aldosteronism (PA) is more prevalent than was previously recognized, and is a potentially curable cause of hypertension and related cardiovascular diseases, the search for a safe and effective means of its diagnosis has reemerged as a topic of interest. 2449394: Primary aldosteronism is an uncommon cause of hypertension but one of particular interest because of its distinctive pathophysiological mechanism of blood pressure elevation. 24682757: We report a case of a 76-year-old woman presenting with recently diagnosed hypertension secondary to primary hyperaldosteronism. 24857581: Primary hyperaldosteronism is an important and commonly unrecognized secondary cause of hypertension. 24944753: Primary hyperaldosteronism (PA) is the most common cause of reversible hypertension, affecting 5%-18% of adults with hypertension. 25365316: Primary aldosteronism (PA) is a condition well worth detecting because it is a common cause of hypertension and is associated with excessive morbidity for the degree of hypertension and reduced quality of life, all of which can be abrogated with specific surgical or medical treatment. 2552113: Our report underlines the importance of a detailed family history in the assessment of hypertension due to primary aldosteronism. 25546991: [Difficulty in diagnosis of primary hyperaldosteronism as the cause of resistant hypertension and severe hypokalemia--case report]. Renovascular hypertension, Cushing syndrome and pheochromocytoma were excluded as potential causes of drug-resistant hypertension in the presented case. 25555247: Primary aldosteronism (PA) is the most common endocrine cause of high blood pressure. 25720606: Primary hyperaldosteronism (PHA) is the most frequent endocrinological, secondary cause of hypertension, rarely diagnosed in pregnant women. 25871964: PURPOSE OF REVIEW: Primary aldosteronism is increasingly recognized as a common secondary cause of hypertension. 25907736: We performed exome sequencing of 40 unrelated subjects with hypertension due to primary aldosteronism by age 10. 25908467: Primary aldosteronism is one of the commonly identified causes of hypertension and is treatable and/or potentially curable. 25944465: OBJECTIVE: Previous studies have investigated the genetic and molecular basis of primary aldosteronism (PA), a common cause of human hypertension, but the effects of microRNAs (miRNAs) on the adrenocortical cell proliferation and aldosterone production are largely obscure. 26193964: BACKGROUND: Primary hyperaldosteronism is a common cause of hypertension, with significant cardiovascular, renal, and metabolic sequelae. 26305168: Approximately 10% of cases of hypertension in Japan are caused by primary aldosteronism (PA), amounting to about 4 million patients in total. 26413481: Primary hyperaldosteronism, the most common of the endocrine cause of hypertension often presents with resistant or difficult to control hypertension associated with either normo-or hypokalemia. 26574803: Primary aldosteronism is the cause of hypertension in 5-10% of the hypertensive population. 26914776: This article describes a patient with hypokalemia, hypertension, and periodic paralysis that were caused by primary hyperaldosteronism. 26971505: Primary aldosteronism (PA) is the most common secondary cause of hypertension, accounting for 10 % of hypertensives and 20 % of those with drug-resistant hypertension. 27035656: Adrenal aldosterone-producing adenomas (APAs) are a main cause for primary aldosteronism leading to arterial hypertension. 27087531: It should be borne in mind that PA can induce hypertension without hypokalemia or, less frequently, hypokalemia without hypertension. 27119751: PURPOSE OF REVIEW: Primary aldosteronism is a major cause of hypertension; aldosterone-producing adenomas (APA) cause about half of primary aldosteronism; idiopathic hyperplasia of adrenal glomerulosa cells are responsible for the rest. 27566330: Primary aldosteronism with a prevalence of 8 % of hypertension and 20 % of pharmacologically resistant hypertension is the most common secondary cause of hypertension. 27648962: CASE DESCRIPTION: We describe the case of a young patient who was diagnosed with severe arterial hypertension due to primary aldosteronism at age 26 years, followed by hemorrhagic stroke 4 years later. 27733767: Primary aldosteronism (PA) is the most common secondary cause of hypertension. 27872236: Primary hyperaldosteronism is a common cause of resistant hypertension. 28228887: Primary hyperaldosteronism often results in resistant hypertension and hypokalemia, which may lead to cardiovascular and cerebrovascular complications. 28416583: Primary aldosteronism is a common cause of hypertension, which becomes refractory if undiagnosed, but potentially curable when caused by an aldosterone-producing adenoma (APA). 28494487: Primary hyperaldosteronism is a common cause of hypertension in the adult population. 28576687: BACKGROUND: Although unilateral primary aldosteronism is the most common surgically correctable cause of hypertension, no standard criteria exist to classify surgical outcomes. 28894201: Adrenocortical hormone excess, due to primary aldosteronism (PA) or hypercortisolemia, causes hypertension and cardiovascular complications. 28992276: As PA represents one of the most common, potentially reversible causes of hypertension, and is associated with significant cardiovascular complications over the long term, it is clear that a pragmatic strategy for targeted case detection in primary care is needed. 29238435: Background: Diabetes mellitus (DM) and primary aldosteronism (PA) have been reported to induce drug-resistant hypertension and atherosclerosis. 29249599: BACKGROUND: Primary aldosteronism causes hypertension and hypokalemia and is often surgically treatable. 29264474: Primary aldosteronism is an important and common cause of hypertension that carries a high burden of morbidity. 29388434: Objective Primary aldosteronism is a curable cause of hypertension which can be treated surgically or medically depending on the findings of adrenal vein sampling studies. 30082690: Primary aldosteronism (PA) is the most common endocrine cause of resistant hypertension. 3034452: Erythrocyte membrane Na+,K+-ATPase activity was measured using a bioluminescence technique in 28 hypertensive patients (24 with essential hypertension, 2 with renovascular hypertension and 2 with hypertension secondary to primary hyperaldosteronism) and in 28 normotensive control subjects matched for age and sex. 30415872: BACKGROUND: Primary aldosteronism is a common but underdiagnosed cause of hypertension. 30430513: Resistant hypertension secondary to coexisting primary hyperaldosteronism and renal artery stenosis. 30707244: Primary aldosteronism (PA) is a frequent cause of resistant hypertension. 31187936: Patients with primary aldosteronism induced hypertension are more likely to experience cardiovascular events compared to patients with essential hypertension. 31195777: BACKGROUND: Primary aldosteronism is the most common specifically treatable and potentially curable cause of hypertension. 31255203: Primary hyperaldosteronism is an important and increasingly prevalent cause of hypertension that is characterized by unregulated aldosterone excess. 31348309: Although unilateral primary aldosteronism (PA) is the most common surgically correctable cause of hypertension, the cure rate varies widely. 31352525: RECENT FINDINGS: Previously considered a rare disease, recent prevalence studies demonstrate that PA is actually a very common, yet vastly under-diagnosed, etiology of hypertension. PA is a common cause of hypertension that leads to disproportionately high rates of cardiovascular disease. 31462725: Primary aldosteronism (PA) is a common curable cause of hypertension. 31482378: RECENT FINDING: PA is the most common endocrine cause of arterial hypertension and unilateral forms of the disease are potentially curable by surgical resection of the overactive adrenal. 31779795: Primary aldosteronism (PA) is a common, but frequently overlooked, cause of arterial hypertension and excess cardiovascular events, particularly atrial fibrillation. 31911970: Hypertension was caused by primary hyperaldosteronism due to an adenoma of the adrenal gland. Hyperaldosteronism causes arterial hypertension and might predispose to stroke, atrial fibrillation, and heart failure. 31998486: Primary aldosteronism (PA) is a potentially reversible cause of uncontrolled hypertension. 32206596: Primary hyperaldosteronism (PA) is one of the most common causes of hypertension that is amenable to surgical cure. 32341439: Primary aldosteronism is a public health issue: challenges and opportunities.A significant proportion of hypertension (potentially more than 5% in the general population) is due to primary aldosteronism (PA) which carries a worse prognosis when compared with blood pressure-matched essential hypertension. Most importantly, a dramatic increase in awareness of PA, as a treatable cause of hypertension, is needed amongst clinicians who manage hypertension. 32449886: The Unrecognized Prevalence of Primary Aldosteronism.BACKGROUND: Primary aldosteronism is a nonsuppressible renin-independent aldosterone production that causes hypertension and cardiovascular disease. 32882712: Primary hyperaldosteronism (PA) is a well-known cause of hypertension although its exact prevalence amongst patients with apparent essential hypertension has been a matter of debate. 33270939: OBJECTIVE: Primary aldosteronism (PA) is a potentially curable cause of hypertension associated with worse cardiovascular prognosis than blood pressure-matched essential hypertension (EH). Routine biochemical screening for PA remained the most reliable way of detecting this treatable secondary cause of hypertension. 33280409: Primary aldosteronism is an underdiagnosed cause of hypertension. 33447758: CONCLUSIONS: After this process, substantial updated information was generated, which could simplify the diagnosis of primary aldosteronism and assist practicing physicians in optimizing treatment and follow-up of patients with one of the most common curable causes of arterial hypertension. 33641355: A similar shift in NaCl taste perception could be detrimental in humans when aldosterone excess in primary aldosteronism (PA) causes hypertension and favors high sodium consumption. 33837588: OBJECTIVE: Primary aldosteronism (PA) is an underdiagnosed cause of hypertension. 34137684: Plasmatic concentration of renin decreases in patients with hypertension due to a primary hyperaldosteronism, contrary to renovascular hypertension where concentrations of renin and aldosterone are both elevated. 34282597: Primary aldosteronism (PA) is the most common endocrine cause of arterial hypertension. In conclusion, DCVT revealed that PA is a highly prevalent cause of hypertension. 34384396: BACKGROUND: Various adrenal disorders including primary aldosteronism and Cushing's syndrome lead to the cause of hypertension. 34488439: Primary aldosteronism (PA) is the cause of arterial hypertension in 4% to 6% of patients, and 30% of patients with PA are affected by unilateral and surgically curable forms. 3450533: Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. 34657442: Primary aldosteronism is a common, yet highly underdiagnosed, cause of hypertension that leads to disproportionately high rates of cardiovascular disease. 35000250: CONTEXT: Primary aldosteronism (PA) is the most common endocrine cause of hypertension. 35904911: Unilateral primary aldosteronism (PA) is the most common surgically correctable cause of hypertension. 36012306: Hypertension due to primary aldosteronism poses a risk of severe cardiovascular complications compared to essential hypertension. 36027139: OBJECTIVE: Primary aldosteronism (PA) leads to hypertension, left ventricular hypertrophy and systolic dysfunction. 36027390: OBJECTIVE: Primary aldosteronism is a common, yet underdiagnosed, cause of hypertension and resistant hypertension. 36045149: Primary aldosteronism is a common cause of hypertension and is a risk factor for cardiovascular and renal morbidity and mortality, via mechanisms mediated by both hypertension and direct insults to target organs. 36246876: Both primary aldosteronism and obstructive sleep apnea are well-known causes of hypertension and contribute to increased cardiovascular morbidity and mortality independently. 36286925: The review discusses the current state of the problem of screening patients for early detection of primary hyperaldosteronism (PHA) as a potential cause of arterial hypertension (AH). 36375972: OBJECTIVES: Primary aldosteronism (PA), the most common endocrine cause of hypertension, is associated with a higher risk of cardiovascular disease (CVD) than blood pressure (BP)-matched essential hypertension (EH). 36646800: Primary aldosteronism (PA) due to a unilateral aldosterone-producing adenoma is a common cause of hypertension. 36945842: BACKGROUND: Primary aldosteronism (PA) is a frequent cause of hypertension. 36965825: Primary aldosteronism suffers from both of these factors and thus, is woefully underdiagnosed as a cause of hypertension and end-organ damage. 37043870: BACKGROUND: To analyze contrast free adrenal vein sampling (AVS) for differentiating unilateral from bilateral disease in patients diagnosed with hypertension due to primary aldosteronism (PA). 37051402: Primary aldosteronism (PA) is a curable cause of hypertension. 37152926: Background: Idiopathic hyperaldosteronism (IHA) is one of the most common types of primary aldosteronism (PA), an important cause of hypertension. 37305032: Aims: Primary hyperaldosteronism (PA) is a common cause of hypertension. 37477017: SUMMARY BACKGROUND DATA: Primary aldosteronism (PA) is the underlying cause of hypertension in 6-18% patients. 37486000: Primary Aldosteronism, or Conn Syndrome, is the most common endocrine cause of hypertension. 37490105: Primary hyperaldosteronism (PA) is a relatively frequent, albeit underdiagnosed, cause of hypertension, and has a specific therapy. 37531636: CONTEXT: Primary aldosteronism (PA) is the most common endocrine cause of hypertension. 37531880: Both patients had hypertension caused by PA and obesity. 37536806: Primary aldosteronism is a prevalent but underdiagnosed cause of hypertension, contributing to increased cardiovascular and cerebrovascular events and end-organ damage independent of blood pressure. 37612380: Primary aldosteronism is the most common single cause of hypertension and is potentially curable when only one adrenal gland is the culprit. 3777074: A case is reported of a primigravid woman presenting in midgestation with severe hypertension caused by primary hyperaldosteronism. 37818947: Primary aldosteronism (PA), characterized by inappropriately high concentrations of the adrenal derived hormone aldosterone, is the most common endocrine cause of arterial hypertension. 38048424: OBJECTIVE: Primary aldosteronism (PA) is the most common surgically curable cause of hypertension. 38095087: BACKGROUND: Primary aldosteronism (PA) is a common but underdiagnosed cause of hypertension. 38134306: INTRODUCTION: Primary Aldosteronism (PA) is a common cause of hypertension. 38313982: Moyamoya Disease Causing Stroke in the Setting of Cocaine Use and Uncontrolled Hypertension Due to Primary Hyperaldosteronism. 38568364: PURPOSE: Primary aldosteronism (PA), a frequent cause of hypertension, is highly associated with cardiovascular risk and mortality. 3884876: Both methods revealed analogous ratios of the two renin forms in its total production in the presence of essential hypertension (in different \renin\ subgroups) and arterial hypertension secondary to PA and may be used as the methods of choice when examining essential hypertension patients with the normal and subnormal plasma renin activity. 474585: Identification and differentiation of surgically correctable hypertension due to primary aldosteronism. 4843255: Salt taste in patients with essential hypertension and with hypertension due to primary hyperaldosteronism. 6462970: Primary aldosteronism is a potentially curable cause of hypertension; it occurs in about 1% of hypertensive patients. 6598066: Surgical management of primary aldosteronism (Conn's syndrome), a correctable cause of hypertension. 7016700: Attention should be paid for the existence of PA as a frequent cause of juvenile hypertension in female, since female were frequently than in male (11 cases of female to 1 case of male) and 10 of 12 patients with PA were pointed out to have high blood pressure at the age of under 40. 7030246: Screening for surgically correctable hypertension caused by primary aldosteronism. 7792813: Primary aldosteronism is the commonest cause of potentially curable hypertension when diagnosed in both florid and less florid forms. 785608: Five patients with low-renin essential hypertension and two with hypertension due to primary aldosteronism, all of whom have normalized their blood pressure on chronic spironolactone therapy, were cotreated in a double-blind fashion with either aspirin or aspirin-placebo during alternate six-week periods. 8582113: In a 19 month period from June 1993 to December 1994, 60 patients (mean age 54.8 +/- 1.5 years s.e.m.; 32 males, 28 females) underwent unilateral laparoscopic adrenalectomy by one of us (JCR) for the treatment of hypertension due to primary aldosteronism (n = 48), phaeochromocytoma (n = 3) and cortisol-producing adenoma (n = 1) or to remove adrenal massess incidentally discovered on abdominal computerized tomography scanning ('incidentaloma') performed for other reasons (seven adenomas without biochemical evidence of excessive steroid hormone or catecholamine secretion and one carcinoma autonomously producing cortisol). Laparoscopic adrenalectomy for adrenal tumours causing hypertension and for 'incidentalomas' of the adrenal on computerized tomography scanning. 8621194: We investigated the effects on the heart of hypertension due to the excess of aldosterone and suppression of the renin-angiotensin system caused by primary aldosteronism with M-mode echocardiography and transmitral Doppler flow velocity measurements. 8634926: BACKGROUND: Primary aldosteronism (PA) is a rare but potentially curable cause of hypertension. 8668294: Although primary hyperaldosteronism is an uncommon cause of hypertension, it is the most common form of renin-independent hypermineralocorticoidism. 8965160: Primary aldosteronism is a potentially curable cause of hypertension, especially when caused by an adrenal adenoma. 938876: Primary hyperaldosteronism is a potentially curable cause of hypertension, and much interest has been shown in methods of diagnosing the associated hypokalaemic hypertension and localising the adrenal adenoma. 9522976: Primary aldosteronism, though an uncommon cause of hypertension, causes significant morbidity, making it important to diagnose and treat this condition. 9538374: Primary hyperaldosteronism (PHA) represents less than 1 to 2% of all causes of hypertension (HT). 9775143: INTRODUCTION: Primary hyperaldosteronism is an uncommon cause of hypertension which classically features hypokaliemia, metabolic alkalosis and excessive urinary potassium excretion. 9782547: Primary aldosteronism is a rare cause of hypertension caused by increased aldosterone secretion. 1115181: In six of the animals, mild hypertension was induced by unilateral renal artery constriction at about the one hundred fifteenth day. 1149331: Plasma renin concentration in hypertension produced by unilateral renal artery constriction in the rat. It is concluded that factors other than the plasma concentration of renin are involved in the early stages of development of hypertension induced by renal artery constriction. 1158426: Peripheral vaso-constriction due to increase in central vasomomotor tone mainly responsible for hypertension whereas stimulation of central beta-receptors with sympathoadr renal discharge responsible for tachycardia. 1190320: The data support the concept that sodium retention causes hypertension almost entirely because of sodium-induced expansion of the extracellular fluid volume. The goal of these studies was to determine whether the hypertension caused by excessive salt loading results from sodium-induced expansion of the extracellular fluid volume or whether the salt increases the pressure in some other way, such as by causing vascular constriction. 1192616: Hypertension induced by renal artery partial constriction and removal of the other kidney is also associated with reduction of interstitial space compliance; a sudden rise in interstitial space compliance may be the primary factor in the course of events that leads to the rapid fall in blood pressure which occurs when the constriction is removed from the renal artery. 12193126: The coronary effects of endothelin-1 (ET-1) during acute hypertension were examined in anesthetized goats, where the left circumflex coronary artery flow was electromagnetically measured and hypertension was induced by constriction of the thoracic aorta. 1236607: It is not clear whether afferent constriction causes hypertension or results from it. 1260974: The similarity of regressions for plasma angiotensin II concentration and arterial blood pressure in the two experiments strongly suggests that the rise of circulating angiotensin II after renal artery constriction is sufficient to account for the hypertension by its direct pressor action. 13190622: Experimental hypertension produced by constriction of the carotid sinus area. 13345072: The relation of heart and adrenal weight to body size and hypertension produced by renal constriction and vitamin B6-deficiency. 13428918: Hypertension in rats produced by constriction of one renal artery was associated with degranulation of juxtaglomerular cells in the contralateral, undamped, kidney. 13473070: Pathogenesis of experimental hypertension produced by carotid sinus area constriction in dogs. 13513919: Hypertension induced by renal artery constriction also intensified the hypercholesterolemia and hyperlipemia. The induction of hypertension by desoxycorticosterone and salt accelerated the development of hypercholesterolemia, hyperlipemia, increase in tissue cholesterol content, and atherosclerotic changes in the intima. 1387507: Constriction of the abdominal aorta just below the diaphragm during periods of 20 days (prevention experiment) and 40 days (regression experiment) resulted in hypertension and cardiac hypertrophy. 14724343: Close to the efferent constriction, it induces intraglomerular hypertension and glomerulosclerosis. 147962: After 1 to 4 weeks of hypertension, induced by constriction of the left renal artery, endocardial myocytes were enlarged 21 per cent, from 10,370 +/- 410 to 12,520 +/- 490 cu. micrometer., while epicardial myocytes showed a 37 per cent hypertrophy, from 12,600 +/- 1,600 to 17,300 +/- 1,100 cu. micrometer. 147963: After 14 weeks of hypertension, induced by constriction of the left renal artery, left ventricular weight is increased by 30 per cent, wall thickness by 42 per cent. 15322325: Such constriction induced intraglomerular hypertension and exaggeratedly reduced peritubular capillary flow (PTCF). 15422098: The pathogenesis of hypertension induced by renal constriction. 15607496: Left circumflex coronary flow was electromagnetically measured, and hypertension was induced by constriction of the thoracic aorta in animals nontreated (7 goats) or treated with the inhibitor of NO synthesis Nw-nitro-L-arginine methyl esther (L-NAME, 6 goats) or the cyclooxygenase inhibitor meclofenamate (6 goats). 16263398: POPH, caused by vasoproliferation/constriction and obstruction of pulmonary arterial blood flow, is associated with higher risk for liver transplantation and increased post-transplantation mortality. 1648301: Diabetes was induced by a streptozotocin (65 mg/kg) injection and hypertension was induced by abdominal aortic constriction; studies were done at 1 and 6 weeks. 16694574: THE GUANIDINE BASES IN THE BLOOD OF DOGS WITH EXPERIMENTAL HYPERTENSION PRODUCED BY CONSTRICTION OF THE RENAL ARTERIES. 17446057: Both extracts decreased the hypertension of spontaneous hypertensive rats, the hypertension induced in rats by L-NAME treatment and that induced by constriction of one renal artery. 183887: Concerning the independence of the basis of hypertension due to ACTH or renovascular constriction. 1860704: At 20 weeks old, the nontreated group exhibited hypertension and a lower arteriolar diameter ratio (afferent to efferent, 0.89 versus 1.22 in control group) because of afferent constriction and efferent dilatation, seen equally in the outer and inner cortexes. 19870737: OBSERVATIONS ON THE PATHOLOGICAL CHANGES FOLLOWING EXPERIMENTAL HYPERTENSION PRODUCED BY CONSTRICTION OF THE RENAL ARTERY. 19870869: The most important factors which determined this elevation of blood pressure in the lower part of the body were probably increased flow of blood into the vascular bed below the clamp and peripheral vasoconstriction of renal and humoral origin, as in the case of the hypertension produced by constriction of the main renal arteries alone (2-86). These facts, are all indicative of the renal origin of the hypertension which results from the constriction of the aorta just above the origin of both main renal arteries. 20274127: Hypertension due to perirenal constriction; case report. 2427888: With experiments on the renal artery constriction in the conscious dog, we have shown that a kidney lesion can produce a form of hypertension not different, in the established phase, from the essential one and that the onset of this form follows a phasic pattern during which the initial stages are crucial for understanding the mechanisms leading to hypertension. 2750542: Hypertension was induced by constriction of the aorta proximal to the renal artery (PAC), by PAC and nephrectomy (PAC + Nx) or by renal artery stenosis (RAS). 28362400: MTAC is a much faster and less invasive way to induce left ventricular hypertension and enables the possibility for high-throughput studies. 29032314: Systemic HT was induced by the constriction of one of the renal arteries (Goldblatt HT), while BF in the CCA was reduced and increased by the constriction of the ipsilateral CCA and the ligation of the contralateral CCA, respectively. However, only in HT/lower BF group, WSS and vascular smooth muscle-activated vascular contraction were smaller than in the other groups, possibly because of wall hypertrophy induced by HT. 29170451: Taken together, these results indicate that CMS of VSMCs induces inflammation-related gene expression, including that of CXCL1 and CX3CL1, which may play important roles in the stress response against CMS caused by hypertension. The expression of Cxcl1 was also induced in VSMCs by hypertension produced by abdominal aortic constriction (AAC). 29628463: Expression of Cxcl1 was also induced in VSMCs by hypertension produced by abdominal aortic constriction in mouse. 2967505: The adrenergic innervation of blood vessel wall was studied in various vascular beds of adult rats with experimental hypertension induced by the constriction of the aorta between the origins of both renal arteries. 3063484: Renal damage in hypertension was thought to be a result of excessive renal arteriolar constriction leading to ischaemia and nephron damage. 31415848: In conclusion, STM could reverse the hypertension and left ventricular remolding caused by abdominal aortic constriction in rats. Tongsaimai reverses the hypertension and left ventricular remolding caused by abdominal aortic constriction in rats. 3164091: To study the role of sodium and renal prostaglandin E2 in the chronic phase of two-kidney one-clip renovascular hypertension, urinary excretion rates of sodium and prostaglandin E2 were measured in rabbits with hypertension induced by left renal artery constriction during alteration in sodium intake. 3534609: To investigate the role of renal prostaglandin E2 (PGE2) in renovascular hypertension, urinary PGE2 was measured in rabbits with hypertension produced by left renal artery constriction. 4463268: Constriction of one renal artery in the presence of the opposite kidney can produce persistent hypertension which is often associated with increase in plasma renin activity, decrease in serum potassium and increase in water intake. 5146234: [Case of hypertension suspected to be due to right renal artery constriction caused by so-called fibromuscular media hyperplasia]. 5630567: A persistent hypertension due to unilateral renal-artery constriction in the rabbit. 6200903: These results suggest that (1) decreases in circulating BK may potentiate the vasoconstrictor effect of angiotensin II and contribute to the hypertension induced by RAC, and (2) urinary kallikrein is an unreliable marker of changes in plasma bradykinin in this model of hypertension. 6670549: The hypertension was induced by constriction of the bilateral renal arteries. 6757203: Immunoreactive renin and angiotensin II in the afferent glomerular arterioles of rats with hypertension due to unilateral renal artery constriction. 7281373: To study the role of renal prostaglandins (PGs) in renovascular hypertension, PGE2 and PGF2 alpha concentrations in both inner and outer medullae of the kidney were measured by radioimmunoassay in rabbits with hypertension produced by left renal artery constriction. 7282952: Therefore, a more gradual pressure overload was produced in female Wistar rats by hypertension due to constriction of the left renal artery. 7418540: Cd pretreatment did not affect the incidence of hypertension produced by unilateral renal artery constriction but slightly decreased its severity. 7485443: Previous studies have shown that both systemic hypertension induced by abdominal aortic constriction (Abcon) and 50% caloric restriction (CR) increase left ventricular (LV) beta-myosin heavy chain (MHC) protein expression in the rat. 7826304: Experimental hypertension, produced by constriction of the abdominal aorta, induced hypertrophy of the left ventricle, with increased perimysium and endomysium of the ECM at the level of the papillary muscles 4 weeks after aortic banding. 8304490: When the rat was subjected to high blood pressure due to constriction of its aorta, the shear modulus does not vary significantly with the length of time the animal was subjected to hypertension. 862332: In the early phase of hypertension produced by renal artery constriction with the opposite kidney intact, infusion of the angiotensin antagonist Sar1-Ala8-angiotensin II or bilateral nephrectomy lowered blood pressure. 870227: The effect of high sodium intake and angiotensin antagonist in rabbits with severe and moderate hypertension induced by constriction of one renal artery. 908239: With modern specific diagnostic studies like isotope renography, angiotensin-infusion-test, peripheral venous renin assay, comparative assays of the renin activity in the individual renal veins, and angiography the renal and renovascular causes for hypertension become more and more significant. When it has been shown that the hypertension is caused by a constriction of the renal arteries, instant operative therapy is indicated. 9211176: DESIGN: Despite the controversy about the origin of essential hypertension and its accompanying vascular changes, it is generally assumed that the characteristic increase in peripheral resistance when hypertension progresses is caused by arteriolar constriction. 966388: Therefore, the initial arteriolar constriction, however slight, may progressively produce hypertension and augment medial hypertrophy by such a positive feedback mechanism. 971555: Role of the renin-angiotensin system in hypertension produced by unilateral renal artery constriction in the rat. 11330874: Angiotensin-converting enzyme and angiotensinogen gene polymorphisms are non-randomly distributed in oral contraceptive-induced hypertension. The genetic contribution to this susceptibility to OC-induced hypertension is poorly understood. CONCLUSION: This statistical interaction of genotype frequencies suggests that the genetic basis of susceptibility to OC-induced hypertension is complex. 1186221: Although the exact mechanisms of OC-induced hypertension are undetermined, it is suggested that subtle alterations in the renin-angiotensin system may contribute to the role. 11966403: Oral contraceptive-induced hypertension (OCIH) is a well-recognized phenomenon characterized by an increase in blood pressure levels after beginning estroprogestin therapy and a reduction to normal levels within 1 year after suspension of the therapy. 1263163: OCs can induce hypertension, though this condition is generally reversible after discontinuation of use. 17203115: CONCLUSION: This study provides evidence that the development of OC-induced hypertension is prevented by calcium channel blockade via improved renal handling of sodium and nitric oxide. This study therefore sought to investigate the effect of L-type calcium channel blocker, nifedipine on OC-induced hypertension. 186375: Some possible factors in the etiology of hypertension induced by oral contraceptives are discussed. 19090344: Oral contraceptive-induced high blood pressure is prevented by renin-angiotensin suppression in female rats but not by sympathetic nervous system blockade. This study sought to investigate the possible roles that renin-angiotensin system (RAS) and sympathetic nervous system (SNS) may play in the development of OC-induced hypertension. The study also suggests that the development of the OC-induced hypertension and cardiac hypertrophy is mediated by RAS, but not by SNS. The results of the present study demonstrate that OC-induced high blood pressure is associated with cardiac hypertrophy, enhanced pressor response to angiotensin II and preserved pressor response to sympathetic activation. 19126663: These data suggest that progesterone-induced increases in AP-P may contribute to the development of OCP-induced hypertension in susceptible Women. INTRODUCTION: The renin-angiotensin and kininogen-kinin hormonal systems are critically involved in regulating blood pressure and are candidates in contributing to oral contraceptive pill (OCP)-induced hypertension. 20036339: The aim of the present study was to investigate the influence of increasing dietary calcium from 0.9 to 3.0% on the development of OC-induced high blood pressure and associated changes in female Sprague-Dawley rats treated with a combination of OC steroids (1 microg ethinyl estradiol and 10 microg norgestrel; p.o.) daily for 10 weeks. 20632668: These results demonstrated that rat model of OC-induced high blood pressure developed cardiac hypertrophy that is not associated with altered sympathetic-mediated cardiovascular responses to arterial baroreceptor stimulation. 21565676: Oral contraceptives and postmenopausal hormone therapy may induce hypertension through multiple mechanisms, including sodium and volume retention. 22314948: Is hypercalcemic diet a possible antidote to oral contraceptive-induced hypertension? These results strongly suggest that high dietary Ca2+ supplementation increases salt and water excretion in OC-treated rats and potentially moderates fluid retention and blood pressure in these animals, and may be of clinical significance in OC-induced abnormal fluid retention and perhaps OC-induced hypertension. 30001502: Elevated circulating uric acid has been postulated to play an important pathophysiological role in estrogen-progestin combined oral contraceptive (COC)-induced hypertension and endothelial dysfunction. 3067841: Oral contraceptives (OCs) may induce high blood pressure in women 35 years old, smokers, and obese women. 33982185: PURPOSE OF REVIEW: Oral contraceptive pill-induced hypertension (OCPIH) and hypertensive disorders in pregnancy (HDP) share common risk factors and pathophysiological mechanisms, yet the bidirectional relationship between these two conditions is not well-established. 392140: [Hypertension caused by oral contraceptives]. 4319180: A possible mechanism for hypertension induced by oral contraceptives. 4324174: [Hypertension caused by oral contraceptives]. 4336457: Plasma renin concentration, activity and substrate in hypertension caused by oral contraceptives. 4559540: Irreversible renal failure secondary to hypertension induced by oral contraceptives. 5360311: Hypertension induced by oral contraceptives containing estrogen and gestagen. 6252632: The small number of hypertensions really induced by oral contraceptives is opposed with the great number of hypertension (essential or not) revealed by oral contraceptives. Careful investigation of these patients revealed that only in some had hypertension been caused by OC treatment, which goes against the commonly held opinion that arterial hypertension in OC patients is always caused by hormonal treatment. Three conditions have to be satisfied in order to incriminate with certainty the responsibility of oral contraceptives inducing hypertension : normal blood pressure before therapy (included pregnancies), normalization of blood pressure in a delay of three months at most after the discontinuation, no other etiology of hypertension. 631040: The described observations--taken together with those on the pathogenesis of hypertension caused by oral contraceptives--provide a pointer to the importance of clotting disorders in the initiation and development of some forms of hypertension. 6393087: Most studies on hypertension caused by OCs were performed with pills containing 50-100 mc of estrogens and 1-4 mg of gestagen. A literature review is presented to show that oral contraceptives (OCs) can cause arterial hypertension in women. Estrogens appear to dominate in the pathogenesis of hypertension caused by OCs. 7294873: In members with renal failure there was no improvement in renal function after treatment of hyperuricaemia, and in 2 sisters oral contraceptives appeared to precipitate hypertension. 793966: In the differential diagnosis of hypertension induced by oral contraceptives, primary aldosteronism and renal artery stenosis have to be excluded; these hypertensive disorders show similar biochemical changes, but should be treated by surgical intervention. A failure in the feedback mechanisms of the renin-angiotensin-aldosterone system is suggested to be an important factor in the etiology of hypertension induced by oral contraceptives. 8479492: OCs can cause hypertension in 4-5% of healthy women and worsen hypertension in about 9-16% of hypertensive women. 857317: In 4 female patients (0.5%) the hypertension was caused by oral contraceptives. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone-producing adenoma of the adrenal gland, and oral contraceptives). In 4 females (.5%) hypertension was caused by oral contraceptives. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone producing adenoma of the adrenal gland and oral contraceptives). 8759093: BACKGROUND: Oral contraceptives induce hypertension in approximately 5% of users of high-dose pills that contain at least 50 micrograms estrogen and 1 to 4 mg progestin, and small increases in blood pressure have been reported even among users of modern low-dose formulations. 8948319: Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. 9171950: However, responses to oestrogen may be dose-dependent and enhancement of vasoconstrictor responses to NA may be relevant to oral contraceptive-induced hypertension. 9280864: It is known that oral contraceptives may induce high blood pressure that usually returns to normal values a few weeks after interruption of the drugs, and without any specific treatment. The precise mechanism by which oral contraceptives cause hypertension is not clear. 9349449: Three of group 1 also had a history of OC-induced hypertension. 961741: Oral contraceptives--induced hypertension--nine years later. In in vitro testing, in which renin was added in a constant amount to the serum of patients with oral contraceptive-induced hypertension, the capacity to generate angiotensin 2 was found to increase linearly with increases in substrate levels. 979870: The question, if and when reversible hypertension due to oral contraceptives becomes persistent renal hypertension, can be answered only after long-term observations with careful documentation (renal biopsy and nephrologic functional diagnosis). Only close long term follow up including renal biopsy and subtile functional tests may provide information whether and/or when hypertension due to oral contraceptives turns to become--at least in part--renal hypertension and also becomes persistent. 11165670: Hypercontraction or abnormal contraction of vascular smooth muscle is a major cause of diseases such as hypertension and vasospasm of the coronary and cerebral arteries. 1153873: The maintenance of high blood pressure could be primarily due to contraction of the arterial wall. 23288166: CONCLUSIONS: We conclude that ER stress increases vascular smooth muscle contractility resulting in high blood pressure, and AMP-activated protein kinase activation mitigates high blood pressure through the suppression of ER stress in vivo. 24871365: Myofibroblastic HSC have taken center stage during liver fibrogenesis, due to their remarkable synthesis of extracellular matrix proteins, their secretion of profibrogenic mediators and their contribution to hypertension, due to elevated contractility. 29394331: Pathophysiological mechanisms contributing to the development of hypertension include increased vascular resistance, determined in large part by reduced vascular diameter due to increased vascular contraction and arterial remodelling. 30339816: Taken together, our data suggest that sibutramine facilitates apoptosis and contraction of aortic smooth muscle cells through elevating production of reactive oxygen species and decreasing exogenous NO supply, leading to pathogenesis of hypertension. 3284357: The resulting Ca2+ increase within arterial cells can be responsible for increased contractility and tone, leading to hypertension. 7297318: It is postulated that increased sodium intake causes hypertension by producing a humoral factor that inhibits sodium transport out of cells and that this alters the calcium content of muscle cells and increases their contractility and thus produces hypertension. 9489363: Narrowing of the retinal artery in hypertension has been considered as an indicator of peripheral vascular resistance, which is largely caused by contraction or narrowness of retinal arterioles. 975149: Rhythmic muscular contraction caused hypotension and vasodilatation; tetanic contraction caused hypertension and vasoconstriction. 10448050: Recent studies have also implicated copper in the pathogenesis of neuronal injury in Alzheimer's disease and the prion-mediated encephalopathies, suggesting that further elucidation of the mechanisms of copper trafficking and metabolism within the nervous system will be of direct relevance to our understanding of the pathophysiology and treatment of neurodegenerative disease. 12920183: Despite the crucial role played by cholesterol and copper in nutrition and normal brain function, recent evidence indicates that they may both be important factors in the etiology of Alzheimer's disease (AD). 17119285: Metals such as aluminum (Al), copper (Cu), zinc and iron have been implicated in the pathogenesis of Alzheimer's disease (AD). 17408857: The decrease in loosely bound iron in mild-moderate AD patients may be associated with myelin breakdown seen in the beginning stages of AD and implicates that iron dysregulation is an early event in AD pathogenesis. Accumulating evidence implicates a role for altered iron and copper metabolism in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). 18376063: Recent studies also point to redox active metals such as iron, copper and zinc in mediating oxidative stress in AD pathogenesis. 21303349: Despite the crucial role of redox active metals like copper and iron in central biological reactions, their elevated levels are involved in the pathogenesis of Alzheimer's Disease (AD). Iron, copper, and zinc are some of the metals, which intensify this process and contribute for the pathogenesis of AD. 21514009: It is now accepted that transition metals, such as iron and copper, are involved in the pathogenesis of the Alzheimer's disease (AD) through their participation in toxic oxidative phenomena. 23669644: These results suggest that the action of copper may be profoundly associated with the pathway of Abeta production in AD pathogenesis. 24343096: In addition, it should be noted the important role that low molecular mass fractions of iron, copper, aluminium and cobalt appear to play in pathogenesis of Alzheimer. 27983558: BACKGROUND: Defective copper regulation, primarily referred to as chelatable redox active Cu(II), has been involved in the etiology of diabetes, and Alzheimer's disease (AD). 28644490: Mounting evidence suggests that copper, a crucial element in normal brain function, plays an important role in the etiology of Alzheimer's disease, which is known as a neurodegenerative mitochondrial disorder. 30598025: Moreover, it is already established that metals (particularly copper, zinc and iron) have a key role in the pathogenesis of AD. 11132610: Subsequently, the effects of L-arginine, D-arginine or L-arginine + N-nitro-L-arginine (NOLA) on corticosterone-induced hypertension (corticosterone 20 mg/kg per day) were examined. We examined the effects of exogenous corticosterone in the male Sprague Dawley (SD) rat to determine whether ACTH-induced hypertension is mediated by corticosterone. It is likely that ACTH-stimulated adrenal production of corticosterone accounts for the features of ACTH-induced hypertension in the rat OBJECTIVE: Corticotrophin (ACTH)-induced hypertension in the rat is prevented by L- but not D-arginine. CONCLUSIONS: The haemodynamic features of ACTH-induced hypertension were reproduced by corticosterone excess, at concentrations of corticosterone similar to those in studies of exogenous ACTH administration. 11703388: We studied nitric oxide synthase (NOS) activity as a possible indicator of NO production in adrenocorticotrophin (ACTH)-induced hypertension in the rat. Previous observations of diminished NO production in ACTH- and corticosterone-induced hypertension in the rat were confirmed, but could not be explained by reduced NOS activity in the present study. Nitric oxide synthase activity in adrenocorticotrophin-induced hypertension in the rat. 12866804: Chronic hypertension in SHR rats is associated with resistance to the lethal effects of lipopolysaccharide, whereas abrupt-onset hypertension induced by corticosterone leads to an increased mortality. 19150652: 11beta-Hydroxysteroid dehydrogenase 2 (11betaHSD2) has been demonstrated to be a mineralocorticoid receptor (MR) protector by inactivating active glucocorticoids including corticosterone (CORT) in rats, and therefore mutation or suppression of 11betaHSD2 causes hypokalemia and hypertension. 1963861: The differences in actions of Na and CS upon the contractile activity of vessels in normo- and hypertensive rats are discussed from the standpoint of the membrane theory of arterial hypertension pathogenesis. 23544271: Neither RU486 nor spironolactone affected corticosterone-induced hypertension, whereas spironolactone, but not RU486, attenuated the effects of corticosterone on LV fibrosis and diastolic function. Glucocorticoid-induced hypertension and cardiac injury: effects of mineralocorticoid and glucocorticoid receptor antagonism. Corticosterone induced hypertension, left ventricular (LV) fibrosis, and LV diastolic dysfunction. 24176792: Neomycin blocks the formation of these steroid metabolites and can blunt the hypertension in rats induced by either ACTH or corticosterone. 2456441: A fall of the arterial blood pressure (ABP) elicited by the intravenous (i.v.) injection of the vasodilatator nitroprusside or the ganglionic blocking agent chlorisondamine decreased the release of corticosterone in the central amygdala (AC) and the ventral hippocampus (VH) whereas an experimentally induced hypertension after i.v. administration of the alpha adrenoreceptoragonist tramazoline led to an enhanced release of the glucocorticoid in the limbic areas mentioned above. 2698926: We conclude that it is unlikely that either aldosterone or the weak mineralocorticoids corticosterone, 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone play a specific role in the pathogenesis of hypertension in Cushing's disease. 28487303: The consequent cortisol deficiency results in a compensatory increase in adrenocorticotropic hormone (ACTH) drive, which stimulates the production of deoxycorticosterone and corticosterone leading to hypertension and hypokalaemia. 436781: An incremental change in circulating PRL, corticosterone, and aldosterone as early as 2 months of age, when blood pressure levels are beginning to rise, suggests that there may be some connection between the genetically programmed pathogenesis of the spontaneous hypertension and the progressively increasing (with age) sensitivity of the pituitary-adrenal axis to stress. 540439: In corticosterone-induced hypertension in rats the activity of the peripheral sympathetic nervous system and its modulation by prostaglandins was studied. Modulation of sympathetic vascular tone by prostaglandins in corticosterone-induced hypertension in rats. 8136112: In the rat, ACTH hypertension is probably due to corticosterone. This study examined the ability of progesterone to antagonize the onset and development of ACTH-induced hypertension in Sprague-Dawley rats (n = 44). DLS may play a role in ACTH-induced hypertension in the rat. Adrenocorticotrophin-induced hypertension in rats. 10100081: Inhibition of glucocorticoid 6 beta-hydroxylation by troleandomycin did not modify adrenocorticotrophin-induced hypertension, suggesting that effects of corticosterone 6 beta-hydroxylation in adrenocorticotrophin-induced hypertension are negligible. Adrenocorticotrophin-induced hypertension: effects of mineralocorticoid and glucocorticoid receptor antagonism. 10474778: Adrenocorticotrophic hormone-induced hypertension in the rat: effects of the endothelin antagonist bosentan. 10513829: The role of the parathyroid glands in adrenocorticotrophin-induced hypertension in the rat. These results do not support a role for the parathyroids in the genesis of ACTH-induced hypertension in the rat. 10658937: These data suggest that increase in RVR may play a role in the pathogenesis of ACTH-induced hypertension in the rat. OBJECTIVES: To investigate the roles of cardiac output and systemic and regional resistances in corticotropin (ACTH)-induced hypertension in the rat METHODS: This study consisted of three series of experiments with eight groups of male Sprague-Dawley rats (n = 132). Haemodynamic mechanisms of corticotropin (ACTH)-induced hypertension in the rat. 11071300: Vasopressin V1a receptor antagonism does not reverse adrenocorticotrophin-induced hypertension in the rat. The role of arginine vasopressin (AVP) was examined in adrenocorticotrophin (ACTH)-induced hypertension in Sprague-Dawley rats using the non-peptide AVP V1a receptor antagonist OPC 21268. These results suggest that AVP (at the V1a receptor) does not play a significant role in the maintenance of ACTH-induced hypertension. 11071304: N-Nitro-L-arginine reversed the blood pressure-lowering effect of L-arginine in ACTH-induced hypertension in the rat, supporting the notion that NO plays a role in the hypertension. To confirm that this effect is mediated through the nitric oxide (NO) system, we examined whether N-nitro-L-arginine (NOLA) could reverse the L-arginine-induced blockade of ACTH-induced hypertension. 11082157: 11beta-Dehydrogenation, converting cortisol to its inactive metabolite, cortisone, mediated by vascular 11beta-hydroxysteroid dehydrogenase type 2 is essential for the control of vascular tone, and the reduced activity may be relevant to the pathogenesis of hypertension. Therefore, the present study provides important information for understanding the mechanism of ACTH-induced hypertension. 11132610: Subsequently, the effects of L-arginine, D-arginine or L-arginine + N-nitro-L-arginine (NOLA) on corticosterone-induced hypertension (corticosterone 20 mg/kg per day) were examined. We examined the effects of exogenous corticosterone in the male Sprague Dawley (SD) rat to determine whether ACTH-induced hypertension is mediated by corticosterone. It is likely that ACTH-stimulated adrenal production of corticosterone accounts for the features of ACTH-induced hypertension in the rat OBJECTIVE: Corticotrophin (ACTH)-induced hypertension in the rat is prevented by L- but not D-arginine. CONCLUSIONS: The haemodynamic features of ACTH-induced hypertension were reproduced by corticosterone excess, at concentrations of corticosterone similar to those in studies of exogenous ACTH administration. 11193135: These data are consistent with previous studies suggesting that functional NO deficiency has a role in ACTH-induced hypertension in rats. 11212977: OBJECTIVE: To determine the effects on pre- and post-glomerular vascular resistance of adrenocorticotrophin (ACTH)-induced hypertension in rats, before and after blockade of nitric oxide formation. Glomerular hypertension and hyperfiltration in adrenocorticotrophin-induced hypertension in rats: the role of nitric oxide. CONCLUSIONS: ACTH-induced hypertension produced glomerular hypertension and hyperfiltration, which may be due to nitric oxide-related vasodilatation of the renal vasculature. 11518849: This study examined circadian (24 h) blood pressure variability in adrenocorticotrophin (ACTH)-induced hypertension in the Sprague-Dawley rat. Circadian blood pressure variability in adrenocorticotrophin-induced hypertension in the rat. 11560123: Telemetric monitoring of adrenocorticotrophin-induced hypertension in mice. This model will allow the selective use of transgenic and/or knockout mice to further elucidate the mechanism of ACTH- and steroid-induced hypertension. We have studied adrenocorticotrophin (ACTH)- and steroid-induced hypertension in both rat and humans. The aim of the present study was to develop a model of ACTH-induced hypertension in the mouse and to assess a chronically implanted telemetric device for measurement of blood pressure (BP). 11703388: We studied nitric oxide synthase (NOS) activity as a possible indicator of NO production in adrenocorticotrophin (ACTH)-induced hypertension in the rat. Previous observations of diminished NO production in ACTH- and corticosterone-induced hypertension in the rat were confirmed, but could not be explained by reduced NOS activity in the present study. Nitric oxide synthase activity in adrenocorticotrophin-induced hypertension in the rat. 12872045: The anti-oxidant Tempol reverses and partially prevents adrenocorticotrophic hormone-induced hypertension in the rat. CONCLUSIONS: ACTH-induced hypertension in the rat is associated with increased oxidative stress. OBJECTIVE: To investigate the effects of the antioxidant Tempol on prevention and reversal of adrenocorticotrophic hormone (ACTH)-induced hypertension in the rat, a model of hypertension characterized by nitric oxide deficiency. 12887135: Lipopolysaccharide (LPS) was used to stimulate nitric oxide (NO) release and investigate the effect of endogenous NO on adrenocorticotrophic hormone (ACTH)-induced hypertension in rats. These data are compatible with the notion that reduced NO availability plays a role in ACTH-induced hypertension. 1321309: Adrenocorticotrophin and steroid-induced hypertension in humans. The role of this increased pressor responsiveness in ACTH/steroid-induced hypertension remains to be determined. 1334993: Role of the renal medulla in adrenocorticotrophin-induced hypertension in rats. OBJECTIVES: The mechanism of hypertension induced by adrenocorticotrophin (ACTH) remains unclear. 15110907: We hypothesized that ACTH-induced hypertension in the rat is characterized by increased EPO production. These data suggest that EPO is not causal in ACTH-induced hypertension. 15132301: Thus, daily injection of BH4 (10 mg/kg i.p.) failed to prevent the development of ACTH-induced hypertension in rat. Accordingly we hypothesized that ACTH-induced hypertension would be reversed by BH4 supplementation. Adrenocorticotropic hormone (ACTH)-induced hypertension in the rat is characterized by nitric oxide deficiency. 15554453: In conclusion, the lowering of SBP by NO donation is consistent with the notion that ACTH-induced hypertension involves an impaired bioavailability or action of NO in vivo. We assessed the ability of NO donation from isosorbide dinitrate (ISDN) to prevent or reverse the hypertension caused by ACTH. 16053986: CONCLUSIONS: Apocynin but not allopurinol prevented and reversed ACTH-induced hypertension in the rat. BACKGROUND: Adrenocorticotropic hormone (ACTH)-induced hypertension in the rat is accompanied by increased oxidative stress. These results suggest superoxide production through NAD(P)H oxidase plays a role in ACTH-induced hypertension. Apocynin (but not allopurinol) co-treatment prevented (142+/-3 ACTH, 120+/-4 mm Hg apocynin+ACTH, P'<0.001) and reversed ACTH-induced hypertension (133+/-4 to 118+/-5 mm Hg, P<.05). 16243970: Chronic administration of ACTH caused hypertension in WT mice but not in mice with an ouabain-resistant alpha2 isoform of Na,K-ATPase. 1649024: The effect of chemical sympathectomy with 6-OH-dopamine (6-OHDA) on the onset of adrenocorticotrophin (ACTH)-induced hypertension was examined in Sprague-Dawley rats (n = 23). 16620303: Ato alone did not alter SBP, but Ato pretreatment prevented ACTH-induced hypertension compared with that in rats treated with ACTH alone (118 +/- 2 and 136 +/- 2 mmHg, respectively, P cent < 0.01). Atorvastatin prevented and partially reversed ACTH-induced hypertension in the rat. Adrenocorticotropic hormone (ACTH)-induced hypertension is associated with nitric oxide (NO) deficiency and increased oxidative stress. The aim of the study was to assess whether pretreatment with Ato would prevent the development of ACTH-induced hypertension and whether established ACTH-induced hypertension could be reversed with subsequent administration of Ato in rats. Ato partially reversed ACTH-induced hypertension (124 +/- 3 and 136 +/- 2 mmHg, respectively, P cent < 0.05). 16922827: Species variability in cardiovascular research: the example of adrenocorticotrophin-induced hypertension. 17324744: Folic acid, but not BH(4), prevented the development of hypertension caused by ACTH and Dex treatment. 17954371: ACTH- but not Dex-induced hypertension was partially reversed by aspirin. The aim of the present study was to investigate the effects of aspirin, a potent antioxidant, on adrenocorticotropic hormone (ACTH) and dexamethasone (Dex)-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with increased oxidative stress. Aspirin prevented the development of hypertension caused by ACTH (P' < .01) and tended to prevent Dex-induced hypertension (P' = .07). 17994356: Antioxidant vitamins and adrenocorticotrophic hormone-induced hypertension in rats. 192514: Further unravelling of the causes of ACTH-induced hypertension in the sheep. 19458537: The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension. HET0016 also prevented the development of hypertension induced by ACTH (P < 0.01). In the present study, we investigated the effect of a specific enzyme inhibitor of 20-HETE production, N-hydroxy-N'-(4-butyl-2-methylphenyl) formamidine (HET0016), on glucocorticoid-induced hypertension in rats, a sodium-independent model. These results suggest that 20-HETE may play a role in the genesis of ACTH-induced hypertension but not in dexamethasone-induced hypertension. 19635986: Dietary sodium depletion also prevented ACTH-induced hypertension. 20659135: These data, together with a previous study showing both ACTH and corticosterone are increased in GRKO mice, show that the GR is required for the development of ACTH-induced hypertension in mice. The glucocorticoid receptor is required for experimental adrenocorticotrophic hormone-induced hypertension in mice. 215361: Pressor responses to angiotensin II, noradrenaline and tyramine were examined in sheep prior to and during the development of corticotrophin-induced hypertension. 2157753: Adrenocorticotrophin-induced hypertension in the rat: haemodynamic, metabolic and morphological characteristics. 22258333: BACKGROUND: We have shown that the ouabain-sensitive alpha2 Na,K-ATPase is required for adrenocorticotropic hormone (ACTH)-induced hypertension and gestational blood pressure regulation. These findings indicate that the underlying mechanisms of hypertension induced by DOCA-salt treatment are different from those of ACTH-induced hypertension. 232025: Haemodynamics of ACTH-induced hypertension in sheep. 23533693: The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. CONCLUSION: Glucocorticoid-induced hypertension in rats is prevented by alpha-lipoic acid via mechanisms other than mitochondrial superoxide reduction. AIMS: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition. 2412029: This study examined the effects of the serotonergic (5-HT2) antagonist ketanserin in sheep on haemodynamic responses to infused serotonin (5-HT), development of adrenocorticotrophin (ACTH)-induced hypertension, and the effect of ACTH on in vivo pressor responsiveness to 5-HT. Thus, 5-HT raises mean arterial pressure in sheep in a dose-related fashion, but there is no evidence of a role for 5-HT in ACTH-induced hypertension. 2542400: Rapid haemodynamic response to adrenocorticotrophin and the role of peripheral resistance in adrenocorticotrophin-induced hypertension in conscious sheep. The haemodynamic effects associated with the onset of hypertension induced by infusion of adrenocorticotrophin (ACTH) were investigated in sheep. The onset of ACTH-induced hypertension in sheep is characterized by very rapid haemodynamic changes with an increase in cardiac output and a relative increase in CTPR after an initial peripheral vasodilatation. These results indicate that constriction of the peripheral vasculature is essential for the onset and maintenance of ACTH-induced hypertension in the sheep, and that the vasoconstriction does not involve a specific Ca21+-dependent mechanism because minoxidil was as effective as nisoldipine in abolishing the pressor response to ACTH. The development of ACTH-induced hypertension was prevented by both nisoldipine, a calcium channel blocker, and minoxidil, a vascular smooth muscle relaxant. 2544114: Although tail-cuff measurements of arterial pressure indicated that the ACTH treatment produced hypertension, this was not confirmed by direct 24-h measurements of mean arterial pressure. ACTH-induced hypertension in rats: fact or artifact? 2551550: Progesterone antagonizes development but not maintenance of ACTH-induced hypertension in sheep. This study investigated the effect of progesterone, which, under certain circumstances, can antagonize both the mineralocorticoid and glucocorticoid activities of steroid hormones, on the development and maintenance of adrenocorticotrophic hormone (ACTH)-induced hypertension in conscious sheep. 2553310: These results do not support a role for centrally mediated increase in sympathetic activity in the genesis of ACTH-induced hypertension. Centrally mediated increased sympathetic activity is not important in the genesis of ACTH-induced hypertension in sheep. This study investigated the proposal that a centrally mediated increase in sympathetic activity is important in the development of ACTH-induced hypertension. 2830066: The study was performed to examine the hypothesis that adrenocorticotrophic hormone (ACTH) induced hypertension in sheep would be enhanced if the blood level of angiotensin II (ANG II), normally suppressed during ACTH administration, was kept at control levels by intravenous infusion of ANG II. 3001556: Studies of ACTH-induced hypertension in sheep have enabled the hypertensinogenic actions of steroid hormones to be separated from their classical glucocorticoid and mineralocorticoid actions. [Hypertension induced by adrenocorticotropin (ACTH)]. 3038444: Dose-response relationships for adrenocorticotrophin-induced hypertension in man. 30780842: Glucocorticoid hormones, both naturally occurring and synthetic, have long been recognized as a major cause of hypertension. Current evidence demonstrates the importance of the nitric oxide (NO) system and interactions between NO and reactive oxygen species in the development of glucocorticoid-induced hypertension. Glucocorticoid-induced hypertension and the nitric oxide system. There are well-described experimental models of glucocorticoid-induced hypertension, such as adrenocorticotropic hormone- and dexamethasone-induced hypertension in rats, although the exact mechanism of glucocorticoid-induced hypertension remains unclear. 4361404: Experimental studies on the mechanism of adrenocorticotrophic hormone-induced hypertension in the sheep. 6096050: This study examines the blood pressure and electrolyte response to adrenocorticotrophic hormone (ACTH) in K loaded sheep to test the hypothesis that ACTH-induced hypertension is blunted in K loaded sheep. 6279500: This study examines whether neural structures in the region of the optic recess of the third ventricle may be involved in the genesis of adrenocorticotrophic hormone (ACTH)-induced hypertension in sheep. 8136112: In the rat, ACTH hypertension is probably due to corticosterone. This study examined the ability of progesterone to antagonize the onset and development of ACTH-induced hypertension in Sprague-Dawley rats (n = 44). DLS may play a role in ACTH-induced hypertension in the rat. Adrenocorticotrophin-induced hypertension in rats. 8261660: The hypothesis that adrenocorticotrophin (ACTH)-induced hypertension is a consequence of steroid-induced hyperinsulinaemia was tested using the somatostatin analogue (sandostatin, octreotide) to inhibit insulin release in Sprague-Dawley (SD) rats (n = 41). These data do not support the notion that insulin-mediated alterations in blood pressure are a major mechanism for ACTH-induced hypertension in the rat. 8713685: This suggests either that ACTH-induced hypertension is not simply a consequence of glucocorticoid activity or that the action of DHEA in dexamethasone hypertension is not through blocking the glucocorticoid receptor. DHEA, which is known to block dexamethasone-induced hypertension, did not modify ACTH-induced hypertension in the rat. 8842566: The possibility that corticotropin (ACTH)-induced hypertension results from a direct central effect of the adrenocortical steroids released by ACTH was investigated in sheep. 9128206: These results suggest the contribution of OLC to ACTH-induced hypertension in rats. Adrenocorticotropin-induced hypertension in rats: role of ouabain-like compound. 9315378: Dexamethasone-induced hypertension differs from adrenocorticotropic hormone (ACTH)-induced hypertension in the rat in that it is not modified by L-arginine. Thus, ACTH-induced hypertension cannot be explained simply in terms of glucocorticoid activity. Dexamethasone-induced hypertension in the rat: effects of L-arginine. 9486303: Thus ACTH-induced hypertension in the ewe had minimal effects on fetal MAP, fetal blood gas status, and pH. ACTH induced hypertension in the ewe. 9493501: The possibility that altered synthesis of vascular nitric oxide (NO) plays a role in the development of corticotropin-induced hypertension in sheep was examined by determining the effect of concomitant infusion of L-arginine, a precursor of NO, on the development of the hypertension. Role of nitric oxide in the development of corticotropin-induced hypertension in sheep. 9535146: Hemodynamic profile of corticotropin-induced hypertension in the rat. CONCLUSION: The hemodynamic profile of corticotropin-induced hypertension in the rat is characterized by a rise in cardiac output and renal vascular resistance, a fall in renal blood flow, but no change in total peripheral resistance, hindquarter blood flow, mesenteric vascular resistance, or hindquarter vascular resistance. OBJECTIVES: To examine hemodynamic variables in corticotropin-induced hypertension in rats and the effects of reversal of the hypertension by L-arginine on the hemodynamic profile. 9794742: DESIGN: We determined the proportions of mRNA for the exon 11+ and exon 11- isoforms in various tissues of SHR and Wistar-Kyoto rats aged 3, 6, 9 and 12 weeks, which span the pre-hypertensive phase through to established hypertension, as well as in Sprague-Dawley rats with adrenocorticotropin-induced hypertension and Sprague-Dawley controls. 10658937: These data suggest that increase in RVR may play a role in the pathogenesis of ACTH-induced hypertension in the rat. OBJECTIVES: To investigate the roles of cardiac output and systemic and regional resistances in corticotropin (ACTH)-induced hypertension in the rat METHODS: This study consisted of three series of experiments with eight groups of male Sprague-Dawley rats (n = 132). Haemodynamic mechanisms of corticotropin (ACTH)-induced hypertension in the rat. 11132610: Subsequently, the effects of L-arginine, D-arginine or L-arginine + N-nitro-L-arginine (NOLA) on corticosterone-induced hypertension (corticosterone 20 mg/kg per day) were examined. We examined the effects of exogenous corticosterone in the male Sprague Dawley (SD) rat to determine whether ACTH-induced hypertension is mediated by corticosterone. It is likely that ACTH-stimulated adrenal production of corticosterone accounts for the features of ACTH-induced hypertension in the rat OBJECTIVE: Corticotrophin (ACTH)-induced hypertension in the rat is prevented by L- but not D-arginine. CONCLUSIONS: The haemodynamic features of ACTH-induced hypertension were reproduced by corticosterone excess, at concentrations of corticosterone similar to those in studies of exogenous ACTH administration. 12878376: The ACTH-induced HT was not affected by huTNFR:Fc coadministration. 1330390: Inhibition of nitric oxide is unlikely to be a major determinant of ACTH-induced hypertension in the rat, since NOLA increased blood pressure whether or not ACTH was administered, indicating an additive effect of ACTH and NOLA administration. Inhibition of NO synthesis has an additive effect on hypertension induced by ACTH in conscious rats. 16467499: Whereas chronic administration of ouabain or ACTH caused hypertension in wild-type mice, it had no effect on blood pressure in mice with a ouabain-resistant alpha2-isoform of Na+-K+-ATPase. 171112: The role of adrenocortical hormones in ACTH-induced hypertension. 17980562: Other forms of hypertension that are known to be mediated by endogenous ouabain-like substances include steroid/salt- (e.g., DOCA-salt) and ACTH-induced hypertension. An endogenous ouabain-like substance (OLS) plays a critical role in the etiology of experimental models of human hypertension induced by a high salt diet. 183887: Concerning the independence of the basis of hypertension due to ACTH or renovascular constriction. 18487447: ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit. Overall, the data establish that the alpha(2)-Na(+)-K(+)-ATPase ouabain-binding site is of central importance in the development of ACTH-induced hypertension. ACTH-induced-hypertension is commonly employed as a model of stress-related hypertension, and despite extensive investigation, the mechanisms underlying elevated blood pressure (BP) are not well understood. 187612: These studies suggest that a steroid other than aldosterone, 18-OH-DOC, or DOC may be the cause of the ACTH-induced hypertension in this patient. Evidence for an unidentified ACTH-induced steroid hormone causing hypertension. 19920212: Although there is evidence that ACTH-induced hypertension is a function of physiological cross talk between glucocorticoids and mineralocorticoids, the present study suggests that the major changes in electrolyte and fluid homeostasis and renal function are attributable to glucocorticoids. 21632957: We have previously shown that ACTH-induced hypertension is abolished in mutant mice expressing ouabain-resistant alpha1- and alpha2-subunits. 2171563: This study investigated the ability of two diuretics, amiloride and frusemide, to prevent the development of ACTH induced hypertension in conscious sheep. Amiloride blocks the onset of ACTH-induced hypertension in the sheep. 21856916: Knockout of the Na,K-ATPase alpha2-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension. These results demonstrate that alpha(2)-expression in heart and vascular smooth muscle is not essential for regulation of basal systolic blood pressure, but alpha(2) is critical for blood pressure regulation under chronic stress such as ACTH-induced hypertension. 221121: ACTH induced hypertension was also potentiated by reduced renal mass, suggesting a volume component for the hypertension when renal excretory capacity for salt and water is reduced. 24176792: Neomycin blocks the formation of these steroid metabolites and can blunt the hypertension in rats induced by either ACTH or corticosterone. 2536448: Studies of the mechanism of ACTH induced hypertension in sheep have led to the hypothesis that adrenocortical steroids may raise blood pressure by a \hypertensinogenic\ action which can be distinguished from effects mediated by occupancy of classical mineralocorticoid or glucocorticoid receptors. 2559253: This study provides additional evidence for an essential mineralocorticoid component in ACTH-induced hypertension. Studies on spirolactone steroid antagonists in ACTH-induced hypertension in sheep. This study investigated the anti-mineralocorticoid potency and haemodynamic effects of a series of mineralocorticoid antagonists of the spirolactone type (RU 28318, spironolactone, K-prorenoate, K-canrenoate and canrenone), for their ability to prevent the development of ACTH-induced hypertension in conscious sheep. 2822310: Effect of sodium depletion on pressor responsiveness in ACTH-induced hypertension in man. 2825944: Autonomic blockade augmented the pressor response to ACTH, indicating that baroreceptor-mediated reflexes normally operate to suppress the degree of hypertension produced by ACTH. The roles of the autonomic nervous system, renin-angiotensin system, and arginine vasopressin (AVP) during the onset of ACTH-induced hypertension were investigated in conscious sheep. 2849322: Thus, in dogs receiving a background infusion of NE, ACTH causes moderate hypertension and natriuresis. 2852074: The course of ACTH-induced hypertension was not altered in animals supplemented with CaCl2 in their drinking water for 6 weeks nor by intravenous injection of vitamin D for 5 days. 2988839: Angiotensin converting enzyme inhibition does not prevent development of ACTH-induced hypertension in sheep. These experiments establish that angiotensin II is not important in the onset of ACTH-induced hypertension in sheep. The role of the renin-angiotensin system in the onset of ACTH-induced hypertension was examined in five conscious sheep. 2989937: It is unlikely on the basis of these results that glucocorticoid-induced inhibition of vasodepressor prostacyclin and resulting increase in pressor responsiveness to circulating agonists is the primary cause of ACTH induced hypertension in sheep. Despite these effects it did not prevent development of ACTH-induced hypertension. The present experiments examine the hemodynamic effects of an intravenous infusion of prostacyclin on the development of ACTH-induced hypertension in conscious sheep. 3011328: As 9 alpha FF did not cause a further increment in blood pressure in sheep with ACTH-induced hypertension it is possible that both ACTH and 9 alpha FF may produce hypertension by similar mechanisms. The effect of treatment with 9 alpha-fluorocortisol (9 alpha FF), a steroid which causes hypertension in sheep, was examined in sheep with ACTH-induced hypertension. The effect of the 'hypertensinogenic' steroid, 9 alpha-fluorocortisol on blood pressure in sheep with ACTH-induced hypertension. 3609396: 17 alpha, 20 alpha-dihydroxy-4-pregnen-3-one (17 alpha, 20 alpha-P) is reportedly a hyper-tensinogenic substance in a model of ACTH induced hypertension in sheep (Scoggins et al). 533676: Cortisol at 20 mg/hr produced hypertension (MAP + 25 mm Hg on day 5, p less than 0.01) but also produced the 'mineralocorticoid' effect of severe hypokalaemia. These results supported the contention that ACTH induced hypertension in sheep represents a mechanism different from a simple 'mineralocorticoid' or 'glucocorticoid' action. 6096893: The aim of this study was to determine the effect of ACTH-induced hypertension on the hemodynamic dose-response curves to intravenous infusion of prostacyclin (PGI2) in conscious sheep. PGI2 was infused for 10 minutes at doses of 0.05-0.50 micrograms/kg per min and hemodynamic dose-response curves were performed before, during and after ACTH-induced hypertension. These studies suggest that in this model of steroid-induced hypertension the resistance vessels are more sensitive to PGI2 and that the blood pressure response to PGI2 is regulated by different mechanisms to those seen prior to ACTH. 6097376: Acute glucocorticoid (corticosterone) hypertension in the rate is significantly attenuated by neomycin administration (Honour 1981), as is ACTH-induced hypertension is the same species (Honour & Kent 1981) presumably by altering gut bacterial steroid metabolism. 6097378: The time of onset and dose threshold for ACTH induced hypertension was examined in conscious sheep. 6100240: The effects of oral neomycin on ACTH induced hypertension were examined in conscious sheep. Failure of neomycin to modify ACTH induced hypertension in sheep. 6200718: Prostaglandin synthesis inhibition with indomethacin in ACTH-induced hypertension. 6256103: Haemodynamic dose-response curves to prostacyclin were performed before, during and after production of ACTH-induced hypertension. After 5 days of ACTH-induced hypertension prostacyclin produced similar effects on mean arterial pressure to those seen prior to ACTH but the effects on heart rate, cardiac output, stroke volume and total peripheral resistance were markedly increased. 6256106: ACTH-induced hypertension in sheep is not associated with enhanced pressor responsiveness to AVP. 6256107: These studies show that while ACTH-induced hypertension is usually associated with increased cardiac output, rather than total peripheral resistance it still occurs, but is associated with a rise in total peripheral resistance if the rise in cardiac output is prevented by beta-adrenoreceptor blockade. 6256118: The aim of the present experiments was to detail the haemodynamic changes associated with restoration of the extracellular potassium concentration in sheep with ACTH-induced hypertension. 6258888: This suggests that the renin-angiotensin system plays no significant role in maintaining the elevated blood pressure of sheep with ACTH induced hypertension. 6276065: The haemodynamic characteristics of ACTH in patients with mild untreated essential hypertension are similar to those in the experimental model of ACTH induced hypertension in sheep. 9056691: Although these data that digibind decreases BP in ACTH but not sham treated rats are consistent with the notion that digitalis-like substances may play a role in ACTH induced hypertension, the evidence that both preimmune sheep IgG and IgG (Fab)2 fragments also decreased blood pressure in rats suggests caution in interpretation of studies that employ digibind preparations. 9128206: These results suggest the contribution of OLC to ACTH-induced hypertension in rats. Adrenocorticotropin-induced hypertension in rats: role of ouabain-like compound. 1115068: It is suggested that glucocorticoid-induced hypertension may be initiated by alterations in vascular responsiveness to pressor agents and that elevated PRS levels may contribute to increase angiotensin formation. Steroid production, plasma renin activity (PRA) and plasma renin substrate (PRS) were measured in eight patients with hypertension due to Cushing's syndrome of benign origin. 11921653: In the case of the Cushing syndrome, which leads to hypertension in about 70% of the patients, the general practitioner should look for the typical cutaneous changes that inevitably accompany this syndrome. 15171429: [Hypertension secondary to Cushing syndrome]. 15702437: Markers of vascular function in hypertension due to Cushing's syndrome. 15900383: Severe hypertension secondary to renal artery stenosis and Cushing's syndrome. 24801134: While endogenous Cushing's syndrome is an uncommon cause of both obesity and hypertension, the recent recognition of other hypercortisolemic states has raised the profile of hypercortisolism as an important contributor in obesity hypertension. 25546991: [Difficulty in diagnosis of primary hyperaldosteronism as the cause of resistant hypertension and severe hypokalemia--case report]. Renovascular hypertension, Cushing syndrome and pheochromocytoma were excluded as potential causes of drug-resistant hypertension in the presented case. 28509248: This is a very rare case of periodic hypokalemia and hypertension caused by cyclic Cushing's syndrome. 29779837: Cushing's syndrome is a rare cause of high blood pressure. 34384396: BACKGROUND: Various adrenal disorders including primary aldosteronism and Cushing's syndrome lead to the cause of hypertension. 10100073: CONCLUSIONS: The findings in the forearm circulation question the concept of generalized increases in vasoconstrictor responses or a disturbance of tonic, basal release nitric oxide in the pathogenesis of cyclosporine-A-induced hypertension. 10212347: Moreover, high percentages of non-dippers have been found among subjects with renal failure, subjects undergoing dialysis (haemofiltration, peritoneal dialysis, continuous ambulatory peritoneal dialysis (CAPD), subjects with renovascular hypertension and with cystic kidney disease, subjects who have had a kidney transplant and subjects with cyclosporine-induced hypertension. 10348094: Cyclosporin-induced hypertension: incidence, pathogenesis and management. 10354289: However, CsA also causes vasoconstriction, which is considered to be at the origin of CsA-induced nephrotoxicity and hypertension. CONCLUSION: These data suggest that CsA preferentially up-regulates the transcription of Ang II receptors, which very likely leads to vasoconstriction in vivo and could be at the origin of CsA-induced hypertension and nephrotoxicity in humans. 10412883: The present study assessed the role of the renin-angiotensin system in the development of CsA-induced hypertension and nephrotoxicity in spontaneously hypertensive rats (SHR) on a high-sodium diet. Cyclosporine A (CsA)-induced hypertension has been shown to be dependent on the level of dietary salt. Our findings thus suggest that increased activity of the renin-angiotensin system is involved in the pathogenesis of CsA-induced hypertension and nephrotoxicity in SHR on a high-sodium diet. Effects of ACE inhibition on cyclosporine A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats on a high-sodium diet. ACE inhibition prevents the CsA-induced hypertension, nephrotoxicity and vascular injuries. 10467627: Cyclosporine A can induce hypertension by its vasoconstrictive effects, particularly on the kidney. 10477041: Nitric oxide in cyclosporine A-induced hypertension: endothelin receptors gene expression. Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. 10551431: Calcium antagonists appear to be extremely useful in patients with cyclosporin-induced hypertension, and in patients with hypertension and concomitant Raynaud's phenomenon and/or migraine. 10604485: This suggest that PKC mediates, in part, CsA-induced hypertension. Nitric oxide in cyclosporine A-induced hypertension: role of protein kinase C. 10635259: Additionally, cyclosporine-induced hypertension is frequently treated with calcium channel blockers, such as nifedipine, both drugs acting synergistically to induce gingival overgrowth. 10720962: Cyclosporine-induced hypertension is a particular problem and has variously been attributed to increased sympathetic nerve activity, salt and water retention, and increased circulating endothelin levels. This may predispose patients to atherosclerosis and may be involved in the etiology of post-transplant hypertension. 10829796: But there were several complications postoperatively: ischaemic-toxic tubular renal failure requiring haemodialysis, underperfusion of the right lobe of the liver due to arterial stenosis, pleural effusion, cytomegalovirus infection and cyclosporin-induced hypertension. 10852615: BACKGROUND: Sympathetic nervous system hyperactivity has been postulated to play a major role in the intense intrarenal vasospasm and hypertension provoked by cyclosporine. 10856274: The decrease in arterial compliance in cyclosporine-induced hypertension seems to imply a degree of ventricular vascular uncoupling more apparent in heart transplantation recipients. 10856453: Cyclosporine A-induced hypertension and nephrotoxicity seem to be associated with renal arterial dysfunction in SHR on high-Na(+) diet. Cyclosporine A causes hypertension and nephrotoxicity in spontaneously hypertensive rats (SHR). 10876188: BACKGROUND: Cyclosporin A-induced hypertension is dependent on the level of dietary salt. 10884522: Cyclosporin-A and tacrolimus can cause hypertension and renal failure through endothelin receptors. 10903974: Comparison of enalapril and valsartan in cyclosporine A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats on high-sodium diet. We compared the effects of the angiotensin converting enzyme (ACE) inhibitor enalapril and the angiotensin AT(1) receptor antagonist valsartan in cyclosporine A (CsA)-induced hypertension and nephrotoxicity in spontaneously hypertensive rats (SHR). 10920204: These results provide a mechanistic explanation for CsA-induced acute hypertension and suggest that synapsins could serve as a drug target in this refractory condition. Cyclosporine A-induced hypertension involves synapsin in renal sensory nerve endings. 10930191: Effects of chronic neutral endopeptidase inhibition in rats with cyclosporine-induced hypertension. CONCLUSION: These results indicate that chronic NEP inhibition may prevent the CysA-induced hypertension by decreasing local ET-1 synthesis and partly increasing vascular nitric oxide production. 10951883: Mechanisms of cyclosporin induced hypertension:enhancement of the vasoconstricting effect of endothelin 1, reduced NO production, activation of neurohumoral vasoconstrictors, increased calcium level in cytosols, increased thromboxane A production, reduced production of vasodilatating prostaglandins and activation of the sympathicus. 10981550: Inhibition of calcineurin-mediated signaling in T lymphocytes is a major mechanism of cyclosporine A (CsA)-induced immunosuppression, and previous rat studies have suggested that inhibition of calcineurin-mediated signaling in central neuronal pools involved in blood pressure regulation plays an important role in causing acute CsA-induced hypertension. However, a central neural mechanism is difficult to reconcile with other data suggesting that CsA-induced hypertension is due to activation of renal and other subdiaphragmtic visceral afferents that reflexively increase efferent sympathetic nerve activity. Calcineurin inhibitors cause renal afferent activation in rats: a novel mechanism of cyclosporine-induced hypertension. 11028414: [Cyclosporine- and tacrolimus-induced hypertension]. 11112045: Cyclosporin-induced endothelial dysfunction and hypertension: are nitric oxide system abnormality and oxidative stress involved? While the mechanism(s) responsible are unclear, CsA-induced endothelial dysfunction and CsA-induced hypertension have been attributed to the CsA effect on the endothelial-derived factors controlling vasomotor tone. Our study evaluates endothelial nitric oxide synthase (ecNOS) gene status (PCR analysis) and plasma levels of NO metabolites (ELISA) in kidney and heart transplant patients under chronic CsA treatment with CsA-induced hypertension. 11115079: In the present study, we tested the hypothesis of whether concurrent supplementation with potassium and magnesium could protect against the development of CsA-induced hypertension and nephrotoxicity more effectively than supplementation with one mineral alone. Dietary potassium and magnesium supplementation in cyclosporine-induced hypertension and nephrotoxicity. CONCLUSIONS: Our findings indicate that both potassium and magnesium supplementations showed beneficial effects against CsA-induced hypertension and nephrotoxicity. BACKGROUND: Cyclosporine A (CsA)-induced hypertension and nephrotoxicity are aggravated by high sodium intake. 11181432: This could be a key mechanism in enhanced vascular responsiveness induced by CsA, causing both hypertension and, via renal vasoconstriction, reduced glomerular filtration. 11207085: BACKGROUND: Hypertension and cyclosporine-induced nephrotoxicity are common complications in heart transplant recipients. 11321510: Functional and morphological changes of blood vessels in cyclosporine A (CsA)-induced hypertension and nephrotoxicity were studied in spontaneously hypertensive rats (SHR). Vascular changes in cyclosporine A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats on high-sodium diet. 11325024: To identify the mechanism of cyclosporine-induced hypertension, we studied the effect of cyclosporine on the catecholamine synthetic pathway in rats. 11369839: Cyclosporin and tacrolimus also induce arterial hypertension. 11579840: Long-acting CCBs have been shown to reduce mortality and morbidity in elderly patients with systolic hypertension, appear to be extremely useful in patients with cyclosporin-induced hypertension, and can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus, renal disease, Raynaud's phenomenon or migraine. 11585243: Although cyclosporine has been influential in the improvement of transplant outcome, it has emerged as a major cause of hypertension after organ transplantation. There is evidence to suggest that the use of tacrolimus-based immunosuppression induces less hypertension compared with cyclosporine. 11688356: Cyclosporin-induced hypertension and endothelial dysfunction have been attributed to the effects of cyclosporin on factors controlling vasomotor tone. In transplanted patients with cyclosporin-induced hypertension, we have recently demonstrated upregulation of the NO system and superoxide and free radical overproduction, which, by increasing NO metabolism, could induce hypertension, vascular remodeling and chronic rejection. 11725176: Cyclosporin-induced hypertension. 11876576: Despite extensive research, the exact mechanisms of cyclosporine A (CsA)-induced hypertension and nephrotoxicity remain obscure. 11926202: BACKGROUND: Arterial hypertension (HT), secondary to cyclosporine A (CsA) used as main immunosuppressive treatment in renal transplantation (RTx), is very frequent (70%), usually severe and explained mostly by vasoconstriction of the glomerular afferent arteriole with secondary sodium and water retention. 11963284: Moreover, our cyclosporin-induced hypertension model could be useful to study drugs that could treat or prevent these changes. 11993718: Nitric oxide in CsA-induced hypertension: role of beta-adrenoceptor antagonist and thromboxane A2. This suggests that PKC mediate, in part, CsA-induced hypertension. Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. 12050171: Our results suggest that cyclosporin A-induced hypertension may involve, at least in part, the attenuation of endothelium-derived NO production through a calcineurin-sensitive pathway regulating eNOS dephosphorylation. 12055538: Ciclosporin provokes serious adverse reactions especially nephrotoxicity and arterial hypertension. 12102255: One mechanism by which cyclosporine induces hypertension is the induction of subtle renal microvascular and tubulointerstitial disease. 12131547: A possible explanation for cyclosporin-induced arterial hypertension may be its action on the adrenergic system. 12193060: Several mechanisms, including endothelin (ET)-1-mediated systemic vasoconstriction, are considered to be responsible for CsA-induced hypertension. 12227681: Oxidative stress and TGFbeta in kidney-transplanted patients with cyclosporin-induced hypertension. In conclusion, carvedilol reduces the oxidative stress and corrects the altered cellular signaling mediated by oxidative stress in CsA-induced post-transplant hypertension. 12352326: In patients with cyclosporine-induced hypertension, upregulation of the nitric oxide system and oxidative stress were shown, which could induce hypertension, remodeling, and chronic rejection by increasing nitric oxide catabolism. Oxidative stress in kidney transplant patients with calcineurin inhibitor-induced hypertension: effect of ramipril. 12588629: An animal model of CsA-induced hypertension was used. 12591008: This suggests that PKC mediate, in part, CsA-induced hypertension. 12874088: These data suggest that ROS generation induced by augmented Ang II levels contributes to the development of CysA-induced hypertension. Treatment with cyclosporine A (CysA), a potent immunosuppressive agent, is associated with systemic and renal vasoconstriction, leading to hypertension. 12893025: The present study aimed to evaluate the CsA effect on the platelet NO-cyclic guanosine-3',5'-monophosphate (cGMP) pathway and the putative benefits of concomitant isosorbide-5-mononitrate (IS-5-MN) administration on CsA-induced hypertension and on platelet hyperactivation. 13679494: CONCLUSIONS: Amlodipine could be more appropriate than tertatolol for CsA-induced hypertension and hyperuricaemia in renal transplant recipients. 1422559: Cyclosporin-induced nephrotoxicity and hypertension. 1498282: Both diuretic and calcium channel blocker therapy are believed to be useful in cyclosporine-induced hypertension. In posttransplant hypertension that is primarily due to cyclosporine, one must balance the risks of reduced cyclosporine dosage against the risks of the hypertension. 15218328: Cyclosporine was perceived as more difficult to swallow (p = 0.001), nephrotoxic (p = 0.005), and to cause more hypertension (p = 0.04) and hyperlipidemia (p = 0.001), while tacrolimus was perceived to be more neurotoxic (p < 0.0001), but not causing more diabetes (p = 0.64). 15466273: In utero exposure to CsA induced a nephron reduction that led to systemic hypertension and progressive chronic renal insufficiency in adulthood. 15589478: Since the mechanism by which CsA induces hypertension is not well defined, the aim of this study is to evaluate the morphological changes and the expression of heat shock proteins (HSPs) in the thoracic aorta of CsA-treated rats. 15860966: Hyperthyroidism, chronic renal failure, adrenal hyperplasia or tumors, amphetamine, cyclosporine, and anabolic steroids are secondary causes of hypertension associated with gynecomastia. 15919496: While its role in cyclosporine-induced hypertension is minimal, its role in tacrolimus-based immunosuppression has not been defined. 15953621: Even though with those effects, hypertension development was totally prevented, suggesting that peripheral SNS per se cannot fully explain CsA-induced hypertension. Increased vascular reactivity associated with cyclosporin A (CsA)-induced arterial hypertension might result from increased vasoconstriction and/or decreased vasodilatation. 16008590: Experimental models suggest that endothelin-1 (ET-1) has a significant role in the pathogenesis of cyclosporin A (CyA)-induced hypertension. 1602404: The possible role of sympathoadrenal stimulation and endothelin release in cyclosporine (CS)-induced hypertension was ascertained in intact and pithed rats. 16087472: This increase in vasopressin receptor is likely at the base of increased vascular responsiveness to vasoconstrictor hormones and hypertension induced by CsA. 1646670: Peripheral vasoconstriction has been suggested as the pathophysiological mechanism for hypertension and renal failure caused by cyclosporine. 16487261: Taurine attenuates hypertension and renal dysfunction induced by cyclosporine A in rats. These data clearly indicate the protective potential of taurine against CsA-induced hypertension and nephrotoxicity and suggest a significant contribution of its anti-oxidant property to this beneficial effect. 1665405: Mechanisms of cyclosporine-induced hypertension. 16915037: INTRODUCTION: The present study evaluated the contribution of 20-hydroxyeicosatetraenoic acid (20-HETE) and its interaction with nitric oxide (NO) in cyclosporin A-induced nephrotoxicity and hypertension. 17578503: We briefly discuss the possible mechanisms of CsA-induced hypertension in light of this information. The mechanisms of CsA-induced hypertension have not been fully elucidated and are still controversial. We present a case of CsA-induced hypertension who was anuric and receiving hemodialysis, and in whom noninvasive cardiothoracic bioimpedence revealed elevated systemic vascular resistance without evidence of fluid-volume overload. 17595192: CONCLUSIONS: Our results pointed to the thick ascending limb of the loop of Henle as an important site of sodium retention in cyclosporine-induced hypertension. Ciclosporin-induced hypertension is associated with increased sodium transporter of the loop of Henle (NKCC2). BACKGROUND: Hypertension induced by cyclosporine is associated with renal sodium and water retention. This data may have potential clinical implications for the treatment of hypertension induced by cyclosporine. Using immunoblotting of kidney homogenates, we investigated the regulation of sodium and water transport proteins in a rat model of cyclosporine-induced hypertension. 1763210: Nevertheless, its performance originates a number of complications derived from: a) conservation techniques of the organ (in our study a prolonged time of hot ischemia was significantly associated with); b) surgery (all patients who required massive blood transfusions developed metabolic alkalosis); c) the graft itself (all the F 1. degrees were significantly infected), and d) extrahepatic causes (cyclosporin was responsible for high blood pressure and nephrotoxicity which appeared as oliguria with good response to furosemide, as well as hyperglycemia). 17954157: Oxidative stress in cyclosporine-induced hypertension: evidence of beneficial effects or tolerance development with nitrate therapy. 17954158: The present study sought to evaluate the prevention and reversion effects of isosorbide-5-mononitrate (Is-5-Mn) on the development of hypertension (HT) and on the underlying vascular and platelet morphofunctional disturbances, using an animal model of cyclosporine (CsA)-induced HT. Our data suggested that Is-5-Mn therapy may be a valid choice to prevent the morphofunctional changes associated with CsA-induced HT, when used as a preventive therapy. Dual effect of nitrate therapy for cyclosporine-induced hypertension on vascular and platelet morphofunctional markers; an animal model. 18370695: Corticosteroids can induce glucose intolerance, hypertension, hyperlipidemia, and weight gain. Cyclosporine and tacrolimus can induce glucose intolerance, hypertension, and hyperlipidemia. 19091785: Cyclosporine A (CsA) is an efficient immunosuppressant used for reducing allograft rejection but with a severe side effect of causing hypertension. We hypothesize that the renal epithelial sodium channel (ENaC) may participate in CsA-induced hypertension. Since enhanced ENaC activity is known to cause hypertension, these data together suggest that CsA may cause hypertension by stimulating ENaC through a pathway associated with inhibition of ABCA1 and consequent elevation of cholesterol in the cells. 1932642: Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. 1941635: The immunosuppressive drug cyclosporin A (CsA) frequently induces hypertension, but the mechanism(s) is unknown. 1963182: Nephrotoxicity is not a feature of cyclosporine A-induced hypertension in this species. This study reports the use of nisoldipine to investigate the role of Ca2(+)-induced smooth muscle contraction in cyclosporine A-induced hypertension in conscious sheep. 20131116: CONCLUSION: After application of nitroglycerin, sBP is reduced immediately in HTX with uncontrolled cyclosporine-induced hypertension. 2039018: The iatrogenic hypertension induced by cyclosporine resembles a low-renin, salt-sensitive form of essential hypertension, which is often controlled with salt restriction and therapies counteracting renal salt acquisition, e.g., diuretics and calcium channel blockers (CCBs). 2069781: Mechanism of cyclosporine-induced hypertension. 2112669: Although the mechanism of cyclosporin (CsA)-induced hypertension is unknown, it has been shown to inhibit prostacyclin (PGI2) production directly, which may be a factor. Decrease in cyclosporin-mediated prostacyclin production in renal versus carotid arteries: a mechanism for cyclosporin-induced hypertension. 2124478: [Hypertension induced by cyclosporin A in insulin-dependent diabetic patients. A one-year follow-up]. 21298017: To better understand the molecular events associated with cyclosporine induced hypertension, we investigated the effect of cyclosporine on HNF4alpha expression and activity and searched for novel HNF4alpha target genes among members of the RAS cascade. HNF4alpha dysfunction as a molecular rational for cyclosporine induced hypertension. Several mechanism for cyclosporine induced hypertension have been proposed, i.e. activation of the sympathetic nervous system, endothelin-mediated systemic vasoconstriction, impaired vasodilatation secondary to reduction in prostaglandin and nitric oxide, altered cytosolic calcium translocation, and activation of the renin-angiotensin system (RAS). 21434893: CONCLUSIONS: These observations may explain in part the mechanism of cyclosporine-induced hypertension, hyperkalemia and hypercalciuria. 22469912: The purpose of our study was to clarify the mechanisms leading to the evolution of hypertension induced by cyclosporine A (CsA). Our results suggest that the best choice for the pharmacotherapy of hypertension induced by CsA would be calcium channel antagonists. 2269381: However, in 1 patient with rapidly advancing systemic scleroderma a short-term therapy with CS in low doses (2-3 mg/kg body weight) resulted in arterial hypertension and renal dysfunction. 22975291: Previous studies including ours showed that cyclosporine (CSA) causes baroreflex dysfunction and hypertension. 2316699: These observations indicate that cyclosporin modifies vascular responsiveness to pressor stimuli in the rat and may explain the relative resistance of this species to cyclosporin-induced hypertension. 23331314: Its etiology has been attributed to renal failure, immunosuppressive drugs such as cyclosporine and tacrolimus, and other potential entities leading to acute hypertension. 23809336: Cyclosporin A (CsA) is a widely used immunosuppressive agent that also causes hypertension. However, the molecular basis for CsA-induced hypertension remains elusive. Furthermore, this organ culture system would be an ideal in vitro tool to study the molecular mechanisms of CsA-induced hypertension. 2388667: CONCLUSIONS: Cyclosporine-induced hypertension is associated with sympathetic neural activation, which may be accentuated by the cardiac denervation that results from heart transplantation. METHODS: To determine whether cyclosporine-induced hypertension is accompanied by sustained sympathetic neural activation in patients, we recorded sympathetic action potentials using intraneural microelectrodes (in the peroneal nerve) in heart-transplant recipients receiving azathioprine and prednisone alone (n = 5) or in combination with cyclosporine (n = 14). 2405549: Cyclosporine-induced hypertension in sheep. We have previously shown that administration of intravenous CsA to sheep for 5 days at 12 mg/kg/day produces a hypertension that is resistance mediated and independent of nephrotoxicity. 24507957: The calcineurin inhibitor tacrolimus is diabetogenic by inhibiting insulin secretion, whereas cyclosporine causes hypertension and increases cholesterol levels. 2457762: Pressor response to graded infusion of angiotensin II, noradrenaline, arginine-vasopressin, and serotonin and blood pressure change following indomethacin, an inhibitor of cyclooxygenase, were examined in conscious sheep, before and during the development of cyclosporin A-induced hypertension. 2475720: Cyclosporin-induced hypertension in marmosets: a new model of hypertension sensitive to angiotensin-converting enzyme inhibition. 25280976: BACKGROUND: Cyclosporine (CsA) is frequently responsible for hypertension in bone marrow transplant children. CONCLUSIONS: Because lacidipine appears to have no effect on CsA exposure, it may be the best option among CCBs for treating high blood pressure caused by CsA in children. 2538392: Arterial hypertension is a common side effect of cyclosporine A therapy; however, the cellular mechanism of cyclosporine A-induced hypertension is still unknown. 25418335: The mechanisms of CsA-induced hypertension and nephrotoxicity are not clear, but several studies suggest the possible involvement of free radicals. 25430438: Central modulation of cyclosporine-induced hypertension. 25772258: However, the exact molecular mechanisms of CsA-induced hypertension remain obscure. 2651756: The present study was undertaken to study the mechanism of cyclosporine-induced nephrotoxicity and hypertension. 26721374: The elucidation of these mechanisms may permit the identification of new therapeutic strategies against CsA-induced hypertension. 2692366: Possible etiological factors of cyclosporine (CyA) induced hypertension were investigated in 10 bone marrow transplanted (BMT) patients followed during one week before and 3 weeks after transplantation. 2708808: Hypertension induced by cyclosporine may, in part, be explained by a reduction in relaxation of peripheral resistance vessels. 27358055: The epoxyeicosatrienoic acid analog PVPA ameliorates cyclosporine-induced hypertension and renal injury in rats. 27567631: Cyclosporine A (CsA) induces hypertension after transplantation. 27701056: RESULTS: Concurrent nebivolol treatment significantly attenuated CsA-induced hypertension, impairment of renal functions, oxidative stress and restored the balance in renal NO system with lowering of the elevated ADMA. 28584011: Regulatory T-Cell Augmentation or Interleukin-17 Inhibition Prevents Calcineurin Inhibitor-Induced Hypertension in Mice. The immunosuppressive calcineurin inhibitors cyclosporine A and tacrolimus alter T-cell subsets and can cause hypertension, vascular dysfunction, and renal toxicity. Daily treatment of mice with cyclosporine A or tacrolimus for 1 week significantly decreased CD4+/FoxP3+ regulatory T cells in the spleen and lymph nodes, as well as induced hypertension, vascular injury and dysfunction, and glomerular mesangial expansion in mice. 29133357: We hypothesized that augmenting MDSCs would ameliorate the CsA-induced hypertension and vascular and renal injury and dysfunction and that CsA reduces MDSCs in mice. Myeloid-Derived Suppressor Cells Ameliorate Cyclosporine A-Induced Hypertension in Mice. These data suggest that augmenting MDSCs can reduce the cardiovascular and renal toxicity and hypertension caused by CsA. Daily interleukin-33 treatment, which increased MDSC levels, completely prevented CsA-induced hypertension and vascular and renal toxicity. 2954283: This study shows that despite the hypertension induced by cyclosporine, myocyte hypertrophy at 3 years posttransplantation does not appear to be significantly greater than in patients treated with conventional immunosuppression. 2973223: Left ventricular hypertrophy in cyclosporine-induced systemic hypertension after cardiac transplantation. 29933079: Treatment of cyclosporine induced hypertension: Results from a long-term observational study using different antihypertensive medications. 30658157: Upregulation of cystathionine-gamma-lyase/hydrogen sulfide pathway underlies the celecoxib counteraction of cyclosporine-induced hypertension and renal insult in rats. 31109455: These data suggest that elevation of intracellular Cho due to blockade of ABCA1 stimulates ENaC, which may contribute to CsA-induced hypertension. Intracellular cholesterol stimulates ENaC by interacting with phosphatidylinositol-4,5-bisphosphate and mediates cyclosporine A-induced hypertension. 3510494: Cyclosporine is known to cause hypertension, and we have recently reported that it causes hypomagnesemia and renal magnesium wasting in marrow transplant recipients. 7490151: We have previously shown that endothelin release from the arteries is increased in rats with cyclosporine-induced hypertension. The specific ETA receptor antagonist FR 139317 may prevent the hypertension induced by cyclosporine. Effects of an endothelin receptor antagonist in rats with cyclosporine-induced hypertension. 7594425: Cyclosporin-induced hypertension occurred in the absence of any change in urinary sodium output or in plasma endothelin. CONCLUSIONS: Cyclosporin-induced hypertension and renal vasoconstriction are well established after 9 days of cyclosporin 5 mg/kg twice a day. OBJECTIVE: To elucidate the sequential mechanisms underlying cyclosporin-induced hypertension and nephrotoxicity. We found no evidence to implicate either circulating endothelin or renal sodium retention in the onset of cyclosporin-induced hypertension. 7688670: Cyclosporine A (CsA)-induced hypertension appears to be caused in part by neurogenic vasoconstriction, but the mechanism by which CsA activates the sympathetic nervous system is unknown. 7697504: A side-effect of CSA is that it induces hypertension and perturbs the lipid profile of transplant recipients. 7814851: CONCLUSION: The reduction in intrarenal prostaglandins clearly played a key role in the development of cyclosporin-induced renal vasoconstriction, but we could not demonstrate a role for prostaglandins or for sodium retention in the initiation of cyclosporin-induced hypertension. 7967781: CONCLUSION: Recognition and treatment of CSA-induced hypertension and vascular injury are important elements in managing the transplant recipient. Cyclosporine-induced hypertension after transplantation. 8007592: We have studied the sequential effects of cyclosporine during the first four days after its initiation in an effort to elucidate the primary and secondary events in the pathogenesis of cyclosporine induced nephrotoxicity and hypertension. Our data show that cyclosporine induced hypertension in the initial stages is not sodium dependent, and that changes in renal water handling were not dependent on alterations in the glomerular filtration rate or effective renal plasma flow. 8021902: The cardiac adaptation to cyclosporine-induced hypertension has more severe concentric left ventricular hypertrophy and impaired left ventricular systolic performance. We studied cardiovascular adaptation to cyclosporine-induced hypertension by determining haemodynamic and echocardiographic indexes in 25 cardiac transplant recipients matched by mean arterial pressure, age, sex, height and weight to 25 patients with established essential hypertension. Cardiovascular adaptation to cyclosporine-induced hypertension. 8076427: These results suggest that the mesenteric vascular RAS does not play a major role in CsA-induced hypertension in the rat. Since plasma renin activity is increased in cyclosporin A (CsA)-induced hypertension in the rat, the role of the vascular renin-angiotensin system (RAS) in CsA-induced hypertension was investigated in rat mesenteric resistance vessels. Vasoconstrictor responses to components of the renin-angiotensin system in cyclosporin-induced hypertension in the rat. 8181542: These results raise a possibility that the up-regulation of endothelial angiotensin AT1A receptors participates in the pathogenesis of cyclosporine induced hypertension. 8182156: Numerous studies have explored the pathogenesis of cyclosporin A (CysA)-induced hypertension; however, none has assessed the impact of CysA treatment on resistance arteries in the setting of elevated blood pressure. We conclude that CysA-induced hypertension is the consequence of a primary effect on resistance vessel relaxation, not increased vasoconstriction, as previously suggested. Vascular mechanisms of cyclosporin-induced hypertension in the rat. 8222166: Cyclosporine-induced hypertension. BACKGROUND: Cyclosporine-induced hypertension may be related to vasoconstriction of the afferent arterioles in the glomeruli caused by changes in the prostaglandin profile. omega-3 Fatty acids have demonstrated vasodilatory properties related to a favorable effect in the prostaglandin profile. 8246369: Both cyclosporine and prednisone can cause hypertension. The higher the dose of either drug, the more likely they will cause hypertension. 8282363: Cyclosporine induces hypertension and wide-spread vasoconstriction after transplantation in addition to reducing kidney function. 8301102: CONCLUSIONS: Our findings contradict previous data and currently held views regarding the pathogenesis of cyclosporin-induced hypertension. Cyclosporin-induced hypertension precedes renal dysfunction and sodium retention in man. 8306543: Hormonal and other mechanisms involved in the pathogenesis of cyclosporin-induced nephrotoxicity and hypertension in man. 8382242: Effects of the blockade of the renin-angiotensin system in cyclosporin-induced hypertension. OBJECTIVE: To compare the acute hypotensive effects of three different methods of inhibiting the renin-angiotensin system in a primate model of cyclosporin-induced hypertension. 8394783: Cyclosporine therapy after cardiac transplantation causes hypertension and renal vasoconstriction without sympathetic activation. 8397889: Cyclosporin-induced hypertension, hyperlipidaemia, hyperkalaemia and hyperuricaemia are generally responsive to appropriate dietary restrictions and pharmacological therapies. 8512668: We propose that cyclosporine-induced hypertension may be due to an increased synthesis of ET-1 in the resistant vessels. 8564450: This article reviews the current state of knowledge concerning cyclosporine A-induced hypertension after heart transplantation, its pathophysiology and management. 8586834: OBJECTIVE: To investigate the role of the renin-angiotensin-aldosterone system as a homoeostatic mechanism by examining whether mild activation of the renin-angiotensin-aldosterone system could enhance cyclosporin-induced renal vasoconstriction and hypertension. 8641746: Cyclosporine-induced hypertension is a major problem in transplant therapy. These data provide further evidence to support a role for endothelin in cyclosporine-induced hypertension and demonstrate the effectiveness of endothelin receptor antagonism as a novel treatment in cyclosporine-induced hypertension. 8771507: Furthermore, because all heart transplant recipients received cyclosporine A, the findings do not support the concept that cyclosporine-induced hypertension is mediated by increased sympathetic nerve activity. 8783602: Dietary salt aggravates cyclosporin A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats: protection by oral magnesium supplementation. 8837316: It is concluded that 5-HT may play a role in the development of hypertension and thrombotic events caused by CyA. The aim of this study was to investigate the mechanism of hypertension and thromboembolic events induced by cyclosporin (CyA) and tacrolimus (FK506) in respect to their action on the serotonergic blood system. 8931845: The immunosuppressant drug cyclosporine A (CsA) has emerged as an important new cause of hypertension in both organ transplant recipients and patients with autoimmune diseases. This article presents a conceptual framework for understanding the pathophysiologic basis of CsA-induced hypertension and focuses on the hypothesis that a common molecular mechanism is involved in mediating the immunosuppressive and the hypertensive effects of CsA. Sympathetic neural mechanisms of cyclosporine-induced hypertension. 9029741: Although several studies have produced promising results, nephrotoxicity and hypertension can result from CyA treatment, and their development must be understood in order to facilitate patient management. 9052902: Effects of dietary sodium and magnesium on cyclosporin A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats. 9072458: Cyclosporine A-induced hypertension in SHR and WKY: role of the sympatho-adrenal system. It is concluded that immunosuppressive agents like cyclosporine or FK506 activate the sympatho-adrenal system in normotensive and genetically hypertensive rats, thereby inducing hypertension. Depletion of catecholamine stores by reserpine also diminished significantly the cyclosporine induced hypertension. Selective alpha1-adrenergic receptor blockade by prazosin blunted acute hypertension induced by cyclosporine. 9112363: Isradipine, a calcium channel entry blocker, has been used successfully in cyclosporine-induced hypertension. 9112676: It is concluded that serotonin may play a role in the development of hypertension caused by CsA. The aim of this study was to investigate the mechanism of cyclosporine-induced hypertension in respect to its action on blood serotonergic system. 9116920: The present study aimed to evaluate whether elevated blood pressure and insulin resistance coexist during CsA therapy to prove the similarity between essential hypertension and CsA induced hypertension. OBJECTIVES: Essential hypertension and insulin resistance frequently coexist; cyclosporine A (CsA) is known to induce hypertension which has been used as a model for essential hypertension. CONCLUSIONS: CsA therapy induces elevated blood pressure and insulin resistance as seen in patients with essential hypertension, thus CsA induced hypertension is considered to have pathophysiological similarities to essential hypertension. 9137231: BACKGROUND: Cyclosporine-induced hypertension is probably related to endothelial dysfunction. 9198362: These results suggest that CyA-induced hypertension is characterized by the loss of nocturnal decline in blood pressure, which is accompanied by volume retention after 1 week and systemic vasoconstriction after 4 weeks. 9229291: Cyclosporine-induced hypertension: evidence for maintained baroreflex circulatory control. CONCLUSIONS: These data indicate that (1) cyclosporine-induced hypertension in heart transplant recipients is associated with a loss of baroreflex function as a result of cardiac denervation-related uncoupling; (2) compared with patients with hypertension, organ transplant recipients with hypertension demonstrated a maintained baroreflex function as indicated by a lack of reduction of the index alpha; (3) baroreflex heart rate control in dihydropyridine-treated cyclosporine-induced hypertension is well maintained. 9263649: Several mechanisms, including endothelin-mediated systemic vasoconstriction, impaired vasodilatation secondary to reduction in nitric oxide, and altered cytosolic calcium translocation, have been proposed to underlie cyclosporine-induced hypertension. Hemodynamic features of cyclosporine-induced hypertension consist of elevated peripheral vascular resistance, ventricular vascular uncoupling contributing to left ventricular hypertrophy, and abnormalities in the diastolic function of the allograft. 9356601: Calcium antagonists have been particularly effective in managing hypertension induced by cyclosporine. 9356603: Cyclosporine-induced hypertension occurs in more than 90% of patients following cardiac transplantation. This article underlines the clinical characteristics as well as the mechanisms that can be associated with the development of cyclosporine-induced hypertension. Cyclosporine-induced hypertension in cardiac transplantation. 9393945: The mechanisms by which the immunosuppressive drug cyclosporine A (CsA) induces hypertension and nephrotoxicity are still not fully understood. 9462627: Selective impairment of endothelium-mediated vasodilation in liver transplant recipients with cyclosporin A-induced hypertension. 9468460: Cyclosporine-induced hypertension and decline in renal function in healthy volunteers. Thus, the present study confirms and extends earlier observations that renal dysfunction and sodium retention are not the initiating events in CsA-induced hypertension. 9557926: OBJECTIVE: To determine whether cyclosporine A-induced hypertension in renal transplant recipients is accompanied by impairment of endothelium-dependent vasodilatation, which has been suggested by in-vitro and in-vivo animal experiments. Our results do not support the hypothesis that attenuation of endothelial vasodilator functioning contributes to the development of cyclosporine A-induced hypertension. CONCLUSIONS: Our data indicate that cyclosporine A-induced hypertension in renal transplant recipients is not accompanied by an increase in forearm vascular resistance. 9617750: Role of endothelin ET(A) receptors in the hypertension produced by 4-day L-nitroarginine methyl ester and cyclosporine treatment. 9690215: However, CsA can cause nephrotoxicity and hypertension (HTN). Depressed renal and vascular nitric oxide synthase expression in cyclosporine-induced hypertension. These observations suggest that CsA-induced HTN may be, in part, related to impaired NO production. This study was designed to test the hypothesis that CsA-induced HTN is related to depressed nitric oxide (NO) production. 9822443: Cyclosporine A (CsA) is an immunosuppressive agent that also causes hypertension. 9883706: Cyclosporin-induced hypertension is a major complication of immunosuppression in transplant recipients but its pathophysiology is only partly understood. We examined the effects of: (1) nitric oxide enhancement with L-arginine administration and antagonism with N-nitro-L-arginine; and (2) chronic endothelin receptor blockade with the non-peptide endothelin receptor antagonist, bosentan, in two animal models of cyclosporin-induced hypertension. These results support the roles of both increased endothelin synthesis and decreased nitric oxide activity in the pathogenesis of cyclosporin A-induced hypertension. 9889429: Long-term efficacy and adverse event of nifedipine sustained-release tablets for cyclosporin A-induced hypertension in patients with psoriasis. 15247418: To determine whether mtDNA mutations contribute more generally to the etiology of AD, we have investigated the sequence of the mtDNA control region (CR) from AD brains for possible disease-causing mutations. 16408223: We report here the analyses of complete mtDNA coding region sequences from more than 270 Alzheimer's disease (AD) patients and normal controls to determine if inherited mtDNA mutations contribute to the etiology of AD. 16886726: Mitochondrial DNA in pathogenesis of Alzheimer's and Parkinson's diseases. 20798880: In this review we discuss the role of the mitochondria, and especially of the mtDNA, in the cascade of events leading to neurodegeneration, dementia, and AD. 21925769: Future research is needed to clarify the role mtDNA deletions have in normal aging and investigate the relationship between mtDNA deletions and the pathogenesis of sporadic AD. 22442439: OBJECTIVE: Although several studies have described an association between Alzheimer disease (AD) and genetic variation of mitochondrial DNA (mtDNA), each has implicated different mtDNA variants, so the role of mtDNA in the etiology of AD remains uncertain. 26881032: In conclusion these data confirmed peripheral mitochondria impairment in AD and demonstrated that TFAM and mtDNA amount reduction could be two features of early events occurring in AD pathogenesis. 33221353: The current review will focus on alterations and variation in mitochondria/mitochondrial DNA (mtDNA) and the rationale for involvement of related abnormalities in pathogenesis of AD. 8937782: There is increasing evidence for a role of defects of mitochondrial DNA in the etiology of neurodegenerative disorders such as Parkinson's and Alzheimer's disease as well as in normal aging. 10070137: Inhibition of cytochrome P-450 (CYP450) enzymes with cobalt chloride (CoCl2) prevented hypertension, organ hypertrophy, and renal injury induced by DOCA and salt (1% NaCl) in uninephrectomized (UNx) rats. 10861964: Blood pressure depression by the fruit juice of Carica papaya (L.) in renal and DOCA-induced hypertension in the rat. 13204839: [Effect of ascorbic acid, of cortisone, and of adrenalectomy on experimental hypertension produced by DOCA]. 13879964: [The action of 4-hydroxy-17alpha-methyltestosterone on \DOCA-induced hypertension\)]. 15934023: The aqueous extract from Berberis vulgaris fruit (B.V.) was tested to evaluate its antihypertensive effects on DOCA-induced hypertension in the rats. 16857894: In DOCA-salt rats, the time course of the synergistic interaction between osmolality and DOCA to produce hypertension is unknown. 25443088: The rat model was produced by deoxycorticosterone-acetate (DOCA; Sigma Aldrich, St. Louis, MO, USA) induced hypertension and a single injection of elastase into the basal cistern. 28942103: Antagonist of thromboxane A2 receptor by SQ29548 lowers DOCA-induced hypertension in diabetic rats. 2951040: These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, and cardiac hypertrophy in rats. 4553293: [Kidney function in rats with experimental DOCA-induced hypertension]. 5070095: [Effect of propranolol on DOCA-induced experimental hypertension in rats]. 5544582: Uptake of ferritin in rat kidney stimulated by renal and DOCA-induced hypertension. 6102922: A study on the effects of some drugs on DOCA induced hypertension in the rat. 7068182: These results are consistent with the observed enhancement of net Na+ transport in incubated arteries in DOCA-induced hypertension and in the SHR but do not account for the increased Na+ permeability observed in these states. 7250299: Recognising on the one hand the interaction between the coagulation system and the vessel wall and on the other hand the fibrinolysis-blocking properties of EACA, it can be assumed that derangements of the coagulation system are aetiologically involved i hypertension induced by salt/DOCA. The development of hypertension induced by DOCA/salt in rats can be reduced by epsilon-aminocaproic acid. 743619: Evidence for enhanced Na transport in hypertension induced by DOCA in the rat. 9228552: Infusion of ebelactone B, (a selective inhibitor of carboxypeptidase Y-like exopeptidase, a kininase in rat urine), to normal BN-Ki rats during induction of hypertension with DOCA and salt, resulted in the reduction of the raised blood pressure, indicating that a site of action of kinins was at the luminal membrane of the renal tubule cells. 10465060: In humans, with ageing and hypertension, the arteries stiffen as a result of progressive degeneration of the arterial media, increased collagen and calcium content, and dilation and hypertrophy of large arteries and the aorta. 10720885: An increased neural source of endothelin in the SHR may contribute to the development of hypertension or may be a consequence of selective degenerative change. 11452332: Increased elastance (or stiffness, inverse of compliance) of the central elastic arteries is the primary cause of increased systolic and pulse pressure with advancing age and in patients with cardiovascular disease, including hypertension, and is due to degeneration and hyperplasia of the arterial wall; diastolic pressure decreases as arterial elastance increases. 11593105: Role of AT1 and AT2 receptor subtypes in salt-sensitive hypertension induced by sensory nerve degeneration. OBJECTIVE: To define the role of the type 1 angiotensin II (AT1) and type II (AT2) receptors in the development of salt-sensitive hypertension induced by sensory nerve degeneration. 11882629: To determine the role of endothelin-1 (ET-1) and its receptors in salt-sensitive hypertension induced by sensory nerve degeneration, selective ET(A) antagonist (ABT-627) and ET(B) antagonist (A-192621) were used. We conclude that blockade of the ET(A) receptor prevents the development of salt sensitive hypertension induced by sensory nerve degeneration, indicating that activation of the ET(A) receptor by increased plasma ET-1 level contributes to elevation of blood pressure in this model. Function and regulation of endothelin-1 and its receptors in salt sensitive hypertension induced by sensory nerve degeneration. 15569407: CONCLUSIONS: Regardless of increased vascular MnSOD levels, salt sensitive hypertension induced by sensory degeneration is associated with increased vascular superoxide production. AIM: To test the hypothesis that production of superoxide in mesenteric resistance arteries is increased and contributes to the development of hypertension induced by sensory denervation plus high salt intake. 15929825: CONCLUSION: Valsartan or Plendil could prevent the development of salt-sensitive hypertension induced by sensory denervation and the overloading of intracellular [Ca(2+)](i), which indicated that salt-sensitive hypertension induced by sensory nerve degeneration might be related to renin-angiotensin-aldosterone system (RAAS) and the over loading intracellular [Ca(2+)](i), and might be more closely to RAAS. 15994858: ET(A) receptor blockade prevents renal dysfunction in salt-sensitive hypertension induced by sensory denervation. Therefore, the blockade of the ET(A) receptor ameliorates the impairment of renal excretory function and prevents the elevation in blood pressure in salt-sensitive hypertension induced by degeneration of sensory nerves, indicating that the activation of the ET(A) receptor impairs renal function and contributes to the development of a salt-induced increase in blood pressure in this model. 20590524: Chronic hypertension and cerebral amyloid angiopathy (CAA) are the main pathologies which can induce the rupture of cerebral vessels and intracerebral hemorrhages, as a result of degenerative changes in the vascular wall. 2112657: It is concluded that marked degenerative changes in the vessels due to Fabry's disease might be the principal etiology of hypertension and rapid deterioration of renal function. 36487: Experimental central hypertension produced by chemical degeneration of the locus coeruleus in the rat. 7913956: These results implicate a selective degeneration by hypothalamic PVN cells in the pathogenesis of hypertension. 10668988: Two of the most prevalent neurologic disorders that result from degeneration are Alzheimer's and Parkinson's diseases. 11793352: The long-held belief that degeneration of the cholinergic basal forebrain was central to Alzheimer's disease (AD) pathogenesis and occurred early in the disease process has been questioned recently. 12476348: Studies of the pathogenic actions of mutations in presenilins and amyloid precursor protein that cause early-onset familial AD have established central roles for perturbed cellular calcium homeostasis and oxidative stress in the neurodegenerative process. The clinical presentation of patients with AD is dominated by cognitive deficits and emotional disturbances that result from dysfunction and degeneration of neurons in the limbic system and cerebral cortex. 1508410: Alzheimer's, Parkinson's, and Huntington's diseases present unique constellations of behavioral and neurological abnormalities which result from the degeneration of neurons in specific regions of the brain. 15190683: While glutamatergic transmission is severely altered by early degeneration of cortico-cortical connections and hippocampal projections in Alzheimer's disease (AD), the role of glutamate receptors in the pathogenesis of AD is not yet defined clearly. 16125326: Alzheimer disease is regarded as a disorder of neural input modulation caused by the degeneration of four modulatory amine transmitter (MAT) systems, namely the serotoninergic, the noradrenergic, the histaminergic, and the cholinergic systems with ascending projections. 16404228: In Alzheimer's disease, the posterior cingulate cortex itself shows little neuropathologic degeneration, and a hypothesis explaining such a discrepancy is that the functional impairment in the posterior cingulate cortex reflects remote effects caused by degeneration in distant but connected areas, such as the entorhinal cortex. 16963164: We conclude that the intraneuronal accumulation of Abeta-amyloid peptides is followed by axonal degeneration, and thus might be a causative factor for the axonal changes seen in AD. 17378753: They suggest that degeneration of microglia is a factor in the pathogenesis of AD. 1776729: As elucidation of the reasons behind amyloid deposition must shed some light on the pathogenesis of AD, we review the current state of knowledge on the nature of the AD amyloid protein, its origin, and its formation. At the cellular level, Alzheimer's disease (AD) must be the result of neuronal dysfunction and degeneration leading to a reduction in synaptic density. 18569738: We describe a 56-year-old woman with Alzheimer's disease with left hemispatial neglect and left homonymous hemianopsia with macular sparing considered a manifestation of Alzheimer's disease resulting from severe degenerative change in the right primary visual cortex. 19718893: The different organs age in different ways: vessel walls become rigid due to protein glycation and develop atheroma; the heart is invaded by fibrosis; the brain suffers from neurofibrillar degeneration and senile plaques (responsible for Alzheimer's disease); the retina undergoes macular degeneration; renal function declines in parallel with the fall in the glomerular filtration rate due to a gradual decrease in the nephron pool; and immune defenses become less effective due to the functional degradation of B and T lymphocytes and thymus involution. 20032460: Synaptic degeneration, including impairment of synaptic plasticity and loss of synapses, is an important feature of Alzheimer disease pathogenesis. 20575007: These data support the idea that by inducing degeneration of the DG, GSK3beta could be involved in the pathogenesis of AD. 20698821: Numerous studies have indicated that Alzheimer's amyloid-beta protein (Abeta) causes the degeneration of synapses and neurons, finally inducing the pathogenesis of Alzheimer's disease (AD). 20858975: When considering degeneration (ratio to synaptophysin and the post-synaptic marker PSD95), GR expression was similar between controls and AD, suggesting that GR loss was due to synaptic degeneration in AD. 21460623: Genetic, molecular and biochemical evidence indicates that the accumulation of toxic Abeta aggregates plays a critical role in the degeneration of neurons during the pathogenesis of Alzheimer disease (AD). 23670960: Degeneration of the corpus callosum (CC) is evident in the pathogenesis of Alzheimer's disease (AD). 2412232: Degeneration of cholinergic neurons from the basal forebrain nuclei is suspected to be the cause of Alzheimer disease. 2463283: In SDAT, there is a primary loss of cholinergic neurons compounded by a secondary reaction of the remaining cholinergic neurons to the terminal degeneration in the cortex. 25045655: Since synaptic dysfunction and degeneration are early events during the pathogenesis of AD, we aim to investigate the effects of testosterone on oligomeric Abeta-induced synaptic changes. 25512503: The dementia of Alzheimer's disease (AD) results primarily from degeneration of neurons that furnish glutamatergic corticocortical connections that subserve cognition. 2582270: These neurones have previously been shown to respond to substance P3 and are analogous to the nucleus basalis of Meynert in man, which gives a diffuse projection to the cerebral cortex and whose degeneration is the likely cause of Alzheimer's disease. 26025658: The progressive cognitive decline that is associated with Alzheimer's disease has been mainly attributed to a deficit in cholinergic neurotransmission due to the continuous degeneration of cholinergic neurons e.g. in the basal forebrain. 26415025: Progressive degeneration and death of neurons are main causes of neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. 2655587: Alzheimer's disease results from the degeneration of neurons. 26608462: Neurological diseases such as Alzheimer's and Parkinson's diseases are incurable progressive neurological disorders caused by the degeneration of neuronal cells and characterized by motor and non-motor symptoms. 26981406: One of the primary hallmarks of the neuropathological disease is the accretion of amyloid beta peptide in the brain that leads to Alzheimer's disease, but the mechanism is still a mystery. Alzheimer's disease is the prevalent cause of premature senility, a progressive mental disorder due to degeneration in brain and deposition of amyloid beta peptide (1-42, a misfolded protein) in the form of aggregation that prevails for a prolonged time and obstructs every aspect of life. 27023706: AD manifests by progressive decline in cognitive functions and alterations in behaviour, which are the result of the extensive degeneration of brain neurons. 2742360: Insomnia associated with progressive supranuclear palsy appears to be worse than the insomnia of Parkinson's disease or Alzheimer's disease and may be due to degenerative changes in brain structures responsible for sleep maintenance. 27458373: The dysfunction of neurogenesis and increased degeneration of neurons contribute to the pathogenesis of AD. 28133526: OBJECTIVES: Alzheimer's disease (AD) as progressive cognitive decline and the most common form of dementia is due to degeneration of the cholinergic neurons in the brain. 28265241: In association with the amyloid deposits, increasing impairments in learning and memory as well as the degeneration of neurons especially in the hippocampus formation are hallmarks of the pathogenesis of AD. 28671131: Thus, the olfactory activation deficits present in AD and MCI patients are most likely caused by degeneration of the central olfactory nervous system. 29602022: Alzheimer's disease (AD) is a severe neurodegenerative disorder characterized by loss of memory and reduction in cognitive functions due to progressive degeneration of neurons and their connections, eventually leading to death. 30524269: Conclusion: The HPA axis may play a crucial role in synaptic degeneration in AD pathogenesis. 30528858: Synaptic degeneration is central in Alzheimer's disease (AD) pathogenesis and biomarkers to monitor this pathophysiology in living patients are warranted. 31117343: This excellent piece of work identifies a potent hexapeptide, which has exceptional ability to protect neurons as well as microtubule from degeneration and may become potent therapeutics against AD pathogenesis in the future. 31507373: Alzheimer's disease (AD) is the most common type of dementia which characterized by a progressive loss of memory and cognitive function due to degeneration of synapses and axons. Till now, it is far from clear what role autophagy plays in AD, a causative role, a protective role, or just a consequence of the disease process itself. 31605783: Alzheimer's disease (AD) is a progressive dementia caused by degeneration of the central nervous system with a high incidence in the elderly. 34590507: Neurodegenerative disorders such as Alzheimer's Disease (AD) and Parkinson's Disease (PD), have been majorly resulted due to degeneration of neurons and neuroinflammation progressively. 7143014: Is the loss of cerebral cortical choline acetyl transferase activity in Alzheimer's disease due to degeneration of ascending cholinergic nerve cells. 7509608: A substantial body of literature has suggested that the memory and learning deficits associated with Alzheimer's disease are attributable to degeneration of the cholinergic magnocellular neurons of the nucleus basalis of Meynert (nbM). 9111743: Pathological comparison between cases with Alzheimer-type dementia (ATD) and the non-demented cases with infarct showed that hippocampal atrophy in ATD could be caused mainly by degeneration of the stratum lacunosum-radiatum rather than neuronal loss in the pyramidal layer of the hippocampus, and that degeneration of the stratum lacunosum-radiatum could be secondary mainly to the entorhinal cortical degeneration. 9527715: These findings led to consider cholinergic deficit as the main disturbance in AD, due to degeneration of presynaptic cholinergic neurons, and that replacement of acetylcholine could restore the cognitive alterations characteristic of AD. 9619150: OBJECTIVE: Diffuse brain atrophy is one of the gross pathological features of Alzheimer's disease and is a result of degenerative changes. 9632306: The system may eventually be applicable to the development of pharmaceutical agents that interfere with formation and/or degeneration of PHF-tau in Alzheimer's disease. 9794144: The particular contribution of muscarinic receptors, beta-amyloid and tau proteins in the pathogenesis of Alzheimer's disease remains still unclear. Probably Alzheimer's disease could be due to a progressive degeneration in the relationship between the three components covered in this review. 9854137: Alzheimer's disease, the most common form of senile dementia, affects more than 15 million people world-wide and is characterized by a marked deterioration in memory and all cognitive functions, as a result of a progressive degeneration and loss of cortical and limbic neurons. 10867221: Alzheimer's disease (AD) and cerebrovascular dementia (CVD) are two major causes of senile dementia in elderly individuals. 12480441: Different forms of dementia are now distinguished-Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, and dementia secondary to disease, such as AIDS dementia. 15608634: A central unresolved problem in research on Alzheimer disease is the nature of the molecular entity causing dementia. 16037976: These results suggest that the activation of this enzyme occurs early in the course of AD, before the onset of overt dementia, thereby implicating 12/15LOX-mediated lipid peroxidation in the pathogenesis of AD. 16046825: They are consistent with the hypothesis that brain hypoperfusion contributes to dementia, possibly to AD pathogenesis, and raise the possibility that the APOE allele epsilon 4 contributes directly to heart valve and myocardial damage. 16092095: PD-dementia (PDD) and dementia with Lewy bodies (DLB) are second to Alzheimer's disease in causing degenerative dementia in the elderly. 16401890: BACKGROUND: Although QOL is an important indicator to assess multiple facets of life, the QOL of Alzheimer's disease (AD) subjects with impaired cognitive ability due to dementia has not yet been fully investigated. 17143085: Significant changes in personality are typically associated with frontotemporal lobar degeneration (e.g., slowly progressive sociopathy), Alzheimer's disease, mild cognitive impairment due to incipient dementia or underlying medical illness. 18041446: At present, different forms of dementia are distinguished, including Alzheimer's disease (AD), dementia with Lewy bodies, frontotemporal dementia, and dementia secondary to diseases, such as AIDS dementia. 19672571: Homonymous visual field disorders, impaired elementary visual capacities (e.g. acuity, contrast sensitivity, convergent fusion, oculomotor disorders), visual neglect, Balint-Holmes syndrome or dementia (e.g. Alzheimer's disease) are the most frequent causes of such disorders. 20596916: Various innovative diagnostic methods for Alzheimer's disease (AD) have been developed in view of the increasing prevalence and consequences of later-life dementia. 21542885: The clinical and scientific study of dementia in adults with Down syndrome led to the development of the amyloid hypothesis as a fundamental concept in Alzheimer's disease pathogenesis. 22492589: The ROSA and four standard instruments -- the Alzheimer's disease Assessment Scale-cognitive (ADAS-cog), Severe Impairment Battery (SIB), Disability Assessment for Dementia (DAD), and the Neuropsychiatric Inventory (NPI) -- were used in an open-label, multicenter, single-arm clinical study to assess treatment-induced changes in cognitive, functional, and behavioral symptoms in patients with AD at different severity stages. 22574282: Alzheimer's disease (AD), the most common form of dementia, is an age-dependent progressive neurodegenerative disorder. beta-amyloid, a metabolic product of the amyloid precursor protein (APP), plays an important role in the pathogenesis of AD. 23100439: Alzheimer's disease (AD) is the most common progressive neurodegenerative disorder causing dementia. 23338285: Dementia in 2012: Further insights into Alzheimer disease pathogenesis. 23707728: The clinical syndrome of dementia has several aetiologies of which Alzheimer's disease (AD) is the most common. 23828739: Therefore, a disorder primarily affecting structures in medial temporal lobe, with accumulation of amyloid beta and abnormal tau, neuritic plaques and tangles, progressive loss of memory and/or other cognitive deficits, ultimately resulting in dementia should be classified as AD. Alzheimer's disease (AD), the most prevalent disorder causing dementia, is considered a neurodegenerative disease. 24505903: 30 % of the cases are wrongly diagnosed with Alzheimer, being in fact other forms of dementia, or that we deal with several biologic processes, generating rather an Alzheimer's syndrome, meanwhile others are unsatisfied by a poor diagnosed disease and its popular receipt as a part of the normal aging process. 25083748: Alzheimer's disease (AD) is the most prevalent form of dementia, and aggregation of amyloid beta-proteins (Abeta) into soluble oligomers and fibrils has been implicated in the pathogenesis of AD. 25435921: The aim of this study was to examine the relation between AD pathologies and early death in AD caused by dementia. 2545826: The relatively small difference in the prevalence of Lewy bodies between controls and Alzheimer's disease could be explained by the additive effects of Lewy body and tangle pathology causing dementia, rather than a greater than chance association between Parkinson's disease and Alzheimer's disease. 26161148: Emerging evidence for the potential co-contributions of small vessel vasculopathy to dementia has resulted in a more nuanced view of Alzheimer's disease (AD) pathogenesis. 26862951: Molecular alterations in ITM2B are associated with 2 neurodegenerative diseases, Familial British and Danish dementia, and dysregulation of ITM2B function has been implicated in the pathogenesis of Alzheimer disease (AD). 26882509: BACKGROUND AND AIMS: Caregivers of individuals with neurodegenerative diseases, including frontotemporal dementia (FTD), Lewy body dementia (DLB), and Alzheimer's disease (AD), experience high levels of psychological and physical stress, likely due to behavioral and psychological symptoms of dementia (BPSD). 27040140: AD is a neurodegenerative disorder causing dementia with no cure nor means for definitive diagnosis during life. 27554603: Alzheimer's disease (AD) is the general consequence of dementia and is diagnostic neuropathology by the cumulation of amyloid-beta (Abeta) protein aggregates, which are thought to promote mitochondrial dysfunction processes leading to neurodegeneration. 27890830: Vascular cognitive impairment and dementia (VCID) is the second leading cause of dementia behind Alzheimer's disease (AD) and is a frequent co-morbidity with AD. 28522216: DISCUSSION: This large prospective study of French older adults suggests that maintaining adequate vitamin D status in older age could contribute to slow down cognitive decline and to delay or prevent the onset of dementia, especially of AD etiology. 28729192: Alzheimer's disease (AD) is the most common neurodegenerative disorder causing dementia. 29226870: Despite the wide knowledge on factors influencing dementia risk, little is known on what accounts for AD progression. 29383688: APP is involved in the pathology of Alzheimer's disease (AD), the most common neurodegenerative disorder causing dementia. 29389553: Alzheimer's disease (AD) is the most common cause of dementia in the elderly. beta-Amyloid (Abeta) has been proposed to play a role in the pathogenesis of AD. 29957266: When hospitalizations were classified according to the main diagnosis, chronic skin ulcers, functional impairment and daily urinary incontinence were associated with hospitalization due to infectious diseases; impaired cognitive capacity, Alzheimer's disease or other dementia and polypharmacy (protective effect) were associated with hospitalizations due to dementia; age of >=90 years, congestive heart failure, coronary artery disease and using >=10 drugs with hospitalizations due to heart diseases; and moderate or strong pain with hospitalization due to musculoskeletal disorders. 30424485: Hallmarks of Alzheimer's disease (AD), a progressive neurodegenerative disease causing dementia, include protein aggregates such as amyloid beta plaques and tau neurofibrillary tangles in a patient's brain. 30696930: Dementia was further categorised into Alzheimer's disease (AD), vascular dementia (VaD), and dementia caused by other diseases (ODs). 30942758: The brain ventricles are surrounded by periventricular structures that are affected by dementia which results in neurodegenerative disorder such as Alzheimer's Disease (AD). 30949934: Molecular Docking and Cognitive Impairment Attenuating Effect of Phenolic Compound Rich Fraction of Trianthema portulacastrum in Scopolamine Induced Alzheimer's Disease Like Condition. Dementia is considered as the frequent cause of neurodegenerative mental disorder such as Alzheimer's disease (AD) amongst elderly people. 30998476: Mild cognitive impairment (MCI) is the preliminary stage of dementia, which may lead to Alzheimer's disease (AD) in the elderly people. 31182772: Alzheimer's disease (AD) is the most common type of neurodegenerative dementia, but the cause of AD remained poorly understood. Many mutations in the amyloid precursor protein (APP) and presenilin 1 and 2 (PSEN1 and PSEN2) have been reported as the pathogenic causes of early-onset AD (EOAD), which accounts for up to 5% of all AD cases. 31248465: METHOD: Data from the initial administration of the MINT were obtained on NACC participants who were cognitively normal (N = 3,981) or diagnosed with mild cognitive impairment (N = 852) or dementia (N = 1,148) with presumed etiology of AD. 31356838: BACKGROUND: Alzheimer's disease (AD) is the most common neurodegenerative disease causing dementia in the elderly population. 31486140: Recognition of the long-term detrimental consequences of migraines for AD and dementia has implications for migraine management, as well as for our understanding of AD etiology. 32615251: Increased GABAergic Development in iPSC-Derived Neurons from Patients with Sporadic Alzheimer's Disease.Alzheimer's disease (AD) is the most common cause of dementia in the elderly, and the underlying molecular mechanisms of this neurodegenerative disorder are still unclear. gamma-aminobutyric acid (GABA) neurons play an essential role in the excitatory/inhibitory (E/I) balance in the brain, and the GABAergic system may contribute to the pathogenesis of AD. 33126501: Alzheimer's Disease (AD) is a progressive multifactorial age-related neurodegenerative disorder that causes the majority of deaths due to dementia in the elderly. 33207563: Alzheimer's disease (AD) is a fatal neurodegenerative disorder caused by protein misfolding and aggregation, affecting brain function and causing dementia. 33396415: Alzheimer's disease (AD) is the most prevalent neurodegenerative disease causing dementia and poses significant health risks to middle-aged and elderly people. 33472953: Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology in longitudinal studies of normal aging and dementia, including assessment of the central model of Alzheimer's disease (AD) pathogenesis, according to which TAU pathology begins focally but expands catastrophically under the influence of amyloid-beta (Abeta) pathology to mediate neurodegeneration and cognitive decline. 34237255: In 2065, DALYs due to Alzheimer's dementia, vascular dementia, and MCI will account for 38% (3654 per 100,000), 17% (1654 per 100,000), and 27% (2585 per 100,000) of total DALYs due to MCI and all-cause dementia, respectively. In 2016, YLDs due to Alzheimer's dementia, vascular dementia, and MCI composed 37% (177 per 100,000), 18% (85 per 100,000), and 15% (70 per 100,000), respectively, of the total YLDs due to MCI and all-cause dementia. In 2016, DALYs attributed to Alzheimer's dementia, vascular dementia, and MCI accounted for 33% (423 per 100,000), 20% (316 per 100,000), and 24% (123 per 100,000), respectively, of the total DALYs due to MCI and all-cause dementia. In 2065, YLDs due to Alzheimer's dementia, vascular dementia, and MCI will account for 48% (1358 per 100,000), 15% (410 per 100,000), and 10% (290 per 100,000), respectively, of total YLDs due to MCI and all-cause dementia. 35493944: Mild Cognitive Impairment (MCI) is an early stage of dementia, which may lead to Alzheimer's disease (AD) in older adults. 36113115: Despite early mentions of dementia in the ancient literature and the first patient diagnosed in 1906, the underlying causes of AD are not well understood. 36254682: Alzheimer's disease (AD) is the most common form of dementia, and risk-influencing genetics implicates microglia and neuroimmunity in the pathogenesis of AD. 36362376: The biological plausibility of the link between high adiposity, insulin resistance, and dementia is central for understanding AD etiology, and to form bases for prevention efforts to decrease the disease burden. 37223834: Conclusions: We identified a gap in the literature on the description of the psychotic symptoms of dementia, mainly in those of non-AD etiologies. 37425748: ABri plaques are accompanied by tau pathology, neuronal cell death and progressive dementia, with striking parallels to the aetiology and pathogenesis of Alzheimer's disease. 37543811: In particular, Alzheimer disease, the most common type causing dementia, remains an incurable disease. 37629545: Considering the results obtained, DTZ might have a potential therapeutic role in treating and managing AD and related dementia pathologies due to its anti-dementia activity in SAD-type conditions in rats induced by ICV-STZ. Repurposing Diltiazem for Its Neuroprotective Anti-Dementia Role against Intra-Cerebroventricular Streptozotocin-Induced Sporadic Alzheimer's Disease-Type Rat Model. In the present study, the neuroprotective anti-dementia effects of DTZ against intra-cerebroventricular-streptozotocin (ICV-STZ)-induced sporadic AD (SAD)-type rat model was investigated. 38491393: Alzheimer's disease (AD) is the most prevailing form of dementia, with long-term high-fat diet (HFD) consumption being a pivotal contributor to AD pathogenesis. 8739399: This paper summarizes results of the Vienna Longitudinal Study on Dementia obtained during the past few years and presents a critical discussion on the relevance of clinicopathological correlation studies for the pathogenesis of AD. 9058061: In spite of this progress, the pathogenetic events that differentiate normal brain aging from the early stages of dementia and may lead eventually to AD are not completely understood. 9625186: CONCLUSIONS: In a population aged 75 to 85 years, the presence of an apoE e4 allele is associated with impaired cognitive function, clinical dementia, AD, and excess 5-year mortality resulting from dementia and all causes. 1212874: The effect of exogenous angiotensin II on the spectrum of nonesterified fatty acids (NEFA) in blood plasma was studied by gas-chromatographic analysis in 10 normotonic rabbits, 12 rabbits with experimental hypertension induced by sinoaortic denervation, and in 14 rabbits with experimental renal hypertension. One minute after injection of angiotensin II, the following changes were found in the spectrum of NEFA: increase in the fraction of saturated, and decrease in the fraction of unsaturated NEFA;the intensity of these changes was higher in the animals with renal hypertension than in those with hypertension induced by sinoaortic denervation, and lowest in the normotonic rabbits. 13852251: [Hypertension caused by denervation in the adrenalectomized dog]. 1652186: In previous investigations it was shown, that this denervation produces hypertension and tachycardia, which is confirmed by the present study: Mean arterial blood pressure increased from 101 +/- 3 to 123 +/- 6 mmHg (P less than 0.05), and heart rate rose from 85 +/- 6 to 124 +/- 5 beats min-1 (P less than 0.001). 16763077: Afferent renal denervation results in salt-sensitive hypertension, suggesting that activation of the afferent renal nerves contributes to water and sodium balance. 17147924: Three years later, it was reported that MAP was near normal in dogs with both aortic and carotid baroreceptors denervated based on continuous measurements, thus discrediting numerous reports of denervation-induced hypertension. 17880379: We reported previously that bilateral renal denervation abolishes hypertension in adult male IUGR offspring, indicating an important role for the renal nerves in the maintenance of established IUGR-induced hypertension. 25629384: KEY POINTS: The indication for renal denervation should be assessed in an interdisciplinary fashion and according to current guidelines with a special focus on ruling out secondary causes for arterial hypertension. 25846764: Patients with RAH were treated by RAD after exclusion of secondary causes of hypertension. 2612022: Since the renal nerves have been shown to play a role in several animal models of hypertension, the current study sought to determine the effect of bilateral renal denervation on the development of stress-induced hypertension in the BHR. 2698949: Chronic captopril treatment (30 mg/day orally) produced a permanent attenuation of the hypertension induced by sino-aortic denervation, as shown by a beat-to-beat analysis of arterial pressure for 80 min. 27375498: In fact, the wide range in effectiveness of renal denervation could be a consequence of this heterogeneous pathogenesis of hypertension. 2767609: Finally, the development (but not the maintenance) of SAD-induced hypertension is associated with an increase in sympathetic tone. 3772719: The purpose of this study was to examine, using pentobarbital-anesthetized rats, whether vasopressin contributes to hypertension caused by denervation of baroreceptors, in comparison to the contribution of vasopressin to hypertension caused by nucleus tractus solitarius (NTS) lesions. Contribution of vasopressin to hypertension caused by baroreceptor denervation and nucleus tractus solitarius lesions in rats. 4202594: [Effect of an adrenergic beta receptor inhibitor (propranolol) on arterial hypertension induced by carotid sinus denervation and vagotomy in dogs]. 564597: The results imply that hypertension induced by baroreceptor denervation is not of a stable and persistent type in which case structural changes in the cardiovascular system would have developed within the observation period (approximately 4 months). 6518342: Long-term analysis of the hypertension produced by sinoaortic denervation in the rat. 7049925: In the spontaneously hypertensive rate of the Okamoto strain (SHR) and the DOCA-NaCl rat, the delay in the development of hypertension produced by renal denervation is due in part to increased sodium excretion thought to be secondary to interruption of the renal efferent nerves. 8572875: [Absence of the effect of nitric oxide on pulmonary and systemic hypertension induced by sino-aortic denervation]. 9043810: Arterial baroreceptor denervation produces acute hypertension, but chronically denervated animals have an average arterial pressure that is similar to that of baroreceptor intact animals. 9303572: AD led to hypertension and increased the lability of arterial pressure. 9674636: The present study tested the hypothesis that denervation of peripheral osmoreceptors elevates arterial pressure and induces NaCl-sensitive hypertension in normotensive rats. 10392370: Hypertension and virilization caused by a unique desoxycorticosterone- and androgen-secreting adrenal adenoma. 1071621: Renal prostaglandin synthesis in hypertension induced by deoxycorticosterone and sodium chloride in the rat. The role of renal medullary prostaglandin E has been examined in rats with hypertension induced by sodium chloride and deoxycorticosterone (salt-DOC). 1218518: The authors examined the changes in arterial blood pressure and the content of Noradrenaline in the myocardium, brain and aorta of rats with hypertension due to nephrectomy and treatment with desoxycorticosterone and NaCl, and after a chronic 6-month treatment of hypertension with various antihypertensive means. 13167756: [Effect of benzedrine on hypertension produced by desoxycorticosterone]. 13258856: Effect of maturity and desoxycorticosterone-induced hypertension on tissue electrolytes. 13365182: [Cation absorption resins in hypertension caused by desoxycorticosterone in the rat]. 13513919: Hypertension induced by renal artery constriction also intensified the hypercholesterolemia and hyperlipemia. The induction of hypertension by desoxycorticosterone and salt accelerated the development of hypercholesterolemia, hyperlipemia, increase in tissue cholesterol content, and atherosclerotic changes in the intima. 13810289: [Intracellular penetration of sodium in hypertension caused by desoxycorticosterone in the rat]. 13933395: [Urinary elimination of catecholamines in rats during experimental hypertension induced by desoxycorticosterone]. 139619: Effect of some substituted pyrimidines on development of desoxycorticosterone-induced hypertension in rats. 14381724: Influence of hypophysectomy upon the established hypertensive disease induced by desoxycorticosterone. 1614061: Experiments in rats with reduced renal mass, desoxycorticosterone-induced hypertension, chronic angiotensin II infusion, and in spontaneously hypertensive rats support such a view. 18148188: Persistence of desoxycorticosterone-induced hypertension in the nephrectomized rat. 187612: These studies suggest that a steroid other than aldosterone, 18-OH-DOC, or DOC may be the cause of the ACTH-induced hypertension in this patient. Evidence for an unidentified ACTH-induced steroid hormone causing hypertension. 1914200: DOC is produced in excess in both deficiencies and is the cause of the hypertension. 19841522: CONCLUSIONS: Co-administration of vitamin C and E does not have an additive beneficial effect on reducing the kidney damage and hypertension compared to either vitamin C or E alone in DOCA-salt-induced hypertension. Unilateral nephrectomy was carried out in the study groups and hypertension was induced by deoxycorticosterone injection and 1% sodium chloride and 0.2% potassium chloride added to the drinking water. INTRODUCTION: We assessed whether co-supplementation of vitamins C and E has additive beneficial effects on reducing the kidney damage and attenuation of the arterial pressure elevation compared to administration of either vitamin C or vitamin E alone in deoxycorticosterone acetate-salt-induced hypertension. Reduction of kidney damage by supplementation of vitamins C and E in rats with deoxycorticosterone-salt-induced hypertension. 20212272: In 9-week-old C57BL/6J male mice, hypertension was induced by angiotensin II or deoxycorticosterone acetate-salt hypertension; degeneration of elastic lamina was induced by infusion of beta-aminopropionitrile, a lysyl oxidase inhibitor. 214053: The two weeks of desoxycorticosterone and 1% saline-induced hypertension caused myocarditis and hyalinization of the coronary arteries of the nonarteriosclerotic (virgin) rats and definite exacerbation of the preexisting arteriosclerosis in breeder rats, severe myocarditis, and polyarteritis nodosa. 2298466: Considering the inability of the developing kidney to adequately excrete a sodium load, we studied the possibility that DOC alone might induce hypertension when treatment is initiated in rats at the age of 21 days. 26525354: Accumulation of 11-deoxycorticosterone and its metabolites causes hypertension in about two thirds of patients. 26862015: The adrenals of patients with 17OHD synthesize 11-deoxycorticosterone (DOC) and corticosterone but no 19-carbon steroids, similar to the rodent adrenal, and DOC causes hypertension and hypokalemia. 27678262: It is important to note that CXCR2 blockade reversed established hypertension induced by angiotensin II or DOCA-salt challenge (n=10 per group). 28487303: The consequent cortisol deficiency results in a compensatory increase in adrenocorticotropic hormone (ACTH) drive, which stimulates the production of deoxycorticosterone and corticosterone leading to hypertension and hypokalaemia. 2964946: Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). 2965178: Glucocorticoid-induced hypertension in rats has been studied using long-term, low-dose dexamethasone treatment. Glucocorticoid-induced decreases in ANP contrast with ANP increases in response to mineralocorticoid treatment in rats with deoxycorticosterone-induced hypertension. We conclude that low-dose infusions (less than 5 micrograms/day) of dexamethasone are suitable for studying glucocorticoid-induced hypertension without the complications of weight loss that have been reported by others or of the mineralocorticoid-like side effects which endogenous glucocorticoids may exhibit. 31051469: Hypertension due to a deoxycorticosterone-secreting adrenal tumour diagnosed during pregnancy. 3244171: 11-Deoxycorticosterone-induced hypertension, glomerulosclerosis and renal arterial and arteriolar lesions. 3284355: The data acquired in these studies agree with the notion that excess mineralocorticoid production causes hypertension by mechanisms that influence the neurohormonal control of blood pressure by the central nervous system. In this article we summarize studies of the hemodynamic and endocrine effects of desoxycorticosterone (DOC)-induced hypertension in dogs and also review new data of the action of this steroid on baroreceptors. 3346052: Characteristics of hormonal and neurogenic mechanisms of deoxycorticosterone-induced hypertension. We characterized the hemodynamic and endocrine changes associated with the evolution of steroid-induced hypertension in conscious, trained, instrumented dogs given intramuscular injections of deoxycorticosterone (DOC) pivalate on Days 1 (20 mg/kg) and 14 (10 mg/kg) of the study. The data suggest that DOC-induced hypertension changes central hormonal influences of cardiovascular function, and also alters cardiopulmonary baroreceptor reflex control of peripheral sympathetic nerve activity. Compared to normal animals, dogs with DOC-induced hypertension showed a reduced pressor response to carotid occlusion associated with suppression of reflex tachycardia; vagotomy partially restored the pressor response to normal levels. 3395970: The effect of deoxycorticosterone (DOC)-induced hypertension on the calcium content within the aorta was studied before the increase in pressure (one week) and after the pressure had reached hypertensive levels (4 weeks). 3553487: Hypermineralocorticoid hypertension is usually due either to aldosterone or deoxycorticosterone excess. 3683766: In conscious rats with normal arterial blood pressure or with spontaneous or DOC induced hypertension, effects of drugs increasing (cycloserine, ethanolamine-o-sulphate, piracetam, chlordesmethyldiazepam) or depressing (bicuculline, Ro 15-1788, PK 11195) GABAergic reactivity were evaluated on the arterial hypotension and sinus bradycardia induced by clonidine. 4321628: Changes in the enzymic capacity of the rat kidney and heart due to unilateral nephrectomy and deoxycorticosterone induced hypertension. 4459300: Reduction by coenzyme Q10 of hypertension induced by deoxycorticosterone and saline in rats. 4764449: [Significance of water-electrolyte balance in the pathogenesis of glucose tolerance disorder in desoxycorticosterone-induced hypertension of the rat]. 4831119: Deficiency of deoxycorticosterone-binding protein in the hypothalamus of rats resistant to deoxycorticosterone-induced hypertension. 514639: Arterial lesions and hypertension induced by saline, unilateral nephrectomy, and deoxycorticosterone in spontaneously hypertensive SHR rats. 6027455: A study of the effects of renal artery constriction on hypertension caused by deoxycorticosterone. Steroid-induced hypertension in the rat. 6111849: Cerebral aneurysms were induced in rats treated with unilateral ligation of the common carotid artery and hypertension produced by renal infarction with or without beta-aminopropionitrile, one of the lathyrogens. In this experiment, cerebral aneurysms developed more frequently than in the previous experiments in which hypertension induced by deoxycorticosterone and salt had been used. 6986224: Rats with deoxycorticosterone-induced hypertension also showed a significant blood pressure fall. 710367: The occurrence of 11-deoxycorticosterone (DOC)-induced hypertension in the Long-Evans rat. These results, which indicate that Long-Evans rats are not resistant to DOC-induced hypertension, contrast with previous reports by others. 7116668: These experiments were intended to elucidate the role of central mechanisms in the maintenance of high blood pressure produced by deoxycorticosterone (DOC) and salt in rats. 7848614: We conclude that the patients with 17 alpha-HD showed salt-sensitive hypertension due to excessive DOC and B, through the impaired renal function for sodium excretion, disproportionate increase in cardiac output, and inadequate vasodilation. 8386933: Perhaps deoxycorticosterone or a hitherto unknown mineralocorticoid is responsible for the hypertension and altered MR-status. 8516490: Experimental investigations in rats with reduced renal mass, desoxycorticosterone-induced hypertension, or chronic angiotensin II infusion, and in spontaneously hypertensive rats support such a view. 868797: The data implicate defective 11beta hydroxylation and suggest that excessive 11-deoxycorticosterone production may have been responsible for the hypertension. 9259306: The discriminating feature of this form of sex-reversal is the presence of hypertension due to the elevated serum deoxycorticosterone levels. 9478073: The literature reports of DOC-induced hypertension due to adrenal adenoma or hyperplasia are reviewed and the possible pathogenetic mechanisms are discussed. 976188: This suggests a resistance to deoxycorticosterone-induced hypertension in this strain of rat. 11244216: It may also represent, reflect or account for the impaired neuronal transmission in DS and AD, caused by deterioration of the exocytic machinery. 12214126: Because AD is a disease of neuronal and synaptic deterioration, APP may be involved during the course of AD pathogenesis, perhaps secondarily. The presence of mutations around the A beta sequence in APP provides strong argument for the involvement of APP, and A beta in particular, in pathogenesis of Alzheimer's disease (AD). 12657430: There is much evidence suggesting that there is a strong relationship between the deterioration of brain lipid homeostasis, vascular changes and the pathogenesis of Alzheimer's disease (AD). 21809745: In it EN provides evidence that in true Alzheimer dementia (AD), memory loss is the initially dominating problem due to deterioration of the circulation in the hippocampus, which has a vulnerable blood supply to begin with. 23512996: BACKGROUND: Relating to Alzheimer's disease (AD), dependence has been defined as the increased need for assistance due to deterioration in cognition, physical functioning, and behavior. 24499794: The deterioration of subcellular organelles, including the mitochondria, is another major ultrastructural characteristic of AD pathogenesis, in addition to amyloid plaque deposition. 29042514: Our results suggest deterioration of DNA integrity as a central contributing factor in AD pathogenesis. 29604402: BACKGROUND: Alzheimer's disease is a neurodegenerative brain disease resulting from the deterioration of neuronal cells and vascular dementia, the latter of which results from cerebrovascular disorders. 2965684: It is concluded that at this age Down's and mentally retarded with different etiologies generally have rather similar cognitive abilities and that the intellectual deterioration of Down's, which at a later age inevitably leads to Alzheimer's disease, indeed starts only at a later CA. 36056872: The progressive deterioration of neurons leads to Alzheimer's disease (AD), and developing a drug for this disorder is challenging. 10485340: Thus, treatment with Dex altered the levels of these proteases which might have a role in the pathogenesis of hypertension and in altered blood coagulation. This study was designed to investigate the alterations in the levels of various proteases such as angiotensin converting enzyme (ACE), kallikrein, aminopeptidases, urokinase and plasmin in serum-heart and kidney and to find out whether the changes in the levels of these enzymes could explain the pathogeneses of hypertension induced by Dexamethasone (Dex). 11072875: These results suggest that the catecholamine synthetic pathway may be involved in DEX-induced hypertension. Involvement of tyrosine hydroxylase up regulation in dexamethasone-induced hypertension of rats. 11577028: In this study, we hypothesized that dexamethasone-induced hypertension is associated with left ventricular hypertrophy and a reduced cardiac functional reserve (CO(max-0)). 12411469: In conclusion, brief prenatal exposure of the pregnant ewe to dexamethasone leads to hypertension in adult animals of both sexes. 15001201: Tempol prevented and partially reversed Dex-induced hypertension, independent of improvement in systemic oxidative stress measured by F(2)-isoprostane concentrations. Tempol partially reversed Dex-induced hypertension (122 +/- 5 and 136 +/- 3 mm Hg, respectively, P' =.057). This study investigated the effects of Tempol, a superoxide scavenger, on prevention and reversal of hypertension induced by the synthetic glucocorticoid dexamethasone (Dex) in the rat. Tempol alone did not alter SBP, but Tempol pretreatment prevented Dex-induced hypertension compared with that in rats treated with Dex alone (128 +/- 4 and 144 +/- 7 mm Hg respectively, P' <.05). 16644906: The present studies were designed to determine whether there is a lower dose of dexamethasone that does not reduce maternal food intake yet still causes hypertension in the adult offspring. 16820346: Atorvastatin prevented and reversed dexamethasone-induced hypertension in the rat. Atorva reversed dex-induced hypertension (129 +/- 0.6 mmHg, vs. Thus, atorvastatin prevented and reversed dexamethasone-induced hypertension in the rat. To assess the antioxidant effects of atorvastatin (atorva) on dexamethasone (dex)-induced hypertension, 60 male Sprague-Dawley rats were treated with atorva 30 mg/kg/day or tap water for 15 days. 17042910: Dexamethasone (Dex)-induced hypertension is characterized by endothelial dysfunction associated with nitric oxide (NO) deficiency and increased superoxide (O2-) production. 17095646: Prenatal administration of dexamethasone causes hypertension in rats when they are studied as adults. 17324744: Folic acid, but not BH(4), prevented the development of hypertension caused by ACTH and Dex treatment. 17439425: Glucocorticoid-induced hypertension (GC-HT) in the rat is associated with nitric oxide-redox imbalance. We studied the role of xanthine oxidase (XO), which is implicated in the production of reactive oxygen species, in dexamethasone-induced hypertension (dex-HT). 17954371: ACTH- but not Dex-induced hypertension was partially reversed by aspirin. The aim of the present study was to investigate the effects of aspirin, a potent antioxidant, on adrenocorticotropic hormone (ACTH) and dexamethasone (Dex)-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with increased oxidative stress. Aspirin prevented the development of hypertension caused by ACTH (P' < .01) and tended to prevent Dex-induced hypertension (P' = .07). 18252958: Prenatal dexamethasone 'programmes' hypotension, but stress-induced hypertension in adult offspring. 18400872: The purpose of the present study was to determine whether the hypertension due to prenatal dexamethasone was mediated by renal nerves. We have demonstrated that administration of dexamethasone during specific periods of pregnancy in the rat causes hypertension in the offspring when they are studied as adults. 1934541: Characterization of alterations of hemodynamics and neuroendocrine hormones in dexamethasone induced hypertension in dogs. Glucocorticoid-induced hypertension mainly depends on the increases in total peripheral resistance but not volume factors. 19403862: Prenatal administration of dexamethasone and a low-protein diet has been shown to result in hypertension in the offspring when they are adults. 19458537: The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension. HET0016 also prevented the development of hypertension induced by ACTH (P < 0.01). In the present study, we investigated the effect of a specific enzyme inhibitor of 20-HETE production, N-hydroxy-N'-(4-butyl-2-methylphenyl) formamidine (HET0016), on glucocorticoid-induced hypertension in rats, a sodium-independent model. These results suggest that 20-HETE may play a role in the genesis of ACTH-induced hypertension but not in dexamethasone-induced hypertension. 19644504: Hemodynamics of dexamethasone-induced hypertension in the rat. Although dexamethasone (DEX) is known to cause hypertension in humans and in animals, the hemodynamic characteristics of DEX-induced hypertension (DEX-HT) in the rat remain unclear. 20186125: NOLA exacerbated dexamethasone-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with imbalance between nitric oxide (NO) and superoxide. Effects of sepiapterin supplementation and NOS inhibition on glucocorticoid-induced hypertension. In the present study, adrenocorticotrophic hormone (ACTH)- and dexamethasone-treated rats were further treated with sepiapterin, a precursor of tetrahydrobiopterin, or N-nitro-L-arginine (NOLA), an inhibitor of NOS, to investigate the role of eNOS uncoupling in glucocorticoid-induced hypertension. Sepiapterin did not prevent ACTH- (129 +/- 4 mm Hg, NS) or dexamethasone-induced hypertension (135 +/- 3 mm Hg, NS), although plasma total biopterin concentrations were increased. These data suggest that eNOS uncoupling does not play a major role in the genesis of glucocorticoid-induced hypertension in the rat. CONCLUSION: Sepiapterin did not prevent ACTH- or dexamethasone-induced hypertension. 20188070: To determine the site(s) of glucocorticoid receptor action relevant to the development of hypertension, we studied glucocorticoid-induced hypertension in a mouse with a tissue-specific knockout of the glucocorticoid receptor in the distal nephron. We conclude that the glucocorticoid receptor in the distal nephron is not necessary for the development or maintenance of dexamethasone-induced hypertension in our model. The glucocorticoid receptor in the distal nephron is not necessary for the development or maintenance of dexamethasone-induced hypertension. We have developed a mouse model of glucocorticoid-induced hypertension, which is dependent on the glucocorticoid receptor. The mechanism of glucocorticoid-induced hypertension is incompletely understood and has traditionally been attributed to promiscuous activation of the mineralocorticoid receptor by cortisol. 21659825: RESULTS: We show that these mice are relatively resistant to dexamethasone-induced hypertension. 21953707: These findings suggest that oleanolic acid (60 mg/kg i.p.) prevents dexamethasone-induced hypertension in rats, which may be attributed to its antioxidant and nitric oxide releasing action. (Loranthaceae) in glucocorticoid (dexamethasone)-induced hypertension in rats and to propose a probable mechanism of action for this effect. 23533693: The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. CONCLUSION: Glucocorticoid-induced hypertension in rats is prevented by alpha-lipoic acid via mechanisms other than mitochondrial superoxide reduction. AIMS: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition. 24383084: We further investigated whether glucagon-like peptide-2 (GLP-2) was effective for dexamethasone-induced hypertension. Peripheral administration of GLP-2 suppressed dexamethasone-induced hypertension in rats by enhancing inhibitory neuronal activity. In the present study, we investigated the sites associated with dexamethasone-induced hypertension in the central nervous system in rats. AIMS: Dexamethasone-induced hypertension models have been used to study the mechanisms of glucocorticoid induced hypertension, but the role of glucocorticoids in central cardiovascular regulation is not clearly understood. 24555785: Maternal citrulline supplementation prevents prenatal dexamethasone-induced programmed hypertension. Thus we intended to determine if maternal L-citrulline therapy can prevent prenatal DEX-induced programmed hypertension by restoration ADMA/nitric oxide (NO) balance, alterations of renin-angiotensin system (RAS) and sodium transporters, and epigenetic regulation by histone deacetylases (HDACs). Next, prenatal DEX-induced programmed hypertension is related to increased mRNA expression of angiotensin and angiotensin II type 1 receptor, and class I HDACs in the kidney. The beneficial effects of L-citrulline therapy include restoration of ADMA/NO balance and alteration of NCC, to prevent the prenatal DEX-induced programmed hypertension. 24587916: Antioxidant effects of bovine lactoferrin on dexamethasone-induced hypertension in rat. Dexamethasone- (Dex-) induced hypertension is associated with enhanced oxidative stress. 24731552: Since melatonin is a potent antioxidant and has been known to regulate blood pressure, we examined the beneficial effects of melatonin therapy in preventing prenatal dexamethasone-induced programmed hypertension. Although antenatal corticosteroid is recommended to accelerate fetal lung maturation, prenatal dexamethasone exposure results in hypertension in the adult offspring. 25090636: We examined whether melatonin prevented neonatal dexamethasone (DEX)-induced programmed hypertension and how melatonin prevented these processes. Similarly, HDAC inhibition prevented DEX-induced programmed hypertension. In conclusion, melatonin therapy exerts a long-term protection against neonatal DEX-induced programmed hypertension. Neonatal DEX exposure induced hypertension in male offspring at 16 weeks of age, which melatonin prevented. Melatonin prevents neonatal dexamethasone induced programmed hypertension: histone deacetylase inhibition. 2509553: Arachidonic acid exerted antihypertensive effects which were marginal initially but significant in the later phase of dexamethasone-induced hypertension (124 +/- 8 versus 139 +/- 8 mmHg in arachidonic acid-treated versus control rats after 7 days of dexamethasone). The goal of the present study was to determine whether dexamethasone-induced hypertension in Wistar rats is due to inhibition of the synthesis of the vasodilator prostaglandin I2 (PGI2) in vivo. The mechanism of glucocorticoid-induced hypertension is not known. 25171190: BACKGROUND/AIM: It has been demonstrated that dexamethasone-induced hypertension can be prevented by the NADPH oxidase inhibitor apocynin. 25921765: Prenatal dexamethasone-induced programmed hypertension and renal programming. Prenatal DEX-induced programmed hypertension was examined in male offspring at 16 weeks of age. 26015927: M. peregrina extract at a dose of 400 mg/kg prevented (P < 0.01) but did not reverse Dex-induced hypertension in rats. The present study was designed to evaluate the effect of hydroalcoholic extract from the leaves of M. peregrina in dexamethasone (Dex)-induced hypertension in rats. CONCLUSIONS: The findings of the present study indicated the antioxidant and partially antihypertensive effects of the hydroalcoholic extract from the leaves of M. peregrina in Dex-induced hypertension. 26600845: The aim of this study was to assess the effects of hydroalcoholic extract of the aerial parts of O. persica in dexamethasone (Dex) induced hypertension in male Wistar rats. For induction of hypertension, Dex at 30 MUg/kg/day was administered subcutaneously for 14 days. 26600859: The present study was designed to evaluate the effects of hydroalcoholic extract of the stems of F. foetida in dexamethasone (Dex)-induced hypertension in rats. 26696906: Prenatal DEX and postnatal HF diet synergistically induced programmed hypertension in adult offspring, which melatonin prevented. Maternal Melatonin Therapy Rescues Prenatal Dexamethasone and Postnatal High-Fat Diet Induced Programmed Hypertension in Male Rat Offspring. Postnatal HF aggravates prenatal DEX induced programmed hypertension in adult offspring, which melatonin prevented. 26743493: Prenatal DEX and postnatal HF diet synergistically induced programmed hypertension in adult offspring, which was prevented by maternal NAC therapy. 26921678: Thus we tested whether postnatal DEX-induced hypertension is related to changes of melatonin receptors in the kidney and heart, which was preserved by maternal melatonin therapy. Postnatal dexamethasone-induced programmed hypertension is related to the regulation of melatonin and its receptors. We concluded that melatonin therapy has long-term protection on postnatal DEX-induced programmed hypertension, which is associated with regulation on melatonin receptors in the kidney. We found that maternal melatonin therapy prevents postnatal dexamethasone (DEX)-induced programmed hypertension. 27014652: In this study, the effects of hydroalcoholic extract of the aerial parts of K. odoratissima were evaluated in dexamethasone (Dex)-induced hypertension in male Wistar rats. MATERIALS AND METHODS: For induction of hypertension, Dex (30 MUg/kg/day) was administered subcutaneously for 14 days. 2719105: Role of antiglucocorticoid RU 486 on dexamethasone-induced hypertension in rats. 27210044: We found postnatal HF diet aggravated prenatal DEX-induced programmed hypertension, which was similarly prevented by early treatment with AUDA or 15dPGJ2. Early postnatal treatment with soluble epoxide hydrolase inhibitor or 15-deoxy-Delta(12,14)-prostagandin J2 prevents prenatal dexamethasone and postnatal high saturated fat diet induced programmed hypertension in adult rat offspring. 27313228: The effect of ethanolic extract of Morinda citrifolia leaves and fruit on blood pressure in dexamethasone-induced hypertension rat was evaluated. 27405316: A Novel Model of Dexamethasone-Induced Hypertension: Use in Investigating the Role of Tyrosine Hydroxylase. Although this DEX treatment also significantly decreased body weight, pair-fed animals that showed similar decreases in body weight due to lowered food intake were not hypertensive, suggesting that body weight changes may not account for DEX-induced hypertension. 27521802: Given that sex differences exist in the blood pressure (BP) control, and that renal transcriptome is sex-specific, thus we intended to elucidate whether prenatal DEX-induced programmed hypertension is in a sex-specific manner and identify candidate genes and pathways using the whole-genome RNA next-generation sequencing (NGS) approach. Prenatal DEX induced programmed hypertension in adult male but not female offspring, which was related to renal programming affecting sex-biased genes and the RAS. The resistance of female offspring to prenatal DEX-induced programmed hypertension is related to a lower Agt expression. 27653214: OBJECTIVE: This study assesses the effect of methanol extract of walnut [Juglans regia L. (Juglandaceae)] on dexamethasone-induced hypertension and the possible mechanisms in Wistar rats. CONCLUSION: Similar to captopril, walnut extract normalized dexamethasone-induced hypertension. 28228807: For induction of hypertension, Dex was injected subcutaneously for 14 days. These results suggest the antihypertensive and antioxidant effects of PCA against Dex-induced hypertension. The Effect of Protocatechuic Acid on Blood Pressure and Oxidative Stress in Glucocorticoid-induced Hypertension in Rat. 28462145: Hence this study was undertaken to investigate the antihypertensive activity of allicin in dexamethasone induced hypertension in wistar rats. Thus, this study confirmed that allicin treatment for 8 weeks partially reverse dexamethasone induced hypertension in rats. CONCLUSION: This result suggests antihypertensive effects of allicin in dexamethasone induced hypertension. 29054562: Dexamethasone-induced hypertension may be caused by baroreflex alterations or renin-angiotensin system (RAS) exacerbation. In conclusion, exercise training was effective in attenuating hypertension induced by DEX and this response may be mediated by a better autonomic balance through an improvement of baroreflex activity rather than changes in RAS components. 29636848: Early Postweaning Treatment with Dimethyl Fumarate Prevents Prenatal Dexamethasone- and Postnatal High-Fat Diet-Induced Programmed Hypertension in Male Rat Offspring. We found that postnatal HF intake aggravated prenatal DEX-induced hypertension in adult male offspring, which could be prevented by DMF treatment. 29800813: By identifying candidate proteins underlying sex-specific mechanisms, our results could lead to novel offspring sex-specific interventions to prevent hypertension induced by antenatal corticosteroids and postnatal HF intake in both sexes. Postnatal high-fat diet sex-specifically exacerbates prenatal dexamethasone-induced hypertension: Mass spectrometry-based quantitative proteomic approach. We found that postnatal HF diet increased vulnerability of prenatal DEX-induced hypertension in male but not in female adult offspring. 30127255: Maternal resveratrol therapy decreased asymmetric and symmetric dimethylarginine (ADMA and SDMA) levels, thereby preventing combined DEX and TCDD exposure-induced programmed hypertension. Maternal Resveratrol Therapy Protects Male Rat Offspring against Programmed Hypertension Induced by TCDD and Dexamethasone Exposures: Is It Relevant to Aryl Hydrocarbon Receptor? 30481537: In this study, we have evaluated ACE-inhibitory potential of the tripeptide l-Phenylalanyl-d-Histidyl-l-Leucine (l-Phe-d-His-l-Leu) in vitro and its antihypertensive effect in rat model of dexamethasone-induced hypertension. l-Phe-d-His-l-Leu was custom-designed by changing the configuration of penultimate amino acid residue (histidine) from C-terminal of Ang I, the site at which ACE acts upon and generates Ang II. 30548831: In one group, hypertension was induced by dexamethasone (20 MUg/kg/day, subcutaneously for 7 days; Dex-HT); the other group was spontaneously hypertensive rats (SHR). 3074918: The present study was designed to investigate the involvement of the renal nerve in glucocorticoid hypertension and to assess the role of the renin-angiotensin system in dexamethasone-induced hypertension. Thus, our results indicate that the stimulation of the renin-angiotensin system through the activation of the renal nerve may be partially responsible for the dexamethasone-induced high blood pressure and, therefore, bilateral renal denervation reduces, partially but significantly, the elevated blood pressure, suggesting that the attenuation of oversecretion of renin contributes to the lowering of the blood pressure. 30780842: Glucocorticoid hormones, both naturally occurring and synthetic, have long been recognized as a major cause of hypertension. Current evidence demonstrates the importance of the nitric oxide (NO) system and interactions between NO and reactive oxygen species in the development of glucocorticoid-induced hypertension. Glucocorticoid-induced hypertension and the nitric oxide system. There are well-described experimental models of glucocorticoid-induced hypertension, such as adrenocorticotropic hormone- and dexamethasone-induced hypertension in rats, although the exact mechanism of glucocorticoid-induced hypertension remains unclear. 31715212: Further, the anti-hypertensive effect of N-methylated peptides was evaluated using rat model of dexamethasone-induced hypertension. Combinatorial inhibition of Angiotensin converting enzyme, Neutral endopeptidase and Aminopeptidase N by N-methylated peptides alleviates blood pressure and fibrosis in rat model of dexamethasone-induced hypertension. 3346065: Our previous finding that dexamethasone-induced hypertension in rats is associated with enhanced reactivity of mesenteric arteries to arginine vasopressin but not to angiotensin II (Ang II) or norepinephrine has led us to postulate that vasopressin contributes to the development or maintenance of glucocorticoid-induced hypertension. Contribution of vasopressin in dexamethasone-induced hypertension in rats. 3905217: Despite the diminished levels of vasodilator 2-series prostaglandins, the cod liver oil diet prevented the development of glucocorticoid induced hypertension. It therefore seems unlikely that glucocorticoid induced hypertension is a consequence of inhibition of vasodilator prostaglandin synthesis. Dietary fish oil prevents dexamethasone induced hypertension in the rat. 4030047: Possible alterations in mesenteric vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin and its relationship to prostaglandins in dexamethasone-induced hypertension in rats were investigated. The increase in vascular reactivity to arginine vasopressin during long-term dexamethasone treatment may contribute to the development or maintenance, or both, of glucocorticoid-induced hypertension. 4227855: [Study of correlations between ocular pressure, resistance to aqueous outflow and hypertension induced by dexamethasone]. 6373587: These results suggest that DX-induced hypertension in rats is associated with inhibition of prostaglandin synthesis leading to increased sensitivity in the vascular response to norepinephrine. Glucocorticoid hypertension was induced by oral administration of dexamethasone (DX) in male Wistar rats. 6421564: This study was designed to investigate whether the hypertension produced by dexamethasone in the rat is associated with a deficit in circulating and renal prostaglandin E2 (PGE2) and PGI2, PGs that are presumed to contribute to antihypertensive mechanisms. Plasma concentrations, renal excretion, and tissue release of prostaglandins in the rat with dexamethasone-induced hypertension. Altogether, this study demonstrates that the hypertension induced by dexamethasone in the rat is not associated with a deficit in circulating and renal PGE2 and PGI2. 7026195: These results suggest that hypertension induced by DEX may not be dependent on sodium retention or activation of the renin-angiotensin system. 8831080: UNLABELLED: To assess the role of dexamethasone treatment as a cause of systemic hypertension and associated complications, blood pressure was registered prospectively before, during and after a 4-week dexamethasone course in 22 neonates with chronic lung disease. CONCLUSION: Dexamethasone induced hypertension is transient, even after a 4-week course, and is not associated with hypertensive complications, so treatment is not necessary. 8969928: In preliminary studies, we have determined that the W/Fu rat is also resistant to dexamethasone-induced hypertension. 9315378: Dexamethasone-induced hypertension differs from adrenocorticotropic hormone (ACTH)-induced hypertension in the rat in that it is not modified by L-arginine. Thus, ACTH-induced hypertension cannot be explained simply in terms of glucocorticoid activity. Dexamethasone-induced hypertension in the rat: effects of L-arginine. 10792625: CONCLUSION: In the development of diabetes-induced hypertension, the effect of spironolactone on mean systolic blood pressure may be associated with the mineralocorticoid effects of corticosterone on renal MR, as well as an alteration of renal 11beta-HSD2 activity and its mRNA expression in insulin-dependent diabetic rats. 11432121: Hypertension and diabetes are the leading causes of small-artery disease, subcortical brain ischemia, and stepwise or slowing progressive decline in cognitive function. 11479254: These data underscore the importance of diabetes in the pathogenesis of hypertension in patients with diabetes and kidney failure. 11978652: The genetics of hypertension modifies the renal cell replication response induced by experimental diabetes. 12109774: BACKGROUND: Poorly controlled longstanding diabetes frequently results in sustained hypertension (HTN) which plays a major role in the pathogenesis of diabetic nephropathy. 12410847: The present study investigated the participation of TXA2 and ET-1 in the increase in renal vascular resistances (RVR) induced by Ang II, as well as the consequences of diabetes, hypertension, and the combination of both on this response. 12970107: This may be a major cause of the increased vascular contractility induced by insulin administration and by hyperinsulinemia in established diabetes, resulting in hypertension. 14656952: We have shown that the first occurrence of sustained hyperglycemia in type I diabetes causes hypertension when induced in rats that have had nitric oxide synthesis blocked chronically (L-NAME, 10 microg/kg per minute IV). 15855808: The magnitude of GLUT1 overexpression caused by hypertension is higher than that induced by diabetes alone. BACKGROUND/AIM: Diabetes and mesangial stretch caused by hypertension increase mesangial matrix deposition which is induced by local production of transforming growth factor beta 1 (TGF-beta1). 15890893: BACKGROUND: We hypothesized that serum gamma-glutamyltransferase (GGT) would positively predict the risk of microalbuminuria, a frequent consequence of both diabetes and hypertension, because serum GGT predicted diabetes and hypertension in dose-response relationships. 16967284: Our data suggests that exposure to intrauterine diabetes may be an important cause of both impaired renal function and hypertension in offspring, without changes in the nephron number. 17122330: Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension. Results document that ANG AT1a receptors are critical in diabetes-induced hypertension and in cardiac autonomic responses. 17952227: Overall, about 14% of IHD, 10% of stroke, 12% of hypertensive disease and 12% of renal disease burden in adult males and females (30+ years) were attributable to diabetes. 18154717: Various diseases such as arterial hypertension, diabetes and obesity result in renal diseases which are often irreversible and resistant to currently available therapies. 18575070: The blockade of the renin-angiotensin-aldosterone system (RAAS) has been shown to be useful, or even mandatory, in the management of arterial hypertension, congestive heart failure, post-myocardial infarction and nephropathy with albuminuria, due to diabetes or not. 19329412: INTRODUCTION: In this study we reviewed the published literature on the economic evaluation of the use of angiotensin receptor blockers (ARBs) for the treatment of hypertension, either primary or due to diabetes. 19721377: Patients with lifestyle-related diseases such as hypertension, diabetes, and hyperlipidemia are at high risk for the pathogenesis of a life-threatening atherosclerotic disease. 21435165: Critical ischemic disease is often caused by arteriosclerosis due to hypertension or diabetes. 22096028: Interestingly, the pattern of dysregulation within the PGC-1 transcriptional regulatory circuit distinguishes the heart disease caused by hypertension from that caused by diabetes. 23188160: The term diabetic cardiomyopathy was initially introduced in the 1980s when evidence was found that diabetes leads to a distinct cardiomyopathy, independent of coronary artery disease or hypertension. 23353773: SFN significantly prevented diabetes-induced high blood pressure and cardiac dysfunction at both 3 and 6 months, and also prevented diabetes-induced cardiac hypertrophy (increased the ratio of heart weight to tibia length and the expression of atrial natriuretic peptide mRNA and protein) and fibrosis (increased the accumulation of collagen and expression of connective tissue growth factor and tissue growth factor-beta). 23800117: CONCLUSIONS: Suboptimal BP control was common in CKD patients with hypertension in this study, particularly those at highest risk of adverse outcomes due to diabetes and or albuminuria. 24349248: Nm-aFGF significantly prevented diabetes-induced hypertension and cardiac dysfunction at 6 months. 25195695: Excessive arginase activity has been shown to contribute to the progression of aging-, hypertension- and diabetes-induced vascular dysfunction as well as ED. 26793405: This review summarizes the recent updates on the protective role of Ang 1-7 in hypertension and kidney injury in diabetes, as well as the possible underlying mechanism(s) of Ang 1-7 action, suggesting that the ACE-2/Ang 1-7/MasR axis can be developed as a therapeutic target for the treatment of diabetes-induced hypertension and renal damage. 27467877: Diabetes causes contractile myocardial dysfunction through accelerated atherosclerosis and hypertension, termed Diabetic Cardiomyopathy. 29731021: Finally, obesity and the metabolic syndrome, through their effects on various hormones and inflammation, might also contribute to the pathogenesis of hypertension and diabetes. The renin-angiotensin-aldosterone system may be upregulated in diabetes, leading to hypertension through a direct effect mediated by angiotensin II, as well as indirectly through upregulation of sympathetic activity. 30054861: In young and old rats, diabetes resulted in hypertension, weight loss, hyperglycemia, and hypertriglyceridemia, which were partially prevented by SMe1EC2. 31522593: Metformin suppresses aortic ultrastrucural damage and hypertension induced by diabetes: a potential role of advanced glycation end products. 31915331: Among the predialysis group majority of the CKD was caused by glomerulonephritis (48%) followed by diabetes (26%), HTN (2%) and large portion undiagnosed (24%) whereas in the haemodialysis group ESRD was caused by diabetes (46%) followed by glomerulonephritis (16%), HTN (13%) and undiagnosed (23%). 32398603: RECENT FINDINGS: In contrast to the general nontransplant hypertensive patient population, traditional risk factors, including family history of HTN, obesity and diabetes, play a minor role in the genesis of posttransplant HTN. 32653904: VE-PTP inhibition, therefore, represents an attractive novel therapeutic option for diabetes-induced endothelial dysfunction and hypertension. 32694567: While the pathogenesis of diabetes-induced high blood pressure (BP) is not entirely clear, current evidence suggests that Toll-like receptor 4 (TLR4) is a key player in the mechanisms associated with hypertension. 35890963: The results obtained demonstrate the sustainability of health conditions affecting humanity today as a consequence of the social environment in which we live, e.g., economics, stress, smoking, alcoholism, drug addiction, obesity, diabetes, physical inactivity, etc., which leads to hypertension. 36505816: Male sex, Caucasian race, pretransplant malignancy, hypertension- or diabetes-induced ESRD, retransplantation, diabetes history, deceased donor, cyclosporin, and mTOR inhibitor use were independent risk factors for posttransplant skin cancer mortality. 36675205: Therefore, exogenous H 2 S attenuates renin release and promotes renin-vesicular autophagy to relieve diabetes-induced hypertension. 37198444: Mineralocorticoid receptor-associated hypertension is a broad concept of hypertension that includes not only PA, but also hypertension caused by borderline aldosteronism, obesity, diabetes, and sleep apnea syndrome. 37416812: A 54-year-old male with a history of diabetes mellitus type 2 for 12 years and hypertension was seen in the clinic due to poorly controlled diabetes. 7030513: Diabetes appears to cause a cardiomyopathy independent of atherosclerotic coronary artery disease and hypertension. 7789643: In diabetes, loss of renal arteriolar smooth-muscle cell contractility leads to intraglomerular hypertension. 7967147: Microalbuminuria, macroangiopathies and hypertension in elderly diabetic patients may develop interrelatedly depending on common vascular damages due to diabetes and aging. 8392266: Multiple pregnancy, gestational or chronic diabetes, pregnancy-induced or chronic hypertension and premature rupture of the membranes were not related to the risk of RDS. 8516488: The mechanisms of glomerular injury can be separated into nonimmunologically mediated glomerulonephritis (GN) such as diabetes, leading to glomerular hypertension and into immunologically mediated GN. 14702004: Does diabetes protect or provoke Alzheimer's disease? 17130475: These results show that insulin deficiency causes rapid and large increases in tau phosphorylation, a condition that could prime tau for the neuropathology of Alzheimer's disease, thereby contributing to the increased susceptibility to Alzheimer's disease caused by diabetes. 19188609: The finding that synapse vulnerability to ADDLs can be mitigated by insulin suggests that bolstering brain insulin signaling, which can decline with aging and diabetes, could have significant potential to slow or deter AD pathogenesis. 21044348: CONCLUSIONS: Our present data indicate that there is a close link between insulin deficient diabetes and cerebral amyloidosis in the pathogenesis of AD. 22785400: Amyloid-beta and tau pathology of Alzheimer's disease induced by diabetes in a rabbit animal model. AD-type pathology demonstrated in genetically unmodified rabbits calls attention to the considerable potential of the model for investigation of AD pathogenesis, diagnostics, and therapeutics. 23020846: Diabetes is a risk factor in the pathogenesis of Alzheimer's disease. 25096625: To determine whether mitochondrial perturbation is associated with the contribution of diabetes to AD progression, we characterized mouse models of streptozotocin (STZ)-induced type 1 diabetes and transgenic AD mouse models with diabetes. Diabetes is considered to be a risk factor in Alzheimer's disease (AD) pathogenesis. 25976367: Several preclinical and epidemiological studies have linked metabolic risk factors such as hypertension, obesity, dyslipidemia, and diabetes to the pathogenesis of AD. 26969101: Interestingly, recent epidemiological studies indicate that diabetes significantly increases the risk of developing AD, suggesting that diabetes may play a causative role in the development of AD pathogenesis. 28957663: Diabetes and impaired brain insulin signaling are linked to the pathogenesis of Alzheimer's disease (AD). 30043289: Even though the relationship between diabetes and AD was indicated by significant evidences, the critical mechanisms and metabolic alterations in diabetes induced AD are not clear until now. Iron metabolism in diabetes-induced Alzheimer's disease: a focus on insulin resistance in the brain. 30225625: Correction to: Iron metabolism in diabetes-induced Alzheimer's disease: a focus on insulin resistance in the brain. 30364261: Increased risks for Alzheimer's disease (AD) are a well-recognized consequence of diabetes, insulin resistance (IR), and hyperinsulinemia. 30958383: Moreover, diabetes-induced AD-like behavioral and pathological changes were associated with a decrease in neuronal cell autophagy. 31068802: Also, we evaluated the effect of edaravone, an antioxidant on diabetes-induced Alzheimer's-like complications and the additive effect of docosahexaenoic acid (DHA) on the efficacy of TPPU. Docosahexaenoic Acid Increases the Potency of Soluble Epoxide Hydrolase Inhibitor in Alleviating Streptozotocin-Induced Alzheimer's Disease-Like Complications of Diabetes. 31156159: These results provide mechanistic insight into the beneficial effects of insulin, and a possible link between insulin deficient diabetes and cerebral amyloidosis in the pathogenesis of AD. 32436237: Thus, targeting PICALM and mTORC1 to prevent endosomal disorders is a promising strategy for managing diabetes-induced AD. 34256527: Additionally, the risk of increased progression of AD was revealed due to pre-diabetes, T2DM and gut dysbiosis. 34347307: In view of its wide range of pharmacological activities, bergapten is expected to be a potential drug candidate for the treatment of diabetes and diabetes-induced osteoporosis, epilepsy, Alzheimer's disease, depression, and cancer. 34609116: Insulin resistance is also a factor that contributes to pathogenesis of AD. The complications that are discussed in this article are diabetic nephropathy, diabetes induced cardiovascular disease, diabetic neuropathy, Diabetic Foot Ulcer (DFU) and Alzheimer's disease. The progression of AD can be due to the change in DNA methylation of CLOCK gene, followed with worsening of AD by APOE4 gene due to dyslipidaemia condition in T2DM patients. 36262805: Our findings provide insight of targeting ERK as a therapeutic application for diabetes-induced AD. 37414154: Furthermore, we have presented an overview of the main pathways that can be targeted to mitigate the progression of AD and the cognitive impairment caused by diabetes. 1291164: Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. 12916269: 114 women (39.0%) were treated because of hypertension and 41 women (14.0%)--because of diabetes mellitus. 1382169: Arterial hypertension is more common in diabetes mellitus than in nondiabetic subjects, and many metabolic and hemodynamic features of diabetes mellitus contribute to the etiology of hypertension. 16014086: These are possibly related to lower nephron numbers, acquired in utero or later in life, which can increase susceptibility to kidney damage from diseases such as hypertension and diabetes mellitus, or cause arterial hypertension and secondary renal damage. 17415202: Multivariable analysis found that cerebral infarction was significantly associated with increasing patient age, worse neurological grade on admission, history of hypertension or diabetes mellitus, larger aneurysm, use of prophylactically or therapeutically induced hypertension, temperature more than 38 degrees C 8 days after SAH, and symptomatic vasospasm. 18282589: The established synergy between obesity and low nephron number on induction of high blood pressure and further decline of renal function identifies subjects with obesity, metabolic syndrome and diabetes mellitus II as particularly susceptible groups. 18414174: RESULTS: Diabetes mellitus was the most common etiology of renal failure, followed by hypertension, urinary tract infection, and congenital malformation. 18535668: A classic hallmark of early diabetes mellitus includes activation of the renin-angiotensin system (RAS), which may lead to hypertension and renal tissue injury, but the mechanism of RAS activation is elusive. 19011245: In dogs, diabetes mellitus and hyperadrenocorticism are causes of hypertension associated with increases in vascular peripheral resistance. 2035993: Arterial hypertension is more common in diabetes mellitus than in nondiabetic subjects, and many metabolic and hemodynamic features of diabetes mellitus contribute to the etiology of hypertension. 22382225: Diabetes mellitus (DM) is now considered as the major cause of end-stage kidney failure, and hypertension (HTN) is one of the main determinants of progression of renal disease. 23591024: Existing epidemiologic and clinical trial data suggest that the blood pressure in patients with hypertension at high risk for cardiovascular events because of coronary artery disease, diabetes mellitus, chronic kidney disease, stroke, or heart failure should be reduced to <140/90 mm Hg in patients younger than 80 years and the systolic blood pressure be reduced to 140-145 mm Hg if tolerated in patients aged 80 years and older. 29238435: Background: Diabetes mellitus (DM) and primary aldosteronism (PA) have been reported to induce drug-resistant hypertension and atherosclerosis. 34007438: Conclusions: These survivors suffered mainly from hypertension, triggered by psychosocial problems and diabetes mellitus; their stroke seemed fueled by unrecognized hypertension, unrecognized diabetes mellitus, ignorance of hyperlipidemia, and wide-scale belief in witchcraft as risk factor. 38655730: In Switzerland, the main risk factors of cardiovascular diseases lead to a loss of 311 332 DALYs in total, 45 454 DALYs lost by hypertension, 64 445 DALYs lost due to hyperlipidema, 24 283 DALYs due to diabetes mellitus, 47 639 DALYs due to smoking, 21 170 DALYs lost by obesity)and 4 669 DALYs lost due to a lack of exercise. 22829447: Thus, the insulin resistance that underlies the pathogenesis of T2DM might also trigger accumulation of autophagosomes, leading to increased Abeta generation, which might be involved in the pathogenesis of AD. 24121970: Experimental induction of type 2 diabetes in aging-accelerated mice triggered Alzheimer-like pathology and memory deficits. 25082505: Additionally, we provide up-to-date perspectives on critical areas of AD research with special reference to common NO-related etiological factors linking Type 2 diabetes to the pathogenesis of AD. 25230234: With an abundance of common mechanisms underpinning both disorders, a significant question that can be posed is whether T2DM leads to AD in aged individuals and the associations between other protein misfolding diseases. 27810390: Agmatine ameliorates type 2 diabetes induced-Alzheimer's disease-like alterations in high-fat diet-fed mice via reactivation of blunted insulin signalling. The aim of this study was to investigate the ability of agmatine to treat AD induced by brain insulin resistance. Previous studies in high-fat diet-induced AD animal models have shown that brain insulin resistance in these animals leads to the accumulation of amyloid beta (Abeta) and the reduction in GSK-3beta phosphorylation, which promotes tau phosphorylation to cause AD. 29382127: Interestingly, epidemiological studies have described a relationship between type 2 diabetes mellitus (T2DM) and this pathology, being one of the risk factors for the development of AD pathogenesis. 30964050: On the other hand, the increased phosphorylation of IRS1 at several serine sites is observed in the brains from patients with AD and animal models of AD or cognitive impairment induced by type 2 diabetes. 31817238: Human pathologies such as Alzheimer's disease, type 2 diabetes-induced insulin resistance, cancer, and cardiovascular diseases have altered lipid homeostasis. 32602568: However, lack of any significant effect on P-tau load, oxidative stress, neuroinflammation, and insulin resistance raise the question about the ability of donepezil to delay the development or arrest the progression of T2D-induced AD and it is still a matter of debate that require further studies. 33797062: The prevalence of T2D leading to AD is approximately 50-70%. 34256527: Additionally, the risk of increased progression of AD was revealed due to pre-diabetes, T2DM and gut dysbiosis. 35639033: Protective effects of L-arginine on cognitive deficits and biochemical parameters in an experimental model of type-2 diabetes mellitus induced Alzheimer's disease in rats. 36505102: Can Alzheimer's Disease Be Secondary to Type-2 Diabetes Mellitus? 36849855: Therefore, large-scale prospective and comparative studies involving long-term metformin therapy in both diabetic and non-diabetic patients are required to exclude the effect of T2DM-induced AD. 37554106: Exploring the molecular targets for Type 2 diabetes-induced Alzheimer's disease through bioinformatics analysis. Molecular docking was used to predict possible protein targets for T2DM-induced AD. Results: The direct interaction of CD44 and STAT3 may play a significant role in the development of T2DM-induced AD. Aim: The purpose of this study was to elucidate the potential mechanisms of Alzheimer's disease (AD) induced by Type 2 diabetes mellitus (T2DM) through bioinformatics analysis, to provide new treatment targets for this disease. 16673861: INTRODUCTION: Diabetic nephropathy is the leading cause of hypertension in type 1 diabetes. 16961167: INTRODUCTION: There is an established role of clinical risk factors such as arterial hypertension and smoking in causing cardiovascular morbidity and diabetic nephropathy (DNP). 17137404: Diabetic nephropathy may lead to hypertension through direct actions on renal sodium handling, vascular compliance and vasomotor function. 1765755: In IDDM, hypertension occurs usually as a consequence of diabetic renal disease. 19758961: In some cases, hypertension develops as a consequence of diabetic nephropathy. 2335182: Diabetic nephropathy is the dominant cause of hypertension in insulin-dependent diabetics, and long-term rigid antihypertensive treatment inhibits the progression of nephropathy, probably even when there is renal insufficiency. 3292819: Thus, hypertension may be a cause as well as a result of diabetic nephropathy. 34859416: OBJECTIVE: Induction of hypertension by diabetic nephropathy (DN) may be dependent on increased renin secretion from juxtaglomerular cells (JGC). 35059392: DN can lead to hypertension, edema, and proteinuria. 9257079: Diabetic nephropathy, arterial sclerosis, obesity and association of essential hypertension can be the causes of hypertension in patients with non-insulin-dependent diabetes mellitus (NIDDM). 1016098: It was established that prolonged feeding with salt-rich diet led to stable hypertension in some experimental animals, and ultrastructural changes in arterioles were noted only in rats which had developed stable hypertension. 10226871: Dietary NaCl-induced hypertension in uninephrectomized Wistar-Kyoto rats: role of kidney function. This study tests the hypothesis that combination of unilateral nephrectomy and a high sodium chloride (NaCl) diet causes hypertension in otherwise normotensive Wistar-Kyoto (WKY) rats and that this hypertensive response is due to a deficit in the remaining kidney's function. These data suggest that the combination of unilateral nephrectomy and dietary NaCl excess causes hypertension in the normotensive WKY rats, but the hypertensive response is not likely due to a functional deficit in the remaining kidney. 10419070: CONCLUSIONS: These data suggest that lacidipine is effective in reversing hypertension and reducing target organ damage induced by HFD. 10454437: The results demonstrate that (1) kinins protect the developing animal from salt-sensitive hypertension, (2) lack of B(2)R from early development does not alter the maturation of BP under conditions of normal sodium intake, and (3) exposure to a HS diet during fetal life is not sufficient in itself to induce long-term hypertension in either wild-type or B(2)R null mice. 10516193: We addressed the hypothesis that hypercaloric diets induce hyperkinetic hypertension irrespective of day-night cycle and locomotor activity that is associated with altered cardiac myosin isozymes. 10588479: In this study, we investigated the role of an abnormal lipid profile in mediating fructose-induced hypertension. A high fructose diet induces hypertension, hyperinsulinemia - insulin resistance, and hypertriglyceridemia (syndrome X). 10608469: Subjects were characterized for family history of hypertension, plasma parameters of the renin-angiotensin-aldosterone system and blood-pressure response to a high (220 mmol/day) and low (20 mmol/day) salt diet RESULTS: The frequency of the -344T allele (0.45) was similar to that reported previously and genotype distribution was in Hardy-Weinberg equilibrium (CC, n = 55; CT, n = 71; TT, n = 37). 10872553: The mechanisms of fructose-induced hypertension are as yet unknown. Blood pressure increased significantly (P< 0.05) only in the fructose-fed rats receiving the high-salt diet Similarly, increased AT1 receptor mRNA levels were observed only in the fructose-fed rats that were maintained on the high-salt diet CONCLUSIONS: Fructose feeding induces hypertension in normal- or high-salt fed animals and it is associated with an increased expression of the AT1 receptor in adipose tissue. The tissue renin-angiotensin system in rats with fructose-induced hypertension: overexpression of type 1 angiotensin II receptor in adipose tissue. To determine whether fructose-induced hypertension is dependent on dietary salt content, rats were fed standard rat chow and a fructose-enriched diet with low and high sodium chloride concentrations. 10988276: L-NAME-induced HTN was reversible with L-arginine in the LFCC diet group; however, HTN was not corrected by L-arginine supplementation in the HFS diet group. We have recently demonstrated that long-term consumption of a high-fat, refined-carbohydrate (HFS) diet induces hypertension (HTN) in normal rats compared with a low-fat, complex-carbohydrate (LFCC) diet. 11243307: Thus, chronic consumption of a high salt diet resulted in moderate HTN in normotensive Sprague-Dawley rats. Consumption of a high salt diet for 3 weeks induced hypertension (HTN) (158 +/- 6 v 115 +/- 5 mm Hg, P < .01) and widespread downregulation of iNOS expression in renal cortex, renal medulla, aorta, and heart. 11315750: These results suggest that, Dorstenia psilurus treatment could prevent and reverse high blood pressure induced by a diet rich in fructose probably by improvement of plasma insulin levels. We examined the effect of methanol/methylene chloride extract of Dorstenia psilurus given by gastric intubation on systolic blood pressure, plasma glucose, insulin, cholesterol, triglycerides and creatinine in rats with fructose-induced hypertension. 11641337: These results demonstrate that long-term consumption of HFS diet induces hypertension in both genders and is reversible by diet modification. Protective effects of estrogen on gender-specific development of diet-induced hypertension. HFS diet-induced hypertension was accelerated by OVX in female rats, approaching the pattern seen in male rats. Thus hormone status contributes to the delayed onset of diet-induced hypertension in females compared with males. 11863249: Gender difference in diet-induced obesity hypertension: implication of renal alpha2-adrenergic receptors. These data thus suggest a strong relationship between the sexual dimorphism in the cafeteria diet-induced hypertension and altered expression of the alpha2-adrenergic receptor subtypes in the kidney. 11997062: The Dahl- Iwai salt-sensitive (DS) rat develops hypertension due to a high-salt diet without any structural alterations of the brain arteries and arterioles. 12052479: Correction of long-term diet-induced hypertension and nitrotyrosine accumulation by diet modification. We hypothesized that diet modification may reverse diet-induced hypertension via (among other mechanisms) decreased ROS activity and improved nitric oxide (NO) availability. 12130711: Gender differences in hypothalamic tyrosine hydroxylase and alpha(2)-adrenoceptor subtype gene expression in cafeteria diet-induced hypertension and consequences of neonatal androgenization. This study investigated the incidence of cafeteria-diet induced hypertension on hypothalamic tyrosine hydroxylase (TH) and alpha(2)-adrenoceptor subtype gene expression in male, female, and neonatally testosterone-imprinted female rats. 12193127: These results suggest that ET-1 and angiotensin-II are probably involved in the mechanism that leads to hypertension since the effect of these hormones is probably not compensated by kinins in B(2)KO mice. Mice with disruption of the kinin B(2) receptor (B(2)KO mice) are sensitive to salt-rich diets, which causes hypertension. 12372790: After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 +/- 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. 12426085: The purpose of the current study was to investigate the effect of the leaf methanol extract of Bidens pilosa on systolic blood pressure (SBP) and plasma glucose, insulin, cholesterol, triglycerides and creatinine levels in rats with fructose-induced hypertension. Leaf methanol extract of Bidens pilosa prevents and attenuates the hypertension induced by high-fructose diet in Wistar rats. 12427595: The objective of this study was to determine whether the effects of a fructose diet, which causes hyperinsulinemia, insulin resistance, and hypertension in male rats, are dependent on sex. 12433862: Chronic consumption of a high-fat, refined-carbohydrate (HFS) diet causes hypertension. Given the critical role of NO in renal sodium handling, we hypothesized that diet-induced hypertension may be associated with salt sensitivity. Thus chronic consumption of an HFS diet results in hypertension and salt sensitivity, which may be in part due to a combination of ROS-mediated NO inactivation and depressed renal nNOS protein expression. 12605267: Influence of arterial hypertension and diet-induced atherosclerosis on macular drusen. 12623979: Inhibition of renal NO production combined with a high-salt diet produces hypertension, and the THAL has been implicated in salt-sensitive hypertension. 12649390: Sexual dimorphism in cafeteria diet-induced hypertension is associated with gender-related difference in renal leptin receptor down-regulation. Therefore, the present study investigated renal leptin receptor (Ob-Ra and Ob-Rb) mRNA and leptin binding capacities in diet-induced hypertension. 12855427: In Dahl SS but not in SR rats on a high-salt diet, enhanced Na+ entry through FMRFamide-activated brain Na+ channels may increase brain OLC release, thereby leading to hypertension. 12939236: The reduction in the synthesis of these eicosanoids may play an important role in the regulation of renal function and blood pressure in obesity-induced hypertension. Downregulation of renal CYP-derived eicosanoid synthesis in rats with diet-induced hypertension. 1310219: RU28318 was continuously infused intracerebroventricularly or subcutaneously in Dahl S/JR rats before or after the onset of hypertension induced by a high-salt diet. 1332023: The belief that diet is a major cause of stroke, diabetes, and hypertension was weakly associated with the dietary fiber density of lower social status groups. 13492357: Effect of choline on the hypertension of rats induced by high salt diet. 14035282: Effect of methionine on the blood hypertension of rats induced by a high salt diet. 14567503: Male DS rats (5 weeks of age) were fed a high-salt (8% NaCl) diet, resulting in hypertension accompanied by glomerular sclerosis and an increased urinary albumin excretion. 14573337: BACKGROUND: Feeding a high-fructose diet induces hypertension and insulin-resistance in Sprague-Dawley rats. 14707164: Endothelin-1 appears to play an important role in the maintenance of arterial pressure in rats fed HF and NF diets, but it does not appear to contribute to increased MAP in this model of diet-induced hypertension. Endothelial dysfunction has been suggested to play an important role in the development of obesity-induced hypertension. 1486591: After one month on the diets, a group of 19 rats in each diet group was operated upon to induce 2K1C hypertension. 15034204: These data suggest that the HFHSC diet causes dilated cardio-myopathy, whereas the HS diet produces arterial hypertension and the HFHS diet causes a vascular dysfunctional state that was highly responsive to alpha-adrenergic stimulation. 15191907: Activation of the systemic and adipose renin-angiotensin system in rats with diet-induced obesity and hypertension. 15206143: KO also revealed severe neo-intimal thickening in response to vascular-injury and hypertension induced by salt diet. 15221511: The findings confirm the antinatriuretic action of taurine and also suggest a role for the kinins in the mechanism of taurine action in diet-induced hypertension. 15333612: Because blood pressure, which is known to eventually rise in this model, was not as yet significantly elevated, the present data suggest that endothelial dysfunction precedes the onset of diet-induced hypertension. We tested whether consumption of a high-fat, high-sucrose (HFS) diet can affect endothelium-dependent relaxation, whether this precedes the development of diet-induced hypertension previously noted in this model, and whether it is mediated, in part, by changes in nitric oxide synthase (NOS) and/or NOS regulatory proteins. 15496307: We conclude that neonatal treatment with capsaicin plus a high-salt diet, and a high-salt diet alone both induced hypertension development in normal Wistar rats, which are associated with cardiovascular remodeling. 15773226: Oxidative stress has been proposed as important in the pathogenesis of hypertension. In Dahl-S rats, the high salt diet induced hypertension (139 +/- 3 mmHg in LS versus 186 +/- 2 mmHg in HS, p < .05) and significantly increased the U-8-ISO (24.9 +/- 3.6 ng/24 hr in LS versus 63.2 +/- 14.6 ng/24 hr in HS, p < .05). 1614069: In salt-sensitive rats given high salt diet, resulting in hypertension, hypoperfused kidneys and progressive renal damage, felodipine treatment results in reduced blood pressure, increased RBF and GFR, and reduced proteinuria and glomerulosclerosis. 16220202: These findings suggest that 17beta-E(2) may provide protection against the effect of high fructose diet, which causes hypertension, dysfunction of endothelial cells and insulin resistance. 16371062: 1.-- In the rat, a fructose-enriched diet induces hyperglycaemia, hypertriglyceridaemia, insulin resistance and hypertension; a model which resembles the human metabolic syndrome. 16843071: CONCLUSION: A high fructose diet in mice produced nocturnal hypertension and autonomic imbalance which may be related to activation of sympathetic and angiotensin systems. 16868307: The administration of ANG II, followed by exposure to high-salt diet, resulted in hypertension, cortical vasoconstriction, an increase in interstitial inflammatory cells (44.8 +/- 1.3 lymphocytes/mm2, and 30.8 +/- 1.2 macrophages/mm2 ANG II vs. 19.6 +/- 2 lymphocytes/mm2, and 22 +/- 0.7 macrophages/mm2 Sham), and increase in renal ANG II levels (1,358 +/- 74.6 pg/ml ANG II vs. 194 +/- 9.28 pg/ml Sham). 16895548: Addition of fructose to a rat diet for various periods of time leads to hypertension, hyperinsulinaemia and dyslipidaemia and provides a model for testing oxidative stress parameters in the animals. 16940562: Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (C<F10<F60). 17008074: CONCLUSION: Current research supports the notion of physical exercise as a potential non-pharmacological antihypertensive treatment for diet-induced obesity hypertension. The diet-induced obesity caused mild hypertension with adverse cardiovascular changes. 17023572: Since earlier studies have provided compelling evidence for the role of oxidative stress and tubulointerstitial inflammation in the pathogenesis of hypertension, we tested the hypothesis that partial SOD2 deficiency may result in hypertension. High-salt diet induced hypertension in 6-mo-old SOD2-deficient mice but not in wild-type mice. 17132534: Effect of sex hormones on non-esterified fatty acids, intra-abdominal fat accumulation, and hypertension induced by sucrose diet in male rats. 17207869: We previously showed that a high fructose diet in mice produced hypertension and sympathetic activation [8]. 17350697: Three weeks of 8% Na+ diet led to a higher blood pressure in DS rats compared to DR and W rats. 17579794: The present study suggests that both high-saturated and unsaturated fatty acid diets result in hypertension associated with significantly decreased endothelium-dependent vasorelaxation, dyslipidemia and IR, and that decreased endothelium-dependent vasorelaxation induced by high fatty acid diets is associated with impaired L-Arg-NO-cGMP pathways. 17585684: Feeding rats with high cholesterol diet induced hypercholesterolemia and high blood pressure. 17612651: Feeding rats with a high fructose diet results in insulin resistance and hypertension. In this study, we investigated the potential interrelationship between ET-1 and TXA2 in the development of fructose-induced hypertension in vivo. 17822696: Herein, the effects of [6-(nitrooxymethyl)pyridin-2-yl] methyl 4'-[1-(1,7'-dimethyl-2'-propyl-1H,3'H-2,5'-bibenzo[d]imidazol-3'-yl)ethyl] biphenyl-2-carboxylate (WB1106), a novel NO-releasing derivative of telmisartan newly synthesized, on the vasocontraction, hypertension and diet-induced insulin resistance were examined in vitro using rat aortic strips and in normotensive and spontaneous hypertension rats (SHR rats). 17951998: BACKGROUND: Chronic consumption of a high-salt diet causes hypertension (HTN) and renal injury in Dahl salt-sensitive (SSR) but not salt-resistant rats (SRR). The high-salt diet resulted in severe HTN and proteinuria (in SSR but not SRR) and marked elevations of renal tissue monocyte chemoattractant protein 1, p22(phox), NADPH oxidase subunit 4, angiotensin-II-positive cell count, infiltrating T cells and macrophages and further increases in AT(1) receptor, COX-2, PAI-1 and phospho-I kappaB in the SSR group. 17959024: In the present study, we investigated whether the effects of a novel, double-stranded, recombinant adeno-associated virus vector (rAAV)-mediated antisense angiotensin II receptor 1 (AT1R) gene efficiently prevents the development of hypertension induced by a high-salt diet in adult, male Sprague-Dawley (SD) rats. 17980562: Other forms of hypertension that are known to be mediated by endogenous ouabain-like substances include steroid/salt- (e.g., DOCA-salt) and ACTH-induced hypertension. An endogenous ouabain-like substance (OLS) plays a critical role in the etiology of experimental models of human hypertension induced by a high salt diet. 18076476: 1 A fructose-enriched diet induces hypertension, metabolic alterations and insulin resistance in rats, resembling human metabolic syndrome. 18418273: In Dahl S but not R rats, the high-salt diet caused marked hypertension, cardiac and kidney hypertrophy, and fibrosis. Prevention of salt-induced hypertension and fibrosis by AT1-receptor blockers in Dahl S rats. 18487446: Hypertension induced by high-salt diet in Dahl salt-sensitive rats leads to compensatory cardiac hypertrophy by approximately 11 wk, cardiac dysfunction at approximately 17 wk, and death from cardiac dysfunction at approximately 21 wk. Alteration of gene expression during progression of hypertension-induced cardiac dysfunction in rats. 18565278: AIM: To investigate the effects of the expression of human kallikrein (HK) on basal level blood pressure and high-salt diet-induced hypertension. 18804478: We recently found that inhibition of epsilonPKC slows down the progression of hypertension-induced HF in salt-sensitive Dahl rats fed a high-salt diet. Six week-old male Dahl rats were fed with a high-salt diet to induce systemic hypertension, which resulted in concentric left ventricular hypertrophy at the age of 11 weeks, followed by myocardial dilatation and HF at the age of 17 weeks. Mast cells and epsilonPKC: a role in cardiac remodeling in hypertension-induced heart failure. Together, our data suggest that epsilonPKC inhibition attenuates pathological remodeling in hypertension-induced HF, at least in part, by preventing cardiac MC degranulation. 18819643: The aim of present study was to investigate the effect of onion (Allium cepa) peel hydroalcoholic extract (OPE) on rat hypertension induced by high-fructose diet and aorta contractility. Although the extract did not change heart rate but after 3 weeks reduced the hypertension induced by fructose (p < 0.001). 19001546: Chronic infusion of angiotensin-(1-7) improves insulin resistance and hypertension induced by a high-fructose diet in rats. 19122855: We seek to determine: 1) whether a long-term high salt diet induces hypertension and renal injury in Sprague-Dawley (SD) rats and 2) whether the high salt diet-induced hypertension and renal injury are associated with decreased renal VEGF expression. Long-term High Salt Diet Causes Hypertension and Decreases Renal Expression of Vascular Endothelial Growth Factor in Sprague-Dawley Rats. These results suggest that a long-term HS diet induces renal injury and hypertension, which are associated with decreased renal VEGF expression in normotensive rodent animals. 1934539: The present study was performed to determine if chronic administration of a high salt diet induces hypertension similarly in young and adult rats and if treatment with DSP-4 alters the development of the hypertension. Age-dependent salt-induced hypertension in the rat: prevention with DSP-4, a selective noradrenergic neurotoxin. 19622599: Two experimental rat models of cardiovascular remodeling were used in this project: the deoxycorticosterone acetate (DOCA)-salt-induced model of chronic hypertension (study I) and a high-carbohydrate/high-fat diet-induced model producing chronic symptoms of the metabolic syndrome and its associated cardiovascular complications (study II). Our results in these rat models of hypertension and diet-induced obesity show that treatment with Avemar improved cardiac function, decreased macrophage infiltration resulting in decreased collagen deposition in the ventricular myocardium, reversed an increased stiffness of the left ventricle in the diseased hearts and attenuated increased plasma malondialdehyde concentrations. 19633817: These data suggest that the kidneys could be actively participating in the pathogenesis of insulin resistance-induced hypertension through the arachidonic acid CYP 450-RhoA/Rho kinase pathway(s). Renal protein expression for the cytochrome P (CYP) 450 arachidonic acid metabolizing enzymes has been shown to be altered in other models of diet-induced hypertension. 19683046: AIM OF THE STUDY: The present study was aimed to determine the effect of ethanolic extract of Solanum torvum (100 and 300 mg/kg; p.o. for 6 weeks) on systolic blood pressure (SBP), vascular reactivity, serum glucose, triglycerides, cholesterol, insulin and uric acid in fructose-induced hypertension. CONCLUSIONS: In conclusion, ethanolic extract of Solanum torvum could prevent the development of high blood pressure induced by a diet rich in fructose probably by reversing the metabolic alterations induced by fructose. 19749146: Therefore, we investigated the role of intrarenal RAS and oxidative stress in diet-induced hypertension and renal inflammation in spontaneously hypertensive rats (SHR) fed a high-fat diet. 19829664: Functional clustering analysis indicated the following functional pathways related to high salt diet-induced hypertension: (1) pro-inflammatory response ( upward arrowIL-17, CCL28; downward arrow NFkappabib); (2) endothelial dysfunction ( downward arrowVEGF-A, VEGF-B, endoglin); (3) pro-matrix formation ( upward arrowosteopontin, IGFBP-5; downward arrow IFN-gamma); and (4) attenuated cell survival and differentiation ( downward arrowCNTF, IGF-II R, ephrin-B1). OBJECTIVE: The present study examines whether a long-term high salt diet causes hypertension and renal injury in normal subjects [Sprague-Dawley (SD) rats] and alters renal cytokine-related gene expression profiles. Long-term high salt diet causes hypertension and alters renal cytokine gene expression profiles in Sprague-Dawley rats. 19897715: Intervention diet resulted in obesity, hypertension, and dyslipidemia. 20059648: The present study aimed to determine whether a moderate increase of endogenous plasma leptin levels affected arterial blood pressure in rats with diet-induced obesity and hypertension. 20305782: In Dahl salt-sensitive rats, high-salt diet resulted in hypertension, cardiac hypertrophy and subsequent heart failure, and significantly stimulated PARM-1 expression in the hearts, with a concomitant increase in ER stress markers such as GRP78 and CHOP. 20462965: The HS diet led to higher blood pressure (224 +/- 8 mmHg), a 180-fold increase in uAGT (1.8 +/- 0.2 microg x kg(-1) x day(-1)), and increased PROT (98 +/- 9 vs. 7 +/- 1 mg x kg(-1) x day(-1)). 20543715: METHODS AND RESULTS: Male Dahl salt-sensitive rats were fed a high-salt diet from age 7 weeks to induce hypertension and were either vehicle or orally administered benidipine (3 mg/kg daily) or nitrendipine (10 mg/kg daily) from age 10 to 18 weeks. 20596792: In this model, a high-salt diet induced high blood pressure and increased ghrelin levels but reduced food intake. 20645789: (Vitaceae) on systolic blood pressure (SBP), vascular reactivity, serum glucose, triglycerides, cholesterol, and insulin in fructose-induced hypertension. The results suggest that myricetin could prevent the development of high blood pressure induced by a diet rich in fructose, probably by reversing the metabolic alterations induced by fructose. 20729036: RESULTS: The IUGR adults had higher urinary excretion of protein and blood pressure than controls and the HP diet caused more severe hypertension and proteinuria than IUGR itself. 21228113: Protein excretion rose from 20 to 120 mg/day in Dahl S rats fed a high-salt diet (8.0% NaCl) for 4 wk to induce hypertension. 21246380: However, it remains unknown whether activation of TRPV1 by dietary capsaicin could prevent the vascular oxidative stress and hypertension induced by a high-salt diet. TRPV1 activation prevents high-salt diet-induced nocturnal hypertension in mice. 21562602: The aim of this study was to determine the effect of NO depletion on renal sodium handling in a model of diet-induced obesity hypertension. 21642952: RESULTS: In rats injected with control shRNA, high-salt diet (HS) caused higher systolic blood pressure compared with normal-salt diet (NS) (HS:149 +/- 4 mmHg; NS:126 +/- 2 mmHg, P<0.05). 21733336: Carvedilol treatment fully prevented diet-induced insulin resistance and hypertension, mimicking the effect of caffeine. 21790490: The results suggest that A-HRS could prevent the development of high-blood pressure induced by a diet rich in fructose, probably by reversing the metabolic alterations induced by fructose. We have examined the effect of chronic administration of A-HRS (100 and 300 mg kg-1; p.o.) isolated from Hibiscus rosa sinensis (Malvaceae) on systolic blood pressure (SBP), vascular reactivity, serum glucose, triglycerides, cholesterol, uric acid and insulin in fructose-induced hypertension model. 21925350: Feeding the S diet throughout gestation and lactation resulted in higher systolic blood pressure (P < .005), FI (P < .05), and glucagon-like peptide 1 and lower peptide YY at weaning and higher BW during weeks 11 to 15 and fat pad mass at week 15 (all Ps < .05). 21968275: MBG-mediated inhibition of sodium pumps in vascular smooth muscle likely plays a role in the hypertension induced by salty diets in these rodents. 22231675: Metformin administration reversed diet-induced hypertension and glucose intolerance. 22258022: In male coupling factor 6 (CF6)-overexpressing transgenic (TG) mice, a high-salt diet induces hypertension and cardiac systolic dysfunction with excessive reactive oxygen species generation. 22418978: Amiloride treatment also reduced high blood pressure caused by the high-salt diet in these mice. 22449517: CONCLUSIONS: The overall results suggest that, TCW treatment could prevent and reverse high blood pressure induced by high fructose diet probably by inhibition of lipid peroxidation, upregulation of antioxidant status and improved insulin sensitivity. 22517449: MATERIALS AND METHODS: Cyp1a1ren-2 rats received a diet containing 0% or 0.167% indole-3-carbinonl (I3C) for 4 weeks to induce hypertension. 22907982: DIS and DIR rats were fed 8% NaCl-containing diet to induce hypertension, with blood pressure measurement once a week, euthanized at 6, 8, or 12 weeks of age, and subjected to the measurement of plasma nitric oxide (NO) and von Willebrand factor (vWF) concentrations combined with histopathological examinations and immunohistochemical detections of vWF in the pancreas and kidney. 23029690: High-salt diet may cause hypertension. 23033372: Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Enhanced adipose afferent reflex contributes to sympathetic activation in diet-induced obesity hypertension. 23335793: The intervention diet produced obesity, hypertension, dyslipidemia, and impaired glucose tolerance, but not atherosclerosis. 23349943: To clarify the role of vitamin D-deficiency in CVD in vivo, we generated mouse models of diet-induced vitamin D deficiency in two backgrounds (LDL receptor- and ApoE-null mice) that resemble humans with diet-induced hypertension and atherosclerosis. Vitamin D deficiency induces high blood pressure and accelerates atherosclerosis in mice. 23469072: Rats were fed a I3C diet between 4-8 weeks of age to induce hypertension. 23530003: Carotid body denervation prevents the development of insulin resistance and hypertension induced by hypercaloric diets. We demonstrate that CB activity is increased in IR animal models and that CSN resection prevents CB overactivation and diet-induced IR and HT. 23552867: A disease control group received albumin but not potassium or icatibant, and all groups were exposed to a hypersodic diet to induce salt-sensitive hypertension. 23906564: Aldosterone treatment associated with a high salt diet induced not only hypertension but also oxidative stress, collagen synthesis and vascular inflammation. 23932324: CONCLUSIONS: High-phosphate and zinc-free diet induced hypertension and cardiac dysfunction. 23933891: We have previously shown that a high salt diet causes hypertension in MnSOD-deficient (MnSOD(+/-)) mice but not in wild-type mice. CONCLUSION: Salt-induced hypertension in MnSOD(+/-) mice is associated with activation of intra-renal inflammatory and ROS generating pathways. 24124187: Systemic administration of ANG II combined with a high-salt diet induces hypertension that is postulated to involve elevated SNA. 2430013: Resting aortic Ca2+ uptake was shown also to be increased in hypertension-resistant R/JR rats by the extreme treatment of unilateral nephrectomy plus 8% NaCl diet which induces hypertension in R/JR rats. 24322818: RESULTS: Eighty-three percent of adults strongly agreed or agreed that most of the sodium we eat comes from packaged, processed, store-bought, and restaurant foods, and 93.0% thought that a high-salt diet could cause hypertension. 24379189: These results may partially explain the mechanism by which a fructose diet induces hypertension. 24467657: We examined in this study whether fructose affects ATP content in RVLM and its significance in the increase in central sympathetic outflow and hypertension induced by the high fructose diet (HFD). An increase in adenosine-5'-triphosphate (ATP) content in rostral ventrolateral medulla is engaged in the high fructose diet-induced hypertension. 24770651: The AngII inhibition-mediated beneficial effects are likely attributable, at least in part, to restoration of p38/ERK-dependent apelin/APJ expression in diet-induced obesity-related hypertension. 24796088: In particular, inappropriate lifestyle including diet and exercise induces lifestyle-related diseases such as hypertension, diabetes, dyslipidemia, obesity, cigarette smoking which promote cognitive decline and the occurrence of dementia as vascular risk factors. 24890824: It concludes that TRPV1 activation in the cortical collecting ducts by capsaicin increases urinary sodium excretion and avoids HS diet-induced hypertension through antagonizing alphaENaC-mediated urinary sodium reabsorption. 25086377: SIGNIFICANCE: Impaired endothelial Akt activation and increased cav-1 expression and resultant decreased eNOS activation contributes to aggravated high-salt diet-induced endothelial dysfunction and hypertension in DM rats. 25233358: Four weeks of treatment with HS diet induced hypertension, proteinuria, glomerular sclerosis and hypertrophy, glomerular podocyte injury, and tubulointerstitial fibrosis in DSS rats. 25314281: Stress (48.4% vs 60% vs 50%; p = 0.31) and, especially at DRH, diet (62.2% vs 22% vs 36%; p < 0.0001) were identified most frequently as causes of cHTN and an association with symptoms was common (83.5% vs 98% vs 78%; p = 0.15). 25351462: Here, we investigated TRPP2 expression change in VSMCs from high-salt intake hypertensive rats and role of TRPP2 in the development of high-salt diet-induced hypertension. 25370989: MATERIAL AND METHODS: Pregnant Dahl-S rats were fed a high-salt diet to induce the development of hypertension and fetal growth restriction. 25452472: We found that hypertension and renal injury induced by a high-salt diet were substantially attenuated in Dahl SS/JrHsdMcwiCrl (SS/Crl) rats that had been maintained for many generations on the grain-based 5L2F diet compared with SS/JrHsdMcwi rats (SS/Mcw) maintained on the casein-based AIN-76A diet (mean arterial pressure, 116+/-9 versus 154+/-25 mm Hg; urinary albumin excretion, 23+/-12 versus 170+/-80 mg/d). Together, the data suggest that maternal diet during the gestational-lactational period has substantial effects on the development of salt-induced hypertension and renal injury in adult SS rats. Conversely, salt-induced hypertension and renal injury were significantly attenuated in rats developed from SS/Mcw embryos transferred to SS/Crl surrogate mothers. Salt-induced hypertension and renal injury were substantially exacerbated in rats developed from SS/Crl embryos transferred to SS/Mcw surrogate mothers. 25560239: To evaluate the relationship between high BP induced by a high sodium (Na) diet and Mg, and other mineral balances, two experimental rat models of salt-sensitive, induced-hypertension were used: Ang-II infused and Dahl salt-sensitive (SS) rats. Blood pressure, magnesium and other mineral balance in two rat models of salt-sensitive, induced hypertension: effects of a non-peptide angiotensin II receptor type 1 antagonist. 25594546: Next, we administered (99m)Tc-MIBI to Dahl salt-sensitive rats fed a high-salt diet, which leads to hypertension and heart failure. 26038832: Male Sprague Dawley rats were fed with a normal salt diet (NS, 0.3%) or a high salt diet (HS, 8%) for 8 weeks to induce hypertension. 26259506: Experimental studies suggest that a higher intra-cellular ratio of Ca:Mg, which may be induced by a diet high in Ca and low in Mg, may lead to hypertension and insulin resistance. 26261587: Salt-sensitive hypertension was successfully induced by 12-week high salt diet in BHR model. 26265746: Six weeks of high salt diet significantly increased both mean arterial pressure (MAP) and pulse pressure, demonstrating successful induction of HTN in all rats. Dahl salt-sensitive rats (n = 12) were given a high salt diet to induce HTN. 26380524: We concluded that salusin-beta in the PVN markedly increased sympathetic outflow and blood pressure in diet-induced OH rats via NF-kappaB signaling. 26383217: In focus groups, participants cited westernized diets, lack of physical activity, stress, psychological factors, and urbanization as causative factors for hypertension. 26465239: Melatonin prevents kidney injury in a high salt diet-induced hypertension model by decreasing oxidative stress. 26619664: Recently, childhood hypertension might be closely related to the abnormality of maternal gestational period caused by the strict diet and the maternal smoking. Developmental Origins of Health and Disease(DOHaD) theory is now highlighted in the pathogenesis of adulthood hypertension. 26635631: This review will address the new insights on the maternal diet induced-hypertension that include the potential role of the phenotypic plasticity, specifically the perinatal protein malnutrition, and sympathetic-respiratory overactivity. New Insights on the Maternal Diet Induced-Hypertension: Potential Role of the Phenotypic Plasticity and Sympathetic-Respiratory Overactivity. Besides, environmental conditions during perinatal development such as maternal malnutrition can program changes in the integration among renal, neural, and endocrine system leading to hypertension. 26640794: Protective Effect of Enalapril against Methionine-Enriched Diet-Induced Hypertension: Role of Endoplasmic Reticulum and Oxidative Stress. 27027507: We have shown that selective bilateral resection of the nerve of the CB, the carotid sinus nerve (CSN), totally prevents diet-induced insulin resistance, hyperglycaemia, dyslipidaemia, hypertension and sympathoadrenal overactivity. 27179211: METHODS: Seven-weeks old Dahl salt-sensitive rats were fed a high salt diet for 5weeks to induce hypertension. 27296999: Here, we assessed the contribution of leptin, alpha-MSH, and neuropeptide Y signaling in the DMH and VMH to diet-induced hypertension. 2733384: The progression of small vessel renal vascular disease was studied in inbred Dahl salt-sensitive (SS/Jr) and salt-resistant rats with acute hypertension induced by a high salt diet. 27452860: The purpose of this work was to know if oral administration of anti-oxidant and free-radical scavenger CoQ10 may attenuate high salt-induced hypertension via regulating neurotransmitters and cytokines in the hypothalamic paraventricular nucleus (PVN). Adult male Sprague-Dawley (SD) rats were fed with a normal salt diet (NS, 0.3% NaCl) or a high salt diet (HS, 8% NaCl) for 15 weeks to induce hypertension. 27457968: BACKGROUND: Diet plays an important role in the etiology of hypertension. 27779710: The present study investigated the effects of severe hypertension induced by a high-salt (HS) diet and antihypertensive therapy on the pathophysiological condition of spontaneously hypertensive rats (SHRs) with steatohepatitis. 27841023: Although when evaluated in anesthetized rats, only the HSMHF group presented augmented blood pressure, evaluation in conscious animals revealed that both the MHF and HSMHF diets, but not the HS alone, were able to induce tachycardia and hypertension. In conclusion, a MHF diet containing 6% fructose was enough to render the renal vascular bed hyperreactive to phenylephrine and to induce both hypertension and tachycardia. 27922176: EXPERIMENTAL APPROACH: Seven-week-old Dahl salt-sensitive rats were fed a high-salt diet for 5 weeks to induce hypertension. 27993957: A high-fructose diet is shown to induce salt-sensitive hypertension, but the underlying mechanism largely remains unknown. 28338001: This study was designed to explore the precise mechanisms of RAS acting on reactive oxygen species (ROS) in salt-induced hypertension. These results, for the first time, identified that the precise signaling pathway of RAS regulating ROS in PVN is via AT1R/PKCgamma/Rac1 in salt-induced hypertension. Male Wistar rats were administered with a high-salt diet (HS, 8.0% NaCl) for 8 weeks to induced hypertension. Renin-angiotensin system acting on reactive oxygen species in paraventricular nucleus induces sympathetic activation via AT1R/PKCgamma/Rac1 pathway in salt-induced hypertension. 28408634: Previously, we reported that 20% fructose diet causes salt-sensitive hypertension. 28730828: A high-salt diet induces hypertension in the salt-sensitive strain, but not in the salt-resistant strain. The high-salt diet led to salt-induced hypertension, but did not affect the level of adult neurogenesis in the dentate gyrus of the hippocampus. 28782443: Intracerebroventricular infusion of Abeta induced a progressive rise in blood pressure in rats with pre-existing hypertension produced by a high-salt diet ( p < 0.0001), but no change in blood pressure in normotensive rats. 28813008: Fructose-enriched diets cause salt-sensitive hypertension. 29120957: Deletion of protein kinase B2 preserves cardiac function by blocking interleukin-6-mediated injury and restores blood pressure during angiotensin II/high-salt-diet-induced hypertension. CONCLUSION: AKT2 deficiency prevents the development of AngII/HSD-induced hypertension, cardiac dysfunction and myocardial injury including oxidative stress, fibrosis and inflammation by suppressing IL-6 expression. 29315230: We examined whether maternal high-fructose diet increases vulnerability to post-weaning high-fructose or high-fat diets induced hypertension in adult offspring and determined the underlying mechanisms. Maternal high-fructose diet exacerbates post-weaning high-fat diet-induced programmed hypertension. 29366359: Salt intake and poor diet were reported as main causes of hypertension by 27.5% and 21.5% of the participants, respectively, whereas more than 85% acknowledged myocardial infarction and stroke as its main consequences. 29436481: Rats fed a 28-week High Fat/Fruc provide a relevant model of diet-induced hypertension. Long-term diet-induced hypertension in rats is associated with reduced expression and function of small artery SKCa, IKCa, and Kir2.1 channels. Abdominal obesity and/or a high intake of fructose may cause hypertension. 29520237: HS diet induced hypertension and significantly increased cerebrospinal fluid (CSF) sodium concentration ([Na+]) in Dahl S rats, but not in normal SD rats. 29541444: We found that, in PSGL-1+/+ mice, high salt diet resulted in high blood pressure with the increased expression of serum inflammatory cytokines IL-6, IL-1beta and TNFalpha, vascular injury markers MCP-1, ET-1, and VWF, and renal macrophages and T cells infiltration, and endothelium-dependent acetylcholine vasodilation dysfunction. 29701904: Through measurements of arterial tension and protein level, we showed that high-salt diet induced hypertension increases activity of PKC (protein kinase C) and ERK1/2 (extracellular signal-regulated kinase 1/2). 29705701: Protective role of AgRP neuron's PDK1 against salt-induced hypertension. These results demonstrate a novel role of PDK1 in AgRP neurons to counteract the high salt diet-induced hypertension by preventing hyperactivation of PVN nesfatin-1 neurons. 29941515: Male A1KOs and A2BKOs were not protected against 4% salt diet-induced hypertension. 30048986: Therefore, this study aimed to investigate the mechanisms within RVLM that can influence exercise training induced effects in salt-induced hypertension. METHODS: Male Wistar rats were fed with a normal salt (0.3%) (NS) or a high salt (8%) (HS) diet for 12 weeks to induce hypertension. 30059752: However, the molecular mechanism of high-salt diet induced hypertension and the serious complications in cardiovascular system still remain unknown. CONCLUSION: Our study provided new insight about molecular mechanism of high-salt induced hypertension and heart and kidney damage. Differential expression gene (DEG) analysis and further functional annotation including Ingenuity Pathway Analysis (IPA) was performed to reveal the molecular mechanism of high-salt induced hypertension and organ injury. 30279341: We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. 30426340: Salt-sensitive rats received a high-salt (HS) diet to induce hypertension, or a normal-salt (NS) diet as control. 30591086: RESULTS: Twenty-four per cent of rural and 40.5 % of urban participants knew that a high-salt diet causes high blood pressure. 30670332: Fueling Ketone Metabolism Quenches Salt-Induced Hypertension. (Cell Reports 2018;25:677-689) discovered that supplementation with a metabolic precursor produced beta-hydroxybutyrate (BHB), counteracting the pathological effects of high-salt diet-induced hypertension, suggesting a new treatment modality. 30687795: We asked their views on the changes in diet that had taken place over their lifetimes and also on the causes of 'noncommunicable' diseases, such as Type 2 diabetes and hypertension in their communities. 30783421: Mice with high-salt diet-induced hypertension were divided into four groups: Control (standard diet alone for 8 weeks), model (diet containing 8% NaCl for 8 weeks and intragastric administration of distilled water for the last 4 weeks), XJEK + high-salt-treated (diet containing 8% NaCl for 8 weeks and intragastric administration of XJEK for the last 4 weeks) and irbesartan + high-salt-treated (diet containing 8% NaCl for 8 weeks with intragastric administration of irbesartan for the last 4 weeks). Therefore, XJEK exerted protective effects against high salt-induced hypertension and cardiovascular remodeling in mice via improving ED, restoring pro- and anti-inflammatory factor balance and decreasing oxidative stress. 30896408: Testing cognition in high-salt diet models that induce hypertension will increase the translatability of future studies in rodents. 30934709: The antihypertensive effects of VPH and VPH-I were studied during 24 h (short-term effect) and 30 days (long-term effect) using high-salt (18% NaCl) and -fructose (10%) diet (HSFD)-induced hypertension. 31065462: Results: Among CYP2C11-null rats, a high-salt diet (females: 156.79 +/- 15.89 mm Hg, males: 130.25 +/- 16.76 mm Hg, n = 10) resulted in significantly higher blood pressure than a normal diet (females: 118.05 +/- 8.43 mm Hg, P < 0.01; males: 115.15 +/- 11.45 mm Hg, P < 0.05, n = 10). 31071969: Pyrogallol-Phloroglucinol-6,6'-Bieckol from Ecklonia cava Improved Blood Circulation in Diet-Induced Obese and Diet-Induced Hypertension Mouse Models. 31257672: OBJECTIVES: To study the promotive effect of salt-induced hypertension on crystal deposition and urolithiasis using a salt-sensitive rat hypertension model. Hypertension was induced by a high-salt diet. 31295767: Whether maternal 3,3-dimethyl-1-butanol (DMB, an inhibitor for TMA formation) treatment or the predominant SCFA acetate supplementation can prevent programed hypertension induced by a high-fructose diet (HFD) exposure during pregnancy and lactation in adult male offspring is examined. HFD-induced hypertension is relevant to increased plasma levels of TMA and acetate, and alterations of gut microbial composition. Maternal HFD induces programed hypertension in adult male offspring, which is prevented by maternal acetate supplementation or DMB treatment. 31600722: SGK1 activation exacerbates diet-induced obesity, metabolic syndrome and hypertension. 31608671: Dahl salt-sensitive (DSS) rats fed a high-salt diet to induce hypertension and organ damage were treated with the sGC stimulator praliciguat to determine its effects on hemodynamics, biomarkers of inflammation, fibrosis, tissue function, and organ damage. 31641986: Salt-sensitive rats were given a high salt diet for 10 weeks to induce hypertension. Toll-like receptor 4 (TLR4) and cellular Src (c-Src) are closely associated with inflammatory cytokines and oxidative stress in hypertension, so we designed this study to explore the exact role of c-Src in the mechanism of action of the TLR4 signaling pathway in salt-induced hypertension. Blockade of c-Src Within the Paraventricular Nucleus Attenuates Inflammatory Cytokines and Oxidative Stress in the Mechanism of the TLR4 Signal Pathway in Salt-Induced Hypertension. 31683330: CONCLUSION: In conclusion, urate-lowering therapy protects rats against fructose-induced obesity hypertension. Hyperuricemia Inhibition Protects SD Rats Against Fructose-Induced Obesity Hypertension Via Modulation of Inflammation and Renin-Angiotensin System in Adipose Tissue. OBJECTIVE: The present study was aimed to reveal the relationship between uric acid and fructose-induced obesity hypertension and its mechanisms. METHODS: A rat model with obesity hypertension was induced by a high-fructose diet. 31835800: The high fructose-enriched diet induced cardiometabolic disorders (hypertension, hyperglycemia, IR and dyslipidemia), an increase in uric acid concentration, transaminase activities and C-reactive protein level. 32059997: Thus, salt-sensitive hypertension is induced in CKD via activation of the renal WNK1- SPAK-NCC phosphorylation cascade by TNF-alpha, reflecting a link with the immune system. Although chronic kidney disease (CKD) is a common cause of salt-sensitive hypertension, the involvement of the WNK phosphorylation cascade is unknown. Moreover, a high-salt diet did not adequately suppress activation of the WNK1-SPAK-NCC phosphorylation cascade in this model, leading to salt-sensitive hypertension. 32078445: We found that HSD induced hypertension in Wistar rats. Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension. Intestinal flora has been reported to be associated with high salt-induced hypertension (hSIH). 32290913: As shown in multivariate logistic regression analysis, the OR(95%CI) of high school and above, high income level, knowing the recommended intake of salt, knowing that high salt diet can cause high blood pressure on the influence of having salt control spoon was 1. Among the student caregivers who having salt control spoon, the OR(95%CI) of knowing the recommended intake of salt, knowing that high salt diet can cause high blood pressure, and source of salt control spoon(community/unit, friends/relatives) on the influence of using salt control spoon was 1. 32305658: Gut dysbiosis contributes to high fructose-induced salt-sensitive hypertension in Sprague-Dawley rats.OBJECTIVES: Although it is known that high fructose intake causes salt-sensitive hypertension, the underlying mechanism remains unclear. Gut dysbiosis contributes to high fructose-induced salt-sensitive hypertension in Sprague-Dawley rats. METHODS: For 8 wk, Sprague-Dawley rats were given 20% fructose in drinking water and 4% sodium chloride in their diet to induce hypertension. 32360273: Dahl salt-sensitive rats were fed a high-salt diet to induce hypertension and diastolic dysfunction and were then treated with dapagliflozin for six weeks. 3241187: In susceptible people and rats, a high-NaCl diet leads to hypertension. 32475311: An inability to increase EETs in response to a high-salt diet results in salt-sensitive hypertension. 32882266: Maternal exposure to high-fat and high-cholesterol diet induces arterial hypertension and oxidative stress along the gut-kidney axis in rat offspring. SIGNIFICANCE: HFHC diet during pregnancy and lactation induces sex-specific oxidative stress along the gut-kidney axis in offspring, which might induce renal dysfunction and arterial hypertension in later life. Maternal exposure to high-fat and high-cholesterol diet induces arterial hypertension and oxidative stress along the gut-kidney axis in rat offspring.AIMS: Evaluate the effects of maternal high fat and high cholesterol (HFHC) diet consumption on blood pressure (BP), renal function and oxidative stress along the gut-kidney axis in male and female rat offspring. 33061560: Discussion: Thus, short-term consumption of high fructose plus high salt diet by rats results in modest hypertension, insulin resistance, diminished aortic and renal artery compliance, and left ventricular diastolic dysfunction. Existing studies show that a rat model reflecting a diet of fructose and salt consumed by the upper 20th percentile of the human population results in salt-sensitive hypertension mitigated by treatment with an antioxidant. 33250683: The key proteins identified in this study warrant further development as new therapeutic targets or biomarkers of cardiovascular diseases associated with high-salt diet-induced hypertension. To that end, the present study identified and quantitated serum proteins that were differentially expressed in male rats fed regular chow (n = 4) and those fed a high-salt diet (n = 4) to induce hypertension. Although high-salt diets can result in hypertension and impaired vascular function, the molecular mechanisms underlying these dysfunctions are not fully known. 33279469: CFTR plays an important role in the regulation of vascular resistance and high-fructose/salt-diet induced hypertension in mice. Here we studied the function of CFTR Cl - channels in regulation of BP and in the high-fructose-salt-diet (HFSD) induced hypertension in mice. 33361535: In summary, GABA-salt reduced high salt, high cholesterol diet induced hypertension in our mouse model by reducing M1 polarization, EC dysfunction, and VSMC proliferation. Gamma-aminobutyric acid-salt attenuated high cholesterol/high salt diet induced hypertension in mice. 33803946: A high amount of salt in the diet increases blood pressure (BP) and leads to salt-sensitive hypertension in individuals with impaired renal sodium excretion. 33817305: We assessed the effects of PCA at 50 and 100 mg/kg on the activation of signaling pathways for tissue necrosis factor (TNF)-alpha/nuclear factor (NF)-kappaB/nuclear factor erythroid 2 (Nrf-2) on progression and development in an elastase-induced CA model, accompanied by a high-salt diet to induce hypertension. 33864813: In conclusion, sEH inhibition by TPPU alleviated insulin resistance and hypertension induced by a HF-HS diet in mice. 33911065: In vivo experiments showed the lack of ATF4 gene could prevent hypertension in mice induced by high-salt diet and protect endothelial function. 34259014: Conclusion HFr-induced hypertension and renal damage are exaggerated in DS rats via renal renin-angiotensin system activation, which can be controlled by renin-angiotensin system inhibitors. High Fructose-Induced Hypertension and Renal Damage Are Exaggerated in Dahl Salt-Sensitive Rats via Renal Renin-Angiotensin System Activation. Enalapril and candesartan attenuated the HFr-induced hypertension, albuminuria, glomerular hyperfiltration, and renal damage in DS rats. However, it has been unknown whether the HFr-induced hypertension and renal damage are exaggerated in subjects with salt sensitivity. Background High-fructose diet (HFr) induces hypertension and renal damage. 34444769: Both curcumin and vehicle treatment groups exhibited similar degrees of high-salt diet-induced hypertension in DS rats. 34495901: CONCLUSION: Febuxostat ameliorates high salt diet-induced hypertension and renal damage with a reduction of renal oxidative stress in Dahl salt-sensitive rats. RESULTS: Treatment with febuxostat for 8 weeks attenuated high salt diet-induced hypertension, renal dysfunction, glomerular injury, and renal interstitial fibrosis. 34572600: We utilized two common mouse models of experimental hypertension: L-arginine methyl ester hydrochloride (L-NAME)/high-salt-diet-induced hypertension (LSHTN) and angiotensin II induced hypertension (AHTN). 34894804: We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut-kidney axis. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut-kidney axis. 34994761: In conclusion, AO intervention could prevent HS diet-induced hypertension in SS rats by restoring the metabolic homeostasis of the kidneys. 35022384: These results show that Ala alleviates high-salt diet-induced hypertension and renal dysfunction. Dahl rats were fed with high-salt diets to induce hypertension and renal damage in vivo, and HK-2 cells were treated with sodium chloride (NaCl) to induce renal injury in vitro. Ala administration alleviated the high-salt diet-induced hypertension, renal dysfunction, and renal fibrosis and apoptosis in Dahl SS rats. 35114278: Calcitriol ameliorates renal injury with high-salt diet-induced hypertension by upregulating GLIS2 expression and AMPK/mTOR-regulated autophagy. The goal of the present study was to investigate the protective effect of calcitriol on high-salt diet-induced hypertension. 35151723: Diet-induced hypertension in rats is associated with increased renal vasoconstrictor response to angiotensin II after imitated endothelial dysfunction. Our data suggest that diet-induced hypertension is not caused by an increase in renal vascular resistance. The mechanisms behind development of diet-induced hypertension remain unclear. 35181841: Exogenous H 2 S Ameliorates High Salt-Induced Hypertension by Alleviating Oxidative Stress and Inflammation in the Paraventricular Nucleus in Dahl S Rats. These findings suggest that exogenous H 2 S attenuates hypertension caused by an HSD by ameliorating oxidative stress, inflammation, and apoptosis in the PVN. 35222552: Conclusion: The extremely high burden of vascular disease is mainly explained by the unhealthy lifestyle of our patients (i.e., high prevalence of smoking, unhealthy diet and physical inactivity resulting in obesity and hypertension). 35315647: In this study, we explored the salutary effects and relevant mechanisms of coriander ( Coriandrum sativum L.), an herbal plant with culinary and medicinal values, on high-fructose and high-salt diet (HFSD)-induced hypertension in SD rats. Conclusively, long-term consumption of coriander may ameliorate HFSD-induced hypertension by mitigating HFSD-caused abnormal changes in vascular endothelial function, renal and intestinal sodium absorption, glucolipid homeostasis, and gut microbiota in rats. Protective Effect of Coriander ( Coriandrum sativum L.) on High-Fructose and High-Salt Diet-Induced Hypertension: Relevant to Improvement of Renal and Intestinal Function. 35439285: Blockade of Microglial Activation in Hypothalamic Paraventricular Nucleus Improves High-salt Induced Hypertension. Blockade of PVN microglial activation inhibits inflammation and oxidative stress, therefore attenuating the development of hypertension induced by high-salt diet. METHODS: High-salt diet was given to male Dahl salt-sensitive rats to induce hypertension. 35452099: Accordingly, efforts to identify and correct the nutrient deficiencies that promote salt sensitivity hold promise for decreasing population risk of salt-induced hypertension without requiring reductions in salt intake. High-salt diets are a major cause of hypertension and cardiovascular (CV) disease. Suboptimal nutrient intake is a common cause of the hemodynamic disturbances mediating salt-induced hypertension. Mechanism-based strategies to prevent salt sensitivity and salt-induced hypertension. 35500733: These include: insulin resistance, hypertension, dyslipidaemia and abdominal obesity caused by a diet rich in refined carbohydrates and saturated fats. 35551736: We previously demonstrated that a functional knock-out of Clcn6 on the Dahl SS rat background (SS-Clcn6) had significantly reduced diastolic blood pressure (BP) compared to WT rats when challenged with a high 4% NaCl (HS) diet to induce hypertension. 35551753: Rats were fed a 4%NaCl diet to induce hypertension, and then the diet was switched back to normal (0.4%NaCl). 35600813: These findings indicate that GT and OLT can prevent hypertension caused by high-salt diets, which may be due to the regulation of intestinal flora by GT and OLT. However, the interventional effects of GT and OLT on hypertension induced by a high-salt diet and its mechanism have not been fully explored. 35724813: We examined whether sodium butyrate administration in pregnancy and lactation can prevent hypertension induced by a maternal tryptophan-free diet in adult progeny and explored the protective mechanisms. 35745245: The relationship between fructose and a high-salt diet, leading to hypertension and other deleterious cardiovascular parameters, has also become more evident, especially in preclinical studies. 35946264: Acid-producing diets can cause high blood pressure through the kidneys, causing the production of the hormones angiotensin II, endothelin-1, and aldosterone. 35986807: Genistein Alleviates Oxidative Stress and Inflammation in the Hypothalamic Paraventricular Nucleus by Activating the Sirt1/Nrf2 Pathway in High Salt-Induced Hypertension. Our results demonstrated that PVN infusion of Gen could inhibit the progression of hypertension induced by an HS diet by activating the Sirt1/Nrf2 pathway. Hypertension caused by a high-salt (HS) diet is one of the major causes of cardiovascular diseases. This study investigates genistein's (Gen) role in HS-induced hypertension and the underlying molecular mechanism. 36017217: In this study, traditional Chinese medicine (TCM) syndrome of hypertension caused by high salt had been diagnosed and the pathogenesis of hypertension was explored from the perspective of intestinal microecology. Hypertension induced by a high salt diet belongs to liver-Yang hyperactivity syndrome. Rats in a high salt diet-induced hypertension group (CG) and normal group (CZ) were compared by 16S rRNA gene full-length sequencing and liquid chromatography and mass spectrometry to identify differences in the bacterial community structure, metabolites, and metabolic pathways. These findings suggest that a high salt diet induces hypertension of liver-Yang hyperactivity syndrome by mediating the microbiota associated with the glutamate/GABA-glutamine metabolic cycle via the gut-brain axis. 36117446: We hypothesized that a diet high in fructose with or without high salt in young male Sprague Dawley rats will lead to salt-sensitive hypertension, albuminuria, and decreased renal function in maturity. 36136562: We now review the revised concept of postbiotics concerning their potential clinical applications and research in kidney disease, by discussing in detail several formulations that are undergoing preclinical development such as GABA-salt for diet-induced hypertension and kidney injury, sonicated Lactobacillus paracasei in high fat diet-induced kidney injury, GABA-salt, lacto-GABA-salt and postbiotic-GABA-salt in acute kidney injury, and O. formigenes lysates for hyperoxaluria. 36181277: Therefore, the aim of this study was to investigate the antihypertensive effects of green tea on high-salt diet-induced hypertension in old male rats. 3628539: The combination of stress and low diet produced the highest blood pressure and lowest serum ionized calcium values. 36451714: Among environmental factors, a high salt diet is an important cause for hypertension. 36458162: However, its role in the progression of hypertension induced by high salt diet (HSD) has not been elucidated. Together, our results offer evidence that the dietary uptake of glutamine may be associated with attenuating the development of high salt-induced hypertension and slightly alleviating the degree of left ventricular hypertrophy in hypertensive rats. The association of dietary glutamine supplementation with the development of high salt-induced hypertension in rats. 36700429: In the EC fraction, HS-induced hypertension significantly altered protein mediators of contractility, metabolism, mechanotransduction, renal function, and the coagulation cascade. METHODS: We performed systematic molecular characterization of the endothelial glycocalyx and EC proteomes in mice with HS (8%) diet-induced hypertension versus healthy control animals. 36729699: INTRODUCTION: High-fructose diet (HFr) causes metabolic syndrome, and HFr-induced hypertension and renal damage are exaggerated in Dahl salt-sensitive (DS) rats. Exercise Training Prevents High Fructose-Induced Hypertension and Renal Damages in Male Dahl Salt-Sensitive Rats. CONCLUSIONS: Ex prevents HFr-induced hypertension and renal damages in DS rats. 36827228: (Re)modeling high salt diet-induced hypertension in mice. 36925479: The process of hypertension induced by high-salt diet: Association with interactions between intestinal mucosal microbiota, and chronic low-grade inflammation, end-organ damage. 36951047: METHODS AND RESULTS: Male rats overexpressing the cardiac-specific VEGF-B transgene (VEGF-B TG) were treated for 3 or 6 weeks with deoxycorticosterone-acetate combined with a high-salt (HS) diet (DOCA + HS) to induce hypertension and cardiac damage. 37086874: In vivo experiments indicated that high-salt diets can lead to high blood pressure, kidney injury, inflammation, and fibrosis. 37298145: In the current study, targeted metabolomic analysis revealed decreased serum and fecal IPA levels in mice with L-arginine methyl ester hydrochloride (L-NAME)/high salt diet-induced hypertension (LSHTN) compared to normotensive control mice. 3734445: Male Dahl-S rats were randomly assigned to either normal chow (NC) or high-salt (HS) diets to induce hypertension. Effect of exercise on the development of salt-induced hypertension in Dahl-S rats. 37373209: Furthermore, the oxalate diet induced hypertension ( p < 0.05). 37463980: HSD induced hypertension, endothelial dysfunction and proinflammatory Th17 cell differentiation only in SS rats. 37465583: This literature review aims to both summarize the current evidence on high salt diet induced hypertension and discuss the epidemiological aspects including socioeconomic issues in the United States and abroad. 37532951: Our study revealed a considerable effect of TRPV4 channels in smooth muscle-dependent contraction in mice during high-salt induced hypertension. These results suggested that TRPV4 channels regulate smooth muscle-dependent contractions in high salt-induced hypertension, and this contraction involves increased [Ca 2+ ] i , IP 3 R2, and IRF7 activity. Whole-transcriptome analysis by RNA-seq and western blot assays revealed the involvement of interferon regulatory factor 7 (IRF7) in TRPV4-IRF7-IP 3 R2 signaling in HSD-induced hypertension. Aortic smooth muscle TRPV4 channels regulate vasoconstriction in high salt-induced hypertension. 37813819: The low K+ diet caused inflammation, nephromegaly and kidney function decline, whereas the high K+ diet caused hypertension, hyperaldosteronism and kidney fibrosis. 37916287: Male SS CD247-/- and SS CD247+/+ littermates were fed 4.0% NaCl (high salt) diet to induce hypertension. 37958726: We previously demonstrated that a high-salt (HS) diet provoked hypertension and proteinuria in Dahl salt-sensitive (DS) rats, accompanied by gammaENaC activation, which were attenuated by camostat mesilate (CM), an SP inhibitor. 38089998: Background: Previous study confirmed that both TaohongSiwu decoction (THSWD) and Dubosiella newyorkensis improved hypertension-induced endothelial dysfunction. Methods: Eight percent high-salt diet was applied to induce hypertension in a mouse model for 4 weeks. 38159883: CONCLUSIONS: Our study shows that maternal HCD programs neuronal plasticity in the offspring and results in male-specific hypertension and hyperglycemia associated with hypothalamic inflammation in mechanisms and pathways distinct from post-natal HCD exposure. 38189082: METHODS: Rats were fed a high-salt diet to induce hypertension and kidney injury, and physical and physiological indicators were measured afterwards. 38618734: Rats were fed a high salt diet to induce hypertension, and then the diet was switched back to normal sodium content. 3884235: Salt-induced hypertension in the 'Sabra' rat strain: influence of nifedipine treatment. Salt diet for 12 weeks resulted in a sustained hypertension and heart hypertrophy only in SBH. 4099269: Diet-induced hypertension and cardiovascular lesions in mice. 6280903: Feeding 8% NaCl diet for 5 weeks induced hypertension in young S rats but failed to alter renal or brain (Na+,K+)-ATPase activity. It appears unlikely that mutations in the structural locus for the renal (Na+,K+)-ATPase molecule are involved in the strain specific differences in susceptibility to salt-induced hypertension since the physical-chemical properties of the enzyme from the two strains were found to be similar. 6405669: The role of diet in the genesis of hypertension has been hotly disputed. 7034303: Hypertension is a disease more common to advanced societies, possibly due to diet and life style. 7119901: Long-term exposure to cadmium in drinking water can induce hypertension in rats. There were other (non-cadmium) differences between the stock and rye diets and between the remainder of our experimental conditions and those used by other investigators, presumably explaining the failure of some others to induce hypertension with cadmium. 7622854: Low levels of calcium on the diet potentiated the hypertension induced by the vitamin B6-deficient diet when both deficiencies were present from the beginning of the experiment. 7666781: In the present study, rats were fed diets that induce hypertension; 50% of the rats were also treated with pioglitazone, a thiazolidinedione derivative that sensitizes target tissues to insulin and decreases plasma insulin concentration in insulin-resistant animals. 8342672: Adrenal medulla as a mediator of diet-induced hypertension. 8482325: Feeding a vitamin B6-deficient diet to rats causes a moderate hypertension. The results suggest that decreased synthesis of 5-HT in brain regions and the consequent alterations in 5-HT receptors in the vitamin B6-deficient rats may be the underlying cause of the hypertension seen in these animals. 8505091: High fructose diet is known to induce hyperinsulinemia and hypertension in rats. 8572878: Since inhibition of nitric oxide (NO) biosynthesis induced by NO2-arginine enriched diet produced hypertension we measured in vivo cardiovascular responses to PGF2 alpha, L-arginine (L-arg) and cicletanine (Cic, IPSEN, France) which enhances PGI2 production. 8695019: Thus, a high salt diet leads to hypertension and eccentric LV hypertrophy in Dahl-S but not in Dahl-R. 8949371: This preliminary study shows that, like in humans, high fat diet in dogs induced abdominal obesity with systemic hypertension but failed to provoke left cardiovascular hypertrophy after 20 weeks. [Experimental hypertension induced by hypercaloric diet]. 9050983: DESIGN: The influence of moxonidine on glucose tolerance in vivo was determined in healthy control rats, in rats receiving a high fructose diet for 6 weeks to induce insulin resistance, hyperinsulinaemia and hypertension, and in rats receiving in addition to a high fructose diet moxonidine (1.5 mg/kg body weight daily). 9072418: These results reveal that benidipine has protective effects against the development of hypertension and the progression of renal lesions induced by the high salt diet in SHRSP. 9072423: Effect of angiotensin-converting enzyme inhibitors on fructose induced hypertension and hyperinsulinaemia in rats. 60 Sprague-Dawley rats were fed a fructose-enriched diet for 5 weeks, which produced hyperinsulinaemia, hypertriglyceridaemia and hypertension. 9072425: The present study was undertaken to examine the effect of the angiotensin converting enzyme (ACE) inhibitor, enalapril, on blood pressure and spontaneous blood glucose levels in two rat models: our new diabetic hypertensive rat in which genetic hypertension and diabetes develop following cross-breeding of Cohen diabetic rat (CDR) and spontaneous hypertensive rats (SHR); and a rat in which hypertension, hyperinsulinaemia and hyperlipidaemia were induced by fructose diet. 9217881: At week 8, the rats in the F and FT groups were started on a 66% fructose diet to induce hyperinsulinemia and hypertension. 9223452: In Dahl salt-sensitive (DS) rats, chronic hypertension caused by a high-salt diet was followed by sustained activation of aortic p42ERK and p44ERK. 9403593: The high salt diet caused the development of severe hypertension in Dahl-S animals and had no effect on blood pressure in Dahl-R animals. 9504453: After at least 5 wks of treatment, all rats in both groups were placed on a 4.0% NaCl diet for 2 weeks to produce sodium-induced hypertension. 96844: Diet-induced atherosclerosis and experimental hypertension in stumptail macaques (Macaca arctoides). 9797185: Finally, we discuss the significance of environmental factors, such as stress and diet, in the pathogenesis of hypertension, and we describe their interactions with specific hypertension susceptibility genes. 22406440: We have previously demonstrated that cholesterol-enriched diet causes AD-like pathology with iron deposition in rabbit brain. 22533436: Alzheimer disease (AD) and metabolic syndrome are two highly prevalent pathological conditions of Western society due to incorrect diet, lifestyle, and vascular risk factors. 22914588: Diet is an important lifestyle factor implicated in the etiology of Alzheimer's disease (AD), but so far it is not fully elucidated to which nutrients the suggested protective effect of diet can be attributed. 23530509: The more common sporadic form of Alzheimer disease (SAD) and the metabolic syndrome are two highly prevalent pathological conditions of Western society due to incorrect diet, lifestyle, and vascular risk factors. 24286859: The ameliorating effects of the diet on the OBX-induced changes were comparable to those of the NMDA receptor antagonist, memantine, a drug used for the management of Alzheimer's disease. 26075716: The fact that genetic factors account for less than 50% cases of sporadic Alzheimer's disease (AD) highlights the important contribution of environmental factors, such as high-salt diet, in AD pathogenesis. 28575011: Here, we tested this hypothesis by assessing the efficacy of HT against diet-induced obesity and AD-related pathology in female 3xTg-AD mice at early versus late middle-age. 30704467: Overall, our study provides intriguing evidence for the role of diet, as an important environmental factor, in AD etiology. 30954605: Increasing evidence has revealed that vascular risk factors influence the midlife development of AD and that diet-induced obesity accelerates tau phosphorylation in tau transgenic mice and increases the level of serum leptin receptor (leptin-R). 31240575: This literature review indicated that adherence to a healthy dietary pattern has neuroprotective effects on AD prevention, while unhealthy diet can cause neurodegenerative effects in AD etiology. 31600762: Poor Diet, Stress, and Inactivity Converge to Form a \Perfect Storm\ That Drives Alzheimer's Disease Pathogenesis. It is thus likely that lifestyle and environmental factors contribute to neurodegenerative processes implicated in the pathogenesis of AD. 33750486: Ovariectomized Sprague-Dawley rats were fed high-fat(H-F) or H-P diets for two weeks, and then they had a hippocampal infusion of beta-amyloid(25-35) for 4 weeks to induce AD and an injection of monoidoacetate(MIA) into the articular cartilage to induce osteoarthritis. We hypothesized that Alzheimer's-like disease (AD) exacerbates osteoarthritis and that intermittent fasting(IMF) with a high-protein(H-P) diet would enhance memory function and relieve osteoarthritis symptoms in estrogen-deficient animals with surgically induced AD and osteoarthritis. 33880134: High Methionine Diet-Induced Alzheimer's Disease like Symptoms Are Accompanied by 5-Methylcytosine Elevated Levels in the Brain. 34370639: CONCLUSIONS: DNLA alleviated AD-like symptoms induced by HMD via the DNA methylation pathway. Alkaloids on Alzheimer's Disease-like Symptoms Induced by High-methionine Diet. OBJECT: Whether DNLA can improve AD-like symptoms induced by HMD is to be explored. BACKGROUND: High methionine-diet (HMD) causes Alzheimer's disease (AD)-like symptoms. 35205079: Moreover, there has been growing evidence that a combination of antioxidants in conjugation with a nutrient-rich diet might be more effective in tackling AD pathogenesis. 36463453: OBJECTIVE: The purpose of this study was to evaluate the effects of a low-dose lithium supplementation on GSK3 activity in the brain of an early, diet-induced Alzheimer's disease model. 36894557: N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer's disease mouse model. 8940575: This can be further evidence that Hg from amalgam restorations or diet is not related to etiology and pathogenesis of AD. 31906276: Moreover, the hypertension induced by HFD is caused by a diminished both nitric oxide (NO) functional role and release probably due to a diminished neuronal nitric oxide synthase (nNOS) activation by protein kinase A (PKA) pathway. 32195603: Conclusion: Feeding the MHF-diet in male-OP rats led to a greater weight-gain and adiposity followed by the development of atherogenic-hyperlipidaemia and persistently impaired pressure-natriuresis to induce hypertension. 32346448: The aim of the present study was to compare the effect of hesperidin (HES) and crocin (CRO) alone and in combination, on blood pressure in a rat model of high-fat diet (HFD)-induced hypertension, using invasive carotid artery measurements. Hypertension is the most important cause of such conditions. 32388270: We investigated the association of IDH2 between the development of prolonged high-fat diet (HFD)-induced hypertension. These results indicate that prolonged HFD intake disrupts the IDH2-NADPH-GSH-associated antioxidant system and activates the renin-angiotensin system in the kidney, leading to increased BP, suggesting that IDH2 is a critical enzyme in the development of hypertension and that the IDH2-associated antioxidant system could serve as a potential hypertension treatment target. 32507041: Intriguingly, G6PD S188F mutants, as compared with WT rats, developed less large arterial stiffness and hypertension evoked by high-fat diet and nitric oxide synthase inhibition with L-N G -nitroarginine methyl ester. Finally, our results suggested that (1) lower resting membrane potential of smooth muscle caused by increased expression of K + channel proteins and (2) decreased voltage-gated Ca 2+ channel activity in smooth muscle contributed to reduced hypertension and arterial stiffness evoked by L-N G -nitroarginine methyl ester and high-fat diet to G6PD S188F mutants as compared with WT rats. 32748067: Although maternal PETN treatment has no effect on blood pressure in offspring fed with normal chow or high-salt diet, the offspring is at higher risk to develop HFD-induced hypertension. 32750363: Pioglitazone ameliorates high fat diet-induced hypertension and induces catechol o-methyl transferase expression in rats.Our study aimed to investigate the effect of pioglitazone (PIO) on the obesity-associated metabolic effects and whether this effect is associated with modulation of catechol O-methyl transferase (COMT) expression in the high fat diet (HFD) induced obese rats. Pioglitazone ameliorates high fat diet-induced hypertension and induces catechol o-methyl transferase expression in rats. 33547712: SCOPE: Perinatal high-fat (HF) diet induces hypertension in adult offspring. Maternal Garlic Oil Supplementation Prevents High-Fat Diet-induced Hypertension in Adult Rat Offspring: Implications of H2S-generating Pathway in the Gut and Kidneys. Garlic oil supplementation during pregnancy and lactation protected against hypertension induced by HF diet in adult male offspring. We examined whether maternal garlic oil supplementation can prevent hypertension induced by HF diet and elucidated its protective effects. 33574986: Pyrogallol-Phloroglucinol-6 6-Bieckol on Attenuates High-Fat Diet-Induced Hypertension by Modulating Endothelial-to-Mesenchymal Transition in the Aorta of Mice. 33666098: Surviving obese-normotensive males displayed less left ventricular dilation and pulmonary congestion compared with chow-fed males after MI; hypertension reversed left ventricular dilation because of high-fat/fructose diet and promoted significant pulmonary congestion compared with chow-fed controls. Methods and Results Male and female C57BL/6J mice were provided standard chow or high-fat/fructose diet for 8 weeks and then infused with angiotensin II for 2 weeks to induce hypertension. 33815135: Phenotypic Changes in T Cell and Macrophage Subtypes in Perivascular Adipose Tissues Precede High-Fat Diet-Induced Hypertension. We hypothesized that immune cell changes in PVATs precede the development of high fat diet (HFD)-induced hypertension. 33851366: Our results suggest that the hypertension and deterioration of renal function induced by HFD in rats with ARDev are Ang II-dependent and mediated by increments in oxidative stress and immune system activation. 33929898: For males and females, the thoracic aorta exhibited medial hypertrophy in HF diet-induced hypertension vs control but did not display a hyperresponsive contraction to the alpha adrenergic agonist phenylephrine nor endothelial cell dysfunction as measured by acetylcholine-induced relaxation. 34248679: Maternal high-fat diet in rabbits leads to hypertension and elevated renal sympathetic nerve activity (RSNA) in adult offspring but whether this is due to adiposity or maternal programming is unclear. 34397279: Collectively, HFD-induced downregulation of MsrA plays a pivotal role in HFD-induced hypertension by reducing H 2 S levels. Here, we assessed the relevance of MsrA in high-fat diet (HFD)-induced hypertension and the effect of HDAC inhibition on MsrA expression, H 2 S production, and hypertension. Inhibition of HDACs (Histone Deacetylases) Ameliorates High-Fat Diet-Induced Hypertension Through Restoration of the MsrA (Methionine Sulfoxide Reductase A)/Hydrogen Sulfide Axis. 34675590: Results: The present work revealed that: 1) a maternal high fat diet (MHF) led to higher blood pressure in adult offspring; 2) MHF led to downregulation of peroxisome markers PEX3 and 14 in fetal kidneys; 3) the antioxidant SOD2 and catalase were decreased, and oxidative stress marker Ephx2 was increased; 4) MHF-induced activation of the UPR pathway; 5) the KEAP1-NRF2 pathway was activated; 6) activation of the NLRP3 inflammasome led to secretion of pro-inflammation factors; 7) in TECs, the changes in PEXs and NLRP3 are similar to tissues, but UPR and NRF2 pathways showed opposite trends; 8) and the antioxidant PQQ alleviated maternal lipotoxicity by decreasing ROS levels and inhibiting activation of ER stress and inflammasome in fetal kidney. 34852339: Background This study aims to compare whether two different routes of Renal denervation (RDN) from the intima and adventitia of the renal artery can reduce renal fibrosis in a pig model of hypertension induced by a high-fat diet and to explore possible molecular mechanisms. 34916185: METHODS: Sixteen beagles were randomly divided into RDN group ( n 8, fed with a high-salt high-fat diet to establish models of hypertension and treated with RDN), sham-operated group ( n 4, fed with a high-salt high-fat diet to induce hypertension but only examined with renal arteriography) and control group ( n 4, fed with formula dog food). 35344116: Caloric restriction overcomes pre-diabetes and hypertension induced by a high fat diet and renal artery stenosis. 35545941: Although high-fat diets induce hypertension in both sexes, these data reveal that males are at greater risk of salt-dependent hypertension and further suggest that females have more redundant systems that can be productive against salt-sensitive hypertension in at least some circumstances. 35551757: BACKGROUND: The Dahl rat has been used as a model of high fat diet (HFD)-induced hypertension and adiposity. Genetic deletion of T cells blunts HFD-induced hypertension. 35745637: A high-fat diet (HFD) was used to induce OH for 20 weeks. 36145220: The HFD induced hypertension in SS ( p < 0.01) but not SR rats, although it increased body weight gain ( p < 0.05) and tPVAT weight ( p < 0.01) in both rats. A high-fat diet (HFD) frequently causes obesity-induced hypertension. 36457800: Results: Knockout of BMP4 either in adipose tissue or specifically in BAT aggravates high-fat diet (HFD, 40% fat)-induced hypertension and endothelial dysfunction in ApoE -/- mice. 36613328: Compared with Octa monomer, the microcapsule was more effective in alleviating the symptoms of weight gain, hypertension, and hyperlipidemia induced by HFD in mice. 36825708: A 20-week high-fat diet (HFD) was given to produce diabetic hypertension in Wister rats. 37244179: Pathologic HDAC1/c-Myc signaling axis is responsible for angiotensinogen transcription and hypertension induced by high-fat diet. Inhibition of c-Myc downregulated Agt and Ang II levels in kidney and serum, ameliorating HFD-induced hypertension. We have shown a possible link between histone deacetylases (HDACs) and renal angiotensinogen (Agt) upregulation in the HFD-induced hypertension, whereas the underlying mechanisms remain to be elucidated. Here, using a HDAC1/2 inhibitor romidepsin (FK228) and siRNAs, we determined roles of HDAC1 and HDAC2 in HFD-induced hypertension and found the pathologic signaling axis between HDAC1 and Agt transcription. 37375598: We found that geraniin supplementation effectively ameliorated HFD-induced hypertension and abnormal remodelling of the thoracic aorta by suppressing excessive vascular superoxide (O 2 - ) radical generation and overexpression of pro-inflammatory mediators in the circulating leukocytes. 37726069: RESULTS: The weight gain, elevated blood pressure and increased blood lipids induced by high-fat-diet were significantly decreased (p < 0.05) after each prescription medicine intervention in a dose-dependent manner. 37897505: Deletion of adipocyte NOS3 potentiates high-fat diet-induced hypertension and vascular remodeling via chemerin. 38420674: To better understand the molecular processes involved, young mice were treated with either deoxycorticosterone acetate (DOCA) or fed a high-fat diet (HFD) to induce hypertension or obesity, respectively. 38689862: Molecular mechanisms and potential therapeutic targets in the pathogenesis of hypertension in visceral adipose tissue induced by a high-fat diet. 10746100: In rats, the feeding of a low protein diet during pregnancy retards fetal growth and induces hypertension in the resulting offspring. 12060603: An experimental model of prenatal programming of hypertension in the rat, induced by a maternal low-protein diet during pregnancy, was employed to study the role of renal Na reabsorption in the pathogenesis. 14583657: We investigated the factors involved in the development of hypertension induced by LPD in rats with post-cyclosporine (CsA) nephropathy, and determined the appropriate composition for LPD that is to be utilized for renal research. Factors involved in the development of hypertension induced by a low-protein diet in rats with renal injury. 15458966: Adult hypertension was induced by maternal low-protein diet during the second half of gestation. 15746697: CONCLUSION: The day of in utero insult by low-protein diet is critical in the induction of adult hypertension; the severity is gender dependent. 16221217: METHODS: Adult hypertension in rat offspring was induced by maternal low protein diet. 16298266: Indeed at least 2 forms of hypertension appear to be related to the up-regulation of the transporter: the so-called programmed hypertension induced by low-protein diet during pregnancy and the early phase of hypertension in the Milan strain of rats. 16843406: In utero exposure to maternal low protein diets induces hypertension in weanling rats, independently of maternal blood pressure changes. Fetal exposure to maternal low protein diets induces hypertension in rats. 19403862: Prenatal administration of dexamethasone and a low-protein diet has been shown to result in hypertension in the offspring when they are adults. 19516079: We conclude that maternal low-protein diet during gestation leads to significant changes in expression of the systemic renin-angiotensin system in fetal mice and may be important in the genesis of hypertension in the adult. 20844591: We found that: (1) postnatal OB diet increased significantly BP (P<0.0001) and HR (P<0.008) in 3-month old OB-C and OB-LP offspring, respectively; (2) that maternal LP diet induced a significant higher BP (P<0.009) and HR (P<0.004) and (3) an altered circadian rhythm in addition to higher plasma corticosterone concentration in 9 months-old LP offspring; (4) that, although LP offspring showed higher plasma total cholesterol than control offspring, atherosclerosis assessed in aortic roots of 6-mo old mice featured increased plaque area due to OB feeding but not due to early mismatched nutrition. 21272146: AIM: Our previous study showed that a maternal low-protein diet induced hypertension and vascular dysfunction in rat offspring after day 175. 22381101: AIM: A low-protein diet (LPD) during pregnancy induces vascular dysfunction and hypertension in the offspring, prevented by administration of an angiotensin II type 1 (AT(1)) receptor antagonist in early life to the offspring. 22536490: A maternal low-protein diet (MLP) fed during pregnancy leads to hypertension in adult rat offspring. 22932874: Surprisingly, there is a scarcity of data regarding the development of hypertension as a consequence of a maternal low-protein diet (MLPD), particularly in the mouse. 25537745: Thus, a prenatal low-protein diet causes hypertension and a reduction in GFR in mature adult offspring, which can be modified by postnatal rearing. 28381328: BACKGROUND: We investigated whether a chronic low-protein multideficient diet (BRD) from weaning turns on cardiovascular adaptive responses that could culminate in hypertension and heart failure. 7712066: Recent studies have demonstrated that the feeding of low protein diets to rats during pregnancy induces hypertension in their offspring. 9170007: The feeding of low-protein diets to rats during their pregnancy results in higher blood pressure in the offspring from the age of weaning. 10099077: Renal parenchymal hypertension is defined as hypertension caused by disease of the kidneys. 10589265: Hypertension induced by atherosclerotic disease is rarely cured, but more easily controlled. 10618564: BACKGROUND: Renal artery stenosis is a common disorder and is an established cause of hypertension and renal insufficiency. 10795724: BACKGROUND: The relation of blood pressure to Alzheimer's disease (AD) is complex because both an association of high blood pressure with increased risk of the disease and lower blood pressure as a consequence of the disease are possible. 10957653: PURPOSE: This retrospective review describes the surgical management of consecutive patients with severe hypertension and ischemic nephropathy due to atherosclerotic renovascular disease. 11338095: Atheromatous renovascular disease (ARVD) is a common cause of hypertension and chronic renal failure (CRF). 1136324: [Significance of certain diseases and anomalies of the kidneys and renal vessels in the etiology of arterial hypertension in children]. 11416740: Renovascular disease is an important cause of hypertension in children and is associated with considerable morbidity and mortality risks. 11538850: The thrust of this essay will be to organize a growing body of evidence which indicates that an abnormality of the kidney, and the adrenal, involving disordered regulation through the renin-angiotensin system, is responsible for the pathogenesis in about 45% of patients--a discrete subgroup that may be most common cause of hypertension. 11771866: CONCLUSIONS: Although symptoms are relatively uncommon. renovascular disease is a frequent cause of severe hypertension in childhood. 1178838: Arteriography may also reveal juxtaglomerular cell tumors, chronic renal inflammatory disease, or other diseases of renal parenchyma which could cause hypertension. 11800059: Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. 11956860: In patients with neurofibromatosis, hypertension is mainly caused by renovascular disease, whereas in tuberous sclerosis (TSC) reasons for hypertension are renoparenchymal lesions, such as angiomyolipoma or cysts. We report on a girl with TSC and hypertension due to unilateral renal artery stenosis associated with aneurysmatic changes of internal carotid artery. 1199986: It is imperative to recognize this disease in order to distinguish it from other entities that cause hypertension. 12046025: Atherosclerotic renovascular disease (ARVD) commonly causes renal failure and hypertension and is accompanied by high cardiovascular comorbidity and mortality. 12087578: BACKGROUND: Renovascular disease is a common cause of renal impairment and hypertension, particularly in the older population. 12616031: ARVD is a common cause of hypertension and chronic renal failure (CRF), and it is one of the most common renal diagnoses in elderly patients accepted on to dialysis programmes with end-stage renal failure (ESRF). 12629100: Disorders of the lipoprotein metabolism are a major cause of endothelial dysfunction that may result in hypertension and proteinuria, clinical hallmarks of preeclampsia (PE). 12715144: An extrarenal disorder is suggested to be the cause of autosomal-dominant hypertension with brachydactyly: the patients react with a severely impaired baroreflex und show neurovascular contact. 12859402: Pre-eclampsia is a potentially life-threatening disease of women during pregnancy leading to hypertension and proteinuria. 12995807: [Hypertension in children caused by unilateral kidney disease]. 13088054: [Unilateral kidney diseases causing hypertension]. 13210759: [Pathogenetic interpretation of certain forms of hypertension as caused by disorders of arteriolar adaptability]. 1329461: Renovascular disease, one of the most common secondary causes of hypertension, is usually the result of atherosclerosis in older patients and the result of fibromuscular dysplasia in younger patients. 13368264: [Arterial hypertension caused by unilateral kidney disease]. 13401226: [Hypertension caused by unilateral kidney disease]. 13488190: The diagnostic approach to hypertension due to unilateral kidney disease. 13503449: Hypertension due to unilateral kidney disease. 13915669: Diagnosis and treatment of hypertension due to occlusive disease of the renal artery. 14585051: Consequences of diseases related to obesity, such as coronary heart disease, hypertension, diabetes and renal disease, account for much of the morbidity in these patients and are rarely treated adequately. 14594571: The classic disorder of the adrenal medulla resulting in hypertension is pheochromocytoma, although hypertension in obesity might also be associated with catecholamine secretion. 14870027: [Addison's disease in a patient with arterial hypertension due to unilateral kidney disease; the role of the adrenals in arterial hypertension]. 14978155: Many diseases that cause CKD, diabetes, and hypertension are also associated with cardiovascular disease. 14978868: The confirmation of a renovascular disease as the cause of a child's hypertension is based on the elevation of the peripheral plasma renin level, the captopril tests, possibly the renal vein renin determinations and the imaging studies. 1511199: In 351 patients, hypertension was secondary to a known disease. 15223726: In the analysis, female youth and male subjects with diseases in heart, kidney, or other organs that could cause high BP were rejected. 15503182: Patient demographics, BMI, family history, presentation of disease, etiology of hypertension, medication, laboratory data, and findings from other procedures were recorded for all patients with hypertension followed in the Pediatric Nephrology Clinic at Children's Hospital, Columbus, Ohio, over a 4-year period. 15520423: BACKGROUND: Timely, accurate detection of renal artery stenosis is important because this disorder may be a potentially curable cause of hypertension and renal impairment. 15698914: Head injuries, seizures, and diseases that lead to intra-cranial hypertension frequently result in significant alteration of neurologic function. 15728214: In obstructive sleep apnea, we discuss how HPA axis hyperactivity may be a consequence of the disorder and contribute to secondary pathology such as insulin resistance, hypertension, depression, and insomnia. 16126467: It represents the most frequent consequence of atherothrombotic disease associated with hypertension, diabetes and hypercholesterolemia. 16810469: It is the authors' belief that hypertension due to these three diseases is more common than previously appreciated and may account for about 20% of the hypertensive population. 16973313: Obesity is epidemic of 21st century, its visceral form is associated with increased risk for type 2 diabetes, cardiovascular disease, hypertension and increased mortality due to consequences of the disease. 16990369: We report three infants with severe, early hypertension due to unilateral renovascular disease, whose cardiovascular changes, or polycythaemia, or both, indicated they had been affected as fetuses. 17035668: Animals have long provided suitable platforms for the development of innovative surgical procedures and for the study of disease states that are relatively easy to produce in otherwise healthy animals, such as diabetes or hypertension. 17124527: Mechanisms of disease: in utero programming in the pathogenesis of hypertension. 17341996: Atherosclerotic renal artery stenosis is the most common disease of the renal arteries and may lead to ischemic renal disease and hypertension. 17365453: The present study was done in order to understand the trends of maternal deaths due to non-eclamptic and eclamptic hypertensive disorders by analysis of case records of women who died due to these disorders over a period of 20 years. 1762850: The patients with symptomatic arterial hypertension of the nephrogenous and endocrine genesis may turn out more conflicting since they are trying to discover the cause of their life failures in their social surrounding rather than in their personal inability to cope with them because of the disease. 18258535: This article discusses the topics on exercise programme in cardiac rehabilitation, the benefits of cardiac rehabilitation and the importance of cardiac rehabilitation in the setting of different cardiac diseases (congestive heart failure, heart transplantation, heart valve surgery and two important diseases that trigger coronary heart diseases; diabetes and hypertension). 18320238: However, secondary causes of hypertension such as renal parenchymal diseases, congenital abnormalities and renovascular disorders still remain the leading cause of pediatric hypertension, particularly in children under 12 years old. 1833057: In elderly patients with uncontrolled hypertension or increasing azotemia caused by renovascular disease, hepatorenal or splenorenal bypass procedures are helpful alternatives. 18440428: Renovascular disease is an uncommon but important cause of hypertension in children. 18690400: The present study aimed to investigate whether disorders of miRNAs system were involved in the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). 18875506: Hypertension caused by unilateral kidney disease; a follow-up report. 19018740: The deterioration is partly explained by the diseases that cause CKD (hypertension and diabetes), associated comorbid conditions (especially cardiovascular) and complications of CKD (anemia and malnutrition-inflammation). 1914201: Hypertension may be attributable to various disorders involving the central or peripheral adrenergic (catecholamine) pathways. 19523365: The possibility that some underlying disorder may be the cause of the hypertension should be considered in every child or adolescent who has elevated BP. 19543233: Similar to a tsunami wave, a new surge of genome-wide association studies in common complex diseases has succeeded in identifying the causative genetic risk factors of hypertension. 19595533: Atherosclerotic renovascular disease (aRVD) is an increasingly recognized cause of severe hypertension and declining kidney function. 19685045: BACKGROUND: Renovascular disease is an uncommon but important cause of hypertension in children. 19856000: Renovascular disease (RVD) is an important cause of hypertension in children, as it often is amenable to potentially curative treatment. 19918393: Sarcoidosis, a disease of unknown etiology, is also a cause of pulonary hypertension and right heart dysfunction. 20108080: In children, up to 10% of the cases of arterial hypertension may be caused by a renovascular disease. 20308753: Clinical consequences of this disorder may include excessive daytime sleepiness, depressed mood, cognitive impairment, hypertension, as well as increased risk for cardiovascular disease and metabolic dysregulation. 20924335: Atherosclerotic renovascular disease is an increasingly recognized cause of severe hypertension and declining kidney function. 2095001: The significance of microcirculatory disorders in the pathogenesis of arterial pulmonary hypertension, respiratory and heart failure is under discussion. 21118836: Flash pulmonary edema (FPE) is a severe renovascular disease that leads to acute recurring pulmonary edema and acute systemic hypertension. 21404100: Arterial hypertension in childhood is less frequent as compared to adulthood but is more likely to be secondary to an underlying disorder. 21462848: As the prevalence of hypertension in children and adolescents increases within the context of the epidemic of obesity, it is important to recognize that while hypertension may be secondary to an underlying disorder, one must not overlook the impact that overweight and obesity have on the condition. 21924324: Disruption of adrenal steroid production results in a variety of diseases that can lead to hypertension, metabolic syndrome, infertility and androgen excess. 22330627: AIM: Renovascular disease may cause arterial hypertension and decreases renal function, which both impair endothelial function. 22432146: Epidemiological studies have shown that small size at birth is associated with an increased risk of coronary heart disease and its risk factors, including hypertension and Type 2 diabetes.It is suggested that these observations linking low birthweight with disease result from an imbalance between fetal nutrient demand and supply. 22573742: Some diseases (obesity, ascites, heart failure etc.) result in chronic AH. 22872284: Finally, there is a potential of a vicious cycle between OSA and fluid overload disorders, whereby OSA can contribute to the pathogenesis of arterial hypertension, heart failure, and chronic kidney disease, which in turn will significantly contribute to the course OSA. 22932914: This group of mostly monogenic and acquired disorders typically causes hypertension through activation of the mineralocorticoid receptor either directly or indirectly via hormonal mediators and from overactive amiloride-sensitive epithelial sodium channels located in the distal tubule and collecting ducts of the kidneys. 22980042: However, developmental programming also offers a novel approach to prevent cardiovascular and related diseases through so-called Reprogramming: administration of appropriate or inhibition of deleterious perinatal factors in induced or genetic models ameliorated undesirable development that otherwise would inevitably have lead to more severe hypertension, cardiovascular and renal disease. 23166176: Although renal artery aneurysms (RAAs) are an uncommon cause of disease of the renal vessels, they are recognised as a cause of hypertension. 23194278: This case depicts an atypical presentation of this disease where the girl visited many physicians for controlling the level of hypertension and put a diagnostic dilemma about the underlying etiology of young hypertension. CONCLUSION: Takayasu's Arteritis should also be kept in mind while searching for the cause of uncontrolled hypertension in the young age group. 23488307: It remains one of the most common disorders in pregnancy and the leading causes of maternal and fetal morbidity The changes in blood vessel endothelium have impact on the pathogenesis of hypertension and preeclampsia. 24103894: Chronic kidney disease (CKD) is the most costly disease covered by Medicare, and two common causes of CKD, diabetes and hypertension, are increasing worldwide. 2424266: It is speculated whether hypertrophic cardiomyopathy and hypertension are both caused by systemic disorders of calcium channels and calcium uptake and binding by cardiac and smooth muscle membranes, respectively. 24333404: Atherosclerotic renal artery stenosis (ARAS) is a common and complicated disease, which can result in high blood pressure and loss of kidney function. 24522941: Renovascular disease is a cause of hypertension in 10 % to 15 % of prepubertal children. Interventions to address hypertension and causes of renovascular disease continue to advance. 24711842: Amlodipine or sildenafil significantly reduced NT-proBNP levels in COPD-induced PH patients (p < 0.05). 25322850: Mutations of genes encoding WNK kinases underly Gordon's syndrome, a monogenic disease leading to hypertension and hyperkalemia. 25621157: Compared with US-practicing clinicians (N = 46), non-US-practicing clinicians (N = 57) favored collaboration between cardiology and pulmonary medicine for clinical decision making (1 = disagree, 7 = agree; 3.1 +/- 2.2 vs. 4.8 +/- 2.2; P < 0.0001) and PDE-Vi (6.5% vs. 22.4%) as first-line therapy for PAH patients with cardiogenic shock but were less likely to perform vasoreactivity testing in patients with lung disease-induced pulmonary hypertension (4.3 +/- 2.1 vs. 2.2 +/- 1.6; P < 0.0001). 25686864: The mechanisms by which obesity causes HTN are complex and involve several organic mechanisms. For both groups, healthy and a variety of diseased dogs were observed; the correlations between pathologies and obesity were studied, paying special attention to diseases whose pathophysiologies could lead to HTN. 25901003: Further research is needed to determine the effects of oral fludrocortisone in cats with primary hyperaldosteronism and cats with other disorders causing hypertension and/or hypokalemia to determine if this protocol can be used as a tool for the definitive diagnosis of primary hyperaldosteronism. 26193106: The disease is characterised by vascular damage resulting in hypertension and proteinuria with high morbidity for both mother and child. 26271106: BACKGROUND: Hypertension is associated with the occurrence of cognitive deficits and dementia, probably because hypertension is a major risk factor for the occurrence of brain damage as a result of cerebral small vessel disease (cSVD). 26430136: Renovascular disease (RVD) can lead to hypertension and chronic kidney disease (CKD). 2652311: In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. 26619664: Recently, childhood hypertension might be closely related to the abnormality of maternal gestational period caused by the strict diet and the maternal smoking. Developmental Origins of Health and Disease(DOHaD) theory is now highlighted in the pathogenesis of adulthood hypertension. 26849700: The municipalities with a lower gross domestic product showed a higher rate of deaths due to hypertensive disease in years 2009 and 2010, and due to ischemic disease in years 2010 and 2011. 26893930: The 'hypertensive emergencies' have been grouped together in three subsets: (1) diseases that result from acute hypertension that is caused by faulty regulation of the peripheral circulation (acute primary hypertension), (2) diseases that produce hypertension (acute secondary hypertension) and 3) diseases that have hypertension as an effect of the acute stress caused by the principle disease (acute associated hypertension). 27288429: CONTEXT: Autosomal dominant polycystic kidney disease (ADPKD) is a common disorder that can cause hypertension during childhood, but the true prevalence of hypertension during childhood is not known. 273077: Pheochromocytoma represents a potentially life-threatening disease, but alsl is a curable cause of hypertension. 28228456: BACKGROUND: Preeclampsia is a pregnancy-specific disorder resulting in hypertension and multiorgan dysfunction. 2833821: The authors present the indices of blood pressure (BP), plasma renin activity, the concentration of aldosterone, cortisol, adrenocorticotropic and antidiuretic hormones in 56 patients with arterial hypertension resulting from kidney parenchymatous diseases before hemosorption and at varying time after it. [Changes in arterial pressure and concentration of several hormones in the blood effected by hemosorption in patients with arterial hypertension caused by parenchymatous diseases of the kidneys]. 28705740: Hypertensive disorder in pregnancy (HDP) refers to a series of diseases that cause the hypertension during pregnancy, including HDP, preeclampsia (PE) and eclampsia. 28844072: These disorders can lead to hypertension, hypokalemia, hypervolemia and metabolic alkalosis. 29093561: In the present study, we evaluated the incidence of the diseases causing cardiovascular problems (hypertension, diabetes mellitus, dyslipidemia and metabolic syndrome) 5 years after delivery in Japanese women with hypertensive disorders of pregnancy. 29229570: RESULTS: Most healers believed that hypertension was caused by the disorder of fire and wind elements in the body. In Thailand, illness and hospitalisation in the modern public health system due to high blood pressure is increasing. 30108382: CONCLUSIONS: Primary hyperaldosteronism as compared to other renin angiotensin aldosterone system disorders was found to be the leading cause of hypertension in young population. 30642276: Acting upon literature evidence suggesting renovascular disease as a cause of IDH, we referred her to an interventional radiologist for evaluation of the renal arteries. 31045658: PURPOSE OF REVIEW: Renovascular disease (RVD) remains an important cause of hypertension and renal dysfunction. 3160766: We conclude that the RVRR is of no prognostic value in the surgical treatment of hypertension due to unilateral renovascular disease. 31940349: Elevated mortality was observed for conditions with a contributing cause of hypertension that included chronic obstructive pulmonary disease, diabetes, Alzheimer's, Parkinson's, and all types of falls. 32522364: Hypertension secondary to a concurrent disease is the most common form of hypertension in cats, particularly in association with chronic kidney disease or hyperthyroidism. 32652154: The sulfated N-acetylglucosamino-glucuronopyranosyl-arabinopyranan purified from A. neglectus could function as a prospective functional lead against the pathophysiological conditions leading to hypertension. 33013278: The latter condition causes hypertension and eventually progress into congestive heart failure. 33119816: The authors raised concerns regarding the lack of inclusion of obesity by several societies as a formal cause of hypertension considering not only the biologic plausibility but also the huge impact of weight loss therapies such as bariatric surgery on hypertension remission. In contrast, there is no discussion that a very rare condition-namely pheochromocytoma-is the most \typical\ cause of hypertension by promoting hypertension remission in the majority of patients after surgical procedure. If obesity becomes largely accepted by several societies as a secondary form of hypertension, this pandemic condition will be certainly the most common cause of hypertension. 33143642: CONCLUSIONS: This case shows that coarctation of the aorta can be cured and that hypertension caused by the condition can be controlled to some extent with medication. 3316791: [Role of transmembrane ion transport disorders in the pathogenesis of hypertension]. 33405430: RESULTS: Renovascular disease induced hypertension and renal dysfunction. 33840647: Abnormal adrenal steroidogenesis leads to a variety of diseases that can cause hypertension, metabolic syndrome, infertility and premature adrenarche. 3439580: Since she had no blood pressure elevation at initial diagnosis and none following discontinuation of the Imipramine (when she was in florid relapse), we believe that this drug rather than her underlying disease alone caused her hypertension. 34480931: The ER stress is a condition that, if unresolved, might lead to heart failure, atherosclerosis, hypertension, and endothelial dysfunction. 35661540: Agents from this malperfused placenta generate a maternal disease, the second phase, in which endothelial damage leads to hypertension and organ damage due to vasoconstriction and thrombotic microangiopathy. 35685144: Idiopathic interstitial pneumonia (IIP) is a group of progressive lower respiratory tract diseases of unknown origin characterized by diffuse alveolitis and alveolar structural disorders leading to pulmonary fibrillation and hypertension, pulmonary heart disease, and right heart failure due to pulmonary fibrosis, and more than half of them die from respiratory failure. 3578397: Pharmacologic and methodologic advances over the last decade have resulted in a body of information implicating serotonin as a mediator in the genesis of preeclamptic hypertension. While it is generally accepted that preeclampsia is a disease of the microvasculature characterized by an imbalance between prostacyclin and thromboxane and that the evidence for enhanced responsiveness to some vasopressors is present weeks before clinical disease, the specific cause of the hypertension characterizing the syndrome is unknown. 35808997: During the differential diagnostic process, obliterative disease was discovered in the bilateral subclavian and right renal arteries, and the latter resulted in uncontrolled hypertension, which played a significant role in the development of heart failure. 3582454: A badly damaged or functionless kidney was removed in 85 (62.0%) patients for the early control of persistent tuberculous cystitis; in 18 (13.1%) because of chronic, nonspecific urinary infection, dispersed calcifications with subsequent nephrolithiasis, pain or other discomfort; in 16 (11.7%) due to supposed nephrogenic hypertension, and in 3 (2.2%) because of extrarenal disease. 35934604: Renovascular disease is an important cause of pediatric hypertension. 36027404: CONCLUSIONS: Renovascular hypertension is responsible for less than 1% of all cases of hypertension and, when present, it is usually caused by atherosclerotic disease or fibromuscular dysplasia. 36344721: Atherosclerotic renovascular disease (RVD) leads to hypertension, chronic kidney disease (CKD), and heart disease. 36583282: These findings highlight the usefulness of regional MW indices in assessing disease and may help differentiate between etiologies of pediatric hypertension. 36634580: Type 2 diabetes mellitus (T2DM) and hypertension (HT) are very common risk factors.The association between multimorbidity due to both diseases and CD has been understudied in low and middle-income countries, in which the strength of the association might be stronger. 37909881: SUMMARY: NCC and ENaC are integral components, and their malfunctions lead to disorders like LS and PHAII, hereditary causes of hypertension. Although lifestyle choices and environmental factors are known to have a significant impact on its development, there is growing recognition of the influence of genetic factors in the pathogenesis of hypertension. 38133617: BACKGROUND: Pulmonary hypertension (PH) consists of a heterogenous group of diseases that culminate in increased pulmonary arterial pressure and right ventricular (RV) dysfunction. 38484135: BACKGROUND: Secondary hypertension (SH) is a form of high blood pressure caused by an identifiable underlying condition. 3925655: Metoprolol, a beta 1 blocking agent, is being used with increasing frequency during pregnancy for treatment of disorders such as hypertension or beta-mimetic induced tachycardia. 4046308: [Non-invasive diagnosis of diseases causing arterial hypertension]. 4090117: [Treatment of patients with arterial hypertension due to a local disorder of the renal circulation]. 4738846: [Case of juvenile hypertension caused by unilateral renovascular disease and contralateral hypoplastic kidney]. 4773560: [Experimental verification of arterial hypertension induced by disorders of venous outflow from the kidney]. 6222777: Hypertension due to fibromuscular disease in a solitary kidney: treatment by percutaneous transluminal angioplasty. 6249611: In childhood hypertension due to renovascular disease or pyelonephritic scarring peripheral plasma renin is increased. 6287390: Childhood hypertension due to adrenocortical disorders. 6345887: Their use in prehospital screening of patients is expected to contribute to the diagnosis of basic disease provoking arterial hypertension. 6419807: The results of the investigations of all patients who underwent renal arteriography for hypertension due to renovascular disease over a three and a quarter year period prior to January 1st 1981 are reviewed and discussed. 6446514: In conclusion, gestosis is a disease of humoral and cellular hyperreactivity finally resulting in the well-known peripheral symptoms edema, hypertension, and proteinuria. 6624544: Among the remaining patients the excretion of catecholamines was normal in the face of severe hypertension in two, the high blood pressure being probably due to diseases other than pheochromocytoma. 6664353: Renin producing tumors, hyperthyroidism and hyperparathyroidism are rare causes of hypertension in children. Inflammatory, traumatic, and tumorous disorders of the central nervous system rarely result in chronic hypertension but may frequently be associated with acute hypertensive crisis. 6732756: The data support the concept that alterations of arterial chemoreceptor structures and reflex effects found in the established phase of hypertension are the result of this disease. 6753366: This means that this disorder of function constitutes an important link in the pathogenesis of hypertension. 6758676: A disease of the urinary apparatus (nephropathy) or of the cardiovascular system (aorta coarctation) can often be identified as the primary cause of the hypertension. 693862: Renovascular disease often leads to hypertension in children. 7103302: These two cases stress the problem of the respective responsibility of both pheochromocytoma and renovascular disease in hypertension genesis. 713242: Under the effect of high-altitude hypoxia (3,200 m), the disease of the mitral valve is attended with overloading of the left atrium with the volume of blood and leads to acute hypertension of the pulmonary artery with subsequent decompensation of the right heart. 7522784: Chronic experiments in rabbits and rats revealed that, when sympathetic influences on the heart prevail during emotional stress, reduce the heart electric stability, induce disorders in the heart rhythm and lead to arterial hypertension. 7553835: Although renovascular disease may cause hypertension and/or renal insufficiency, it may also occur in the absence of the usual clinical markers that suggest renovascular hypertension. 7603072: Hypertension is a complex disease, the treatment of which should not only lower systolic and diastolic blood pressure but also attenuate the secondary consequences of the disease. 7610567: Therefore, a disorder of the venous outflow from the spinal channel, on the one hand, and intensification of the venous blood inflow, on the other, may develop under certain conditions, resulting in intrachannel hypertension. 7667614: Renovascular hypertension (RVH) remains a leading cause of potentially curable hypertension. Advances in percutaneous transluminal renal angioplasty (PTRA) have renewed interest in developing better noninvasive screening tests for identifying patients with potentially correctable hypertension or renal impairment due to renovascular disease caused by either fibromuscular dysplasia (FMD) or arteriosclerosis. 7889060: Clinician questions in nephrovascular hypertension are: 1) Is hypertension secondary to nephrovascular disease? 7967780: RESULTS: Renovascular disease is an important cause of resistant hypertension and progressive renal insufficiency, particularly in the elderly population. 8052439: Seventeen of the 29 allografts had recurrent mesangial IgA deposits and of these three patients have negative urinalysis, normal glomeruli by light microscopy, and stable renal function; six patients have microhaematuria, mesangial proliferative nephritis, but at present stable renal function; and five have mesangial proliferative glomerulonephritis with microhaematuria, heavy proteinuria, hypertension, and progressive allograft failure secondary to IgA disease alone, and one of these is now back on dialysis. 8160862: Blood pressure and body weight rise with age, and hypertension is hypothesized to result from an early disorder of growth. 8225886: The patients' charts were reviewed for the presence of hypertension and diseases that might cause hypertension. 8361607: The study of viscosity and erythrocytes deformability, and of erythrocytes and platelets stickiness could pharmacologically correct the haemorheological disorders which can be some of the causes of hypertension. 8365497: Accumulating data suggest that the disorder of the renin-angiotensin system is not essentially a primary factor of hypertension, but it apparently plays an indispensable role in the pathogenesis of hypertension. 8377262: Excluding those with diseases which might induce hypertension or those under 20 yr and over 60 yr of age, 570 male subjects were eligible for analysis. 8404957: This work suggests that a screening investigation with a low radiation burden can be carried out at most institutions; if the investigation is positive, there will be a high index of suspicion that renovascular disease is the cause of the hypertension. In children over 1 year of age, renal disease is the commonest cause of hypertension. 8496635: The tumor time-density curve following IP was characterized by a markedly delayed washout, with many hypovascular portions noted in the vascular model and a clear decrease in tumor vessels measuring 30 microns or less. in contrast, the peak value increased in the time-density curve and there was washout in the excretory phase following ATII induced hypertension. In view of the results, we suggest that a microcirculatory disorder resulting from IP administration could be improved under ATII induced hypertension. Following intraperitoneal(IP) administration of cis-diamminedichloroplatinum(CDDP), a dynamic study was conducted on rabbits in Angiotensin II(ATII) induced hypertension to investigate hemodynamic changes in VX2 ovarian tumors. 8527810: Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. 8586940: Renovascular disease is the leading cause of surgically-curable arterial hypertension and one of the few cause of reversible chronic renal failure, but its exact prevalence remains unknown. 8723806: Renovascular disease is a frequent cause of severe hypertension in children and may result in significant morbidity or mortality. 8984121: OBJECTIVE: To investigate whether mutations in the beta subunit of the epithelial sodium channel (Scnn1b) contribute to the pathogenesis of hypertension in the spontaneously hypertensive rat (SHR) and the Dahl salt-sensitive rat. If disordered activity of the epithelial cell sodium channel contributes to the pathogenesis of hypertension in the SHR or Dahl models, it must stem from genetic lesions in sequences that regulate Scnn1b function or in sequences important to the structure or function of the other sodium channel subunits. 9055283: It might be postulated that sinus hypertension caused by stenocclusive disease of the venous sinuses triggers the development of fistulous connections between arteries and veins in the dural wall, which may result in increasingly dilated venules and the formation of DAVFs. 9203196: Renovascular disease is an important cause of remediable hypertension in childhood. 9423201: Renovascular disease is an important cause of hypertension in children because it is potentially treatable by surgical or angioplasty techniques. 9536103: The anatomic presence of atherosclerotic RVD as a threat to renal function has become a more pressing concern than that of hypertension secondary to RVD. 9568855: BACKGROUND: Renovascular disease is the most frequently encountered secondary cause of hypertension and is one of the few potentially reversible causes of chronic renal failure. 10570621: UNLABELLED: BASIC: The loss of verbal fluency in Alzheimer's disease (AD) has been related to the cognitive and functional impairment caused by the disorder. 10879068: These novel findings regarding the protein aggregates and causative genes for AD and related disorders will facilitate our understanding of the pathogenesis of AD, as well as development of therapeutic strategies against it. 11006125: As NSP-C was also reduced in AD frontal cortex, NSP-C deficits in these disorders may be reflecting neurodegenerative changes rather than a primary and specific finding of DS or AD pathogenesis. 11741391: In addition, it has revealed differences in apoC-I expression based on site, genotype, and disease status that may reflect a role for apoC-I in the pathogenesis of AD. 12480441: Different forms of dementia are now distinguished-Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, and dementia secondary to disease, such as AIDS dementia. 12740808: The enigmatic proteases alpha-,beta-, and gamma-secretase are the three executioners of amyloid precursor protein processing, and disruption of their delicate balance is suspected to result in Alzheimer's disease. Despite the dramatic progress that has been made in understanding the disease, the exact cause of Alzheimer's disease is still unknown. 14758627: For the first time the Alzheimer disease in monkeys was shown to entail a deficit of operative memory due to disorders in the sensory and cognitive components of the memory. 15340159: Because enhanced neurogenesis occurs in both AD and an animal model of AD, it seems to be caused by the disease itself and not by confounding clinical factors. 16120299: Mitochondrial dysfunction causes dozens of debilitating diseases, and is implicated in the etiology of type 2 diabetes, Parkinson's, and Alzheimer's diseases, among others. 17337008: However, evidence from epidemiological, neuropathological, clinical, pharmacological, and functional studies suggest considerable overlap in risk factors and pathological changes suggesting shared common pathogenic mechanisms between these two diseases such that vascular factors play a vital role in the pathogenesis of Alzheimer disease. 17892369: The onset of disease is not manifested clinically and little is known regarding the cause of nonfamiliar AD. 17922309: Moreover, accumulating evidence that mitochondria failure, reduced glucose utilization and deficient energy metabolism occur already very early in the course of the disease suggests a role of impaired insulin signalling in the pathogenesis of AD. 18041446: At present, different forms of dementia are distinguished, including Alzheimer's disease (AD), dementia with Lewy bodies, frontotemporal dementia, and dementia secondary to diseases, such as AIDS dementia. 1976213: Disorders in somatostatin metabolism have been proposed to contribute to the pathogenesis of Alzheimer's disease, epilepsy, GI motility disorders, and diabetes. 19777328: The markers of oxidative stress have been localized in the brain regions of AD and MCI that show pathological hallmarks of this disease, suggesting the possible role of Abeta in the initiation of the free-radical mediated process and consequently to the build up oxidative stress and AD pathogenesis. 20059701: For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re-entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. 20305996: BACKGROUND: During the course of the Alzheimer's disease (AD), many patients need to be hospitalized either due to the direct consequences of the disease itself, or due to associated diseases or life event. 20413848: The accumulation of toxic amyloid-beta42 (Abeta42) peptide oligomers and aggregates in AD brain has been proposed to be primarily responsible for the pathology of the disease, an idea dubbed the 'amyloid hypothesis' of AD etiology. 20442493: Since its proposal in 1992, the amyloid cascade hypothesis implicates Abeta overproduction as a causative event in disease pathogenesis, and this thinking has predominated the field's understanding of AD pathogenesis and the development of potential therapeutics (i.e., Abeta-reducing agents). 20552018: In neurodegenerative disorders such as Alzheimer's disease (AD), brain miRNA profiles are altered; thus miRNA dysfunction could be both a cause and a consequence of disease. 20601643: While partially effective in improving symptoms, currently available treatments approved by the US Food and Drug Administration (FDA) do not halt progression of AD, or address the underlying mechanism of the disease, in part because the etiology of AD is still an active area of investigation. 21391278: BACKGROUND: Cerebral small vessel disease (SVD) and hippocampal atrophy are related to verbal memory failures and may ultimately result in Alzheimer's disease. 21504127: Mild cognitive impairment (MCI) is recognized as a prodromal phase of dementing disorders, and it has been suggested that oxidative stress may play a role in the pathogenesis of Alzheimer's disease (AD), and in predicting progression of MCI to AD. 22886015: While macroscopic stroke can clearly produce cognitive deficits and accelerate Alzheimer's disease, the prevalence and implications of microvascular disease in Alzheimer's disease pathogenesis has been harder to define. 2313044: Alzheimer's disease is a major public health problem, yet little is known about the potential oral consequences of the disease. 23811083: Some significant novel genes and other variants for various biological processes have been reported as being associated with AD, AG, and other diseases, and these could be implicated in biochemical events leading to AD from AG through pathways, interactions, and associations. The present study aimed to identify genes with differential topology and their further association with other biological processes that regulate causative factors for AD, ageing (AG) and other diseases. 24059308: Our findings implicate diabetic disorders in the pathogenesis of AD, and provide a basis for future candidate studies based on specific pathways. 24899710: Few animal models of AD have been capable of isolating the relative contribution made by soluble and insoluble forms of Abeta to the behavioral symptoms and biochemical consequences of the disease. 25435363: Within this group, the top five leading causes of DALYs were: depressive disorders, Alzheimer's disease, migraine, substance-use disorders, and anxiety disorder, which accounted for 70.9% of all DALYs due to neuropsychiatric disorders. 26283893: Although no single model of AD is capable of providing the solution to the growing epidemic of the disease, we encourage a comprehensive approach that acknowledges the complex etiology of AD with the goal of enhancing the bidirectional translatability from bench to bedside and vice versa. 26618971: Tests of processing speed, working memory, verbal symbolic functions, and visuoperceptual and visuospatial judgment and problem solving are sensitive to the severity of TBI and AD, as well as to the functional consequences of these disorders, including ability to work, financial and medical decision-making capacities, and driving ability. 27094492: Mitochondrial dysfunction has been widely associated with the pathology of Alzheimer's disease, but there is no consensus on whether it is a cause or consequence of disease, nor on the precise mechanism(s). 27313503: Whether these changes are an initial cause for the onset of AD or occur as a result of the disease in late stages is still under debate. 27699087: Evidence from rodent and cell models show a number of neurotrophic and neuroprotective effects of guanosine preventing deleterious consequences of seizures, spinal cord injury, pain, mood disorders and aging-related diseases, such as ischemia, Parkinson's and Alzheimer's diseases. 28122529: Because the burden of AD on patients, families, healthcare providers, and society is substantial and increasing, it is important and necessary to understand the economic burden caused by this disease. 28261376: Studying AD from a metabolic perspective provides new insights into AD pathogenesis and may lead to the discovery of dietary metabolite supplements that can partially compensate for alterations of enzymatic function to delay AD or alleviate some of the suffering caused by the disease. 28387677: To date, neither any effective treatment nor prevention of Alzheimer's disease (AD), a major dementia causing disorder, are available. 29301530: OBJECTIVES: To understand AMD pathogenesis by analogy and suggest ideas for future research, this study summarizes main commonalities in disease pathogenesis of AMD, Alzheimer's disease, atherosclerosis and glomerulonephritis. 2941815: The theories put forward to explain the association between these two disorders and their possible significance to the understanding of the aetiology of Alzheimer's disease are discussed. 30546389: Although both amyloid beta peptide deposition and neurofibrillary tangle formation in the AD brain have been established as pathological hallmarks of the disease, many other factors contribute in a complex manner to the pathogenesis of AD before clinical symptoms of the disease become apparent. 30696930: Dementia was further categorised into Alzheimer's disease (AD), vascular dementia (VaD), and dementia caused by other diseases (ODs). 30740049: Nevertheless, the relationships between the morphological and functional changes of dendrodendritic synapses, particularly the local field potentials (LFPs) as a consequence of olfactory disorders in patients with AD have not been investigated. 30937343: The identification of the molecular underpinning of the disease not only provided the framework of AD pathogenesis but also targets for therapeutic inventions. 31127574: BER deficiency is associated with development of diseases causing neurodegenerative disorders, such as Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). 31228376: Despite the fact that this disease is considered, of course, age-associated pathology, which is the main cause of senile dementia, its diagnosis in Russia is exhibited rather rarely compared with dementia, for example, of vascular origin. 31456206: Increasing evidence suggests that disorders of metal ion metabolism in the brain are one of the risk factors for the pathogenesis of AD. 31521231: Amyloid-beta (Abeta) and alpha-synuclein (alphaS) are two intrinsically disordered proteins (IDPs) at the centers of the pathogenesis of Alzheimer's and Parkinson's diseases, respectively. Intrinsically disordered proteins in various hypotheses on the pathogenesis of Alzheimer's and Parkinson's diseases. 31605538: While Abeta has been suggested to be critical in inducing and, potentially, driving the disease, the molecular basis of AD pathogenesis is still under debate. 31607780: Similar to other complex disorders, the etiology of Alzheimer disease is multifactorial and characterized by an interplay of biological and environmental risk and protective factors. 31894361: Knowing the intrinsic disorder status and disorder-based functionality of proteins associated with amyloid cascade signaling pathway may help to untangle the mechanisms of AD pathogenesis and help identify therapeutic targets. 31900899: Excitotoxicity is a modern clinical condition included in the pathogenesis of Alzheimer's disease. 32225073: Importantly, there is also clinical evidence supporting their potential use as biomarker candidates for AD, due to reduced serum and CSF levels that correlate with amyloid burden in AD patients compared with controls. Although the exact etiology of the disease remains elusive, accumulating evidence highlights the key role of lipid rafts, as well as the endocytic pathways in amyloidogenic amyloid precursor protein (APP) processing and AD pathogenesis. 32696388: Measuring Interactions Between Tau and Aggregation Inducers with Single-Molecule Forster Resonance Energy Transfer.Tau is an intrinsically disordered protein implicated in the pathogenesis of Alzheimer's disease and other neurodegenerative disorders. 33302541: AD is considered a multifactorial disease: two main hypotheses were proposed as a cause for AD, cholinergic and amyloid hypotheses. 33457489: Models or combinations of new models are needed that incorporate genetics with environmental interactions, timing of disease development, heterogeneous mechanisms and pathways, comorbidities, and other pathologies that lead to AD and related dementias. 33512819: Although it has not been possible to determine the origin of this disease, the amyloid hypothesis is one of the most accepted to explain the etiology of AD. 33629978: Although it has not been possible to determine the origin of this disease, the amyloid hypothesis is one of the most accepted to explain the etiology of AD. 33806317: Identifying the molecular characteristics of the disease is imperative to understanding the pathogenesis of AD. 34439596: No drug class was associated with the least severe AD (cluster-1), likely due to lesser antecedent disease. 34609116: Insulin resistance is also a factor that contributes to pathogenesis of AD. The complications that are discussed in this article are diabetic nephropathy, diabetes induced cardiovascular disease, diabetic neuropathy, Diabetic Foot Ulcer (DFU) and Alzheimer's disease. The progression of AD can be due to the change in DNA methylation of CLOCK gene, followed with worsening of AD by APOE4 gene due to dyslipidaemia condition in T2DM patients. 35463002: Background: Recent Alzheimer's disease (AD) hypotheses implicate that hepatic metabolic disorders might contribute to the disease pathogenesis of AD, but the mechanism remains unclear. 35563253: As research progresses, it has become known that AD can be caused by diseases that have been experienced over the course of a lifetime, which could also affect other organs. 36430144: The identification signatures overlapping for AD, PD, and MS raise the question of whether these reflect a common etiology or rather common consequence of these diseases. 36431219: This state of affairs has made neuroscientists suspicious, so much so that for several years the idea has gained ground that AD is not a direct neuropathological consequence taking place downstream of the deposition of the two toxic proteins, but rather a multifactorial disease, including mitochondrial dysfunction as an early event in the pathogenesis of AD, occurring even before clinical symptoms. 36436686: Animal model of Alzheimer's disease induced by streptozotocin: new insights about cholinergic pathway. Disorders of the cholinergic system are well known to be involved in the pathogenesis of AD, characterized by increased acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) and decreased acetyltransferase (ChAT) enzymatic activities. 37000425: Although it is largely unclear whether dysfunctions in sleep and circadian rhythms contribute to the etiology of AD or are a consequence of the disease, there is evidence that these conditions are involved in a complex self-reinforcing bidirectional relationship. 37693644: We suggest that Abeta is not a culprit of Alzheimer's disease, but merely a byproduct of autophagy/lysosomal failure resulting from hydroxynonenal-induced Hsp70.1 disorder. 37811614: Furthermore, despite the disease hallmarks commonly manifested in all AD cases, considerable evidence suggests complex heterogeneity of AD pathogenesis. 37934647: For Alzheimer's Disease, the proposed method demonstrated remarkable performance in predicting the brain ventricle changes induced by the disease, achieving the state-of-the-art result on TADPOLE cross-sectional prediction challenge dataset. 38064104: Even though a century has passed since the discovery of AD, the exact cause of the disease still remains unknown. Since dysregulation of this kinase affects all the major characteristic features of the disease, such as tau phosphorylation, amyloid formation, memory, and synaptic function, it is thought to be a major player in the pathogenesis of AD. 38203429: After several years of research in the field of Alzheimer's disease (AD), it is still unclear how amyloid-beta (Abeta) and Tau, two key hallmarks of the disease, mediate the neuropathogenic events that lead to AD. 38549636: Background: Increasing evidence suggests that both amyloid-beta metabolism disorders in the liver and cerebral hypoperfusion play an important role in the pathogenesis of Alzheimer's disease (AD). 7542917: CONCLUSION: These results indicate that optic nerve degeneration is not a feature of AD and suggest that the visual deficits in the disease result from cortical dysfunction. 8198393: Alzheimer's disease (AD), the most common dementing disorder of late life, is a major cause of disability and death in the elderly. 8290042: This mutation was present in DNA from all four examined affected individuals and linked to the disease with a lod score of 3.25, and was the most probable cause of AD in this family. 8871938: Despite a large amount of evidence that suggests an association between oxidative stress and the pathogenesis of AD, it is not yet known whether oxidative stress is a cause or consequence of the disorder. 8912490: Further studies will determine whether this alteration could provide a peripheral biochemical marker of the disorder and whether it could intervene in the pathogenesis of Alzheimer disease. 1033105: 2) TLP-607 slightly hypertension induced by dopamine, adrenaline and noradrenaline, but had no effect on hypotension induced by acetylcholine and histamine. 11408422: Blood-brain barrier permeability during dopamine-induced hypertension in fetal sheep. Using time-dated pregnant sheep, we tested the hypothesis that dopamine-induced hypertension increases fetal BBB permeability and cerebral water content. 12879669: Over a specific dose range, systemic hypertension induced by adrenaline, noradrenaline and dopamine did not significantly increase cerebral blood flow under 2% isoflurane anaesthesia. 1453933: The purpose of this study is to describe our technique of applying fibrin glue at the microvascular anastomotic site and to evaluate the effect of fibrin glue on anastomotic hemostasis and patency under various high pressure states using dopamine-induced acute hypertension in rats. 1574468: Effects of clonidine-induced hypotension and dopamine-induced hypertension on blood flows in prostatic adenocarcinoma (Dunning R3327) and normal tissues. In the present study it was investigated whether hypertension induced by dopamine or hypotension induced by clonidine could influence the relative blood distribution in a s.c. transplanted prostatic adenocarcinoma in relation to blood flow in normal tissues in rats. 18615257: Dopamine is important in the pathogenesis of hypertension because of abnormalities in receptor-mediated regulation of renal sodium transport. 21701066: Intrarenal dopamine deficiency leads to hypertension and decreased longevity in mice. 23786005: Determined the decrease in dopamine activity with age, that contributes to the pathogenesis of hypertension, abdominal obesity, the development of left ventricular hypertrophy. 2844127: In the control state, DA-induced arterial hypertension (i.v. administration) and augmented inotropism (i.v. and i.c. administration) were accompanied by a dose-dependent coronary vasodilatation (increase of CBF and decrease of CVR). 31809283: We found information regarding the role of the brain-gut--bone marrow axis, the brain-gut--kidney axis, the high-salt diet, short-chain fatty acids (SCFAs), neurotransitters, such as serotonin, dopamine and norepinephrine, nitric oxide, endothelin and steroids in modulating gut microbiota and in contributing to the pathogenesis of hypertension. 3443545: Increased outputs of lymphocytes in lymph efferent from the lymph nodes of sheep during systemic arterial hypertension induced by phenylephrine or dopamine. 3766759: Blood-brain barrier (BBB) permeability was increased during moderate hypertension induced by dopamine and not when induced by norepinephrine. The effects of hypertension induced by norepinephrine and dopamine infusion on the relationship between local cerebral blood flow (CBF) and local glucose use (GU) were examined in rats with the use of quantitative autoradiographic techniques. 3951751: Hypertension induced by DA resulted in significant increases (median = 44%) in local CBF in 38 of the 40 brain regions investigated. 465876: 5 It is suggested that dopamine injected into the cerebral ventricles of the unanesthetized dog causes hypertension and tachycardia by activating central dopamine receptors. 466431: No significant changes in DA content were observed in any region of the brain following induction of hypertension by the three different methods. NA content increased significantly in various areas: the increase of NA in the pons-medulla was common to all procedures inducing hypertension. In two substrains, selected from the Hebrew University strain, for their respective sensitivity (H) or immunity (N) to hypertension induced by DOCA--salt treatment, there were no significant increases in NA or DA in any part of the brain following DOCA--salt treatment. Noradrenaline (NA) and dopamine (DA) distribution in different brain areas was assayed following induction of hypertension. 4802783: [Effects of cocaine on hypertension induced by dopamine (hydroxytyramine) and action on posthypophyse extracts on blood pressure effect induced by this dopamine previously treated with adrenalin antagonists]. 6147763: They also show that the ventricular cardioaccelerator effect of dopamine is attenuated by a reflex vagal depressor effect consequent to the induced hypertension. 6599658: Increased DA release, tissue content and urinary excretion of DA and its metabolites are thus selectively involved in the sequence of events leading to hypertension in SHR. 6766538: We evaluated the treatment regime of dopamine-induced hypertension in association with volume expansion and ventilatory support in an experimental subarachnoid hemorrhage (SAH) model using the cynomolgus monkey. 690680: All were treated with dopamine-induced hypertension, mannitol, and large quantities of intravascular fluids. 7144267: The possibility is that dopamine along with noradrenaline may be playing an important role in peripheral organs, such as adrenal gland and heart, in the pathogenesis of hypertension. The noradrenaline and dopamine contents of heart and adrenal gland were estimated in rats with spontaneous, renal and stress-induced hypertension. 7642168: Recent aspect of the role of peripheral dopamine and its receptors in the pathogenesis of hypertension. 7850410: Several lines of evidence now suggest that abnormalities of the renal dopamine system can lead to salt-sensitive hypertension. 8169626: Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. 8262273: However, it is plausible that the impairment of dopamine generation and/or the defective responses of a dopamine receptor might induce sodium retention and hypertension. Since dopamine is one of the important endogenous hypotensive and natriuretic substances, it is speculated that impaired dopamine generation and/or the disturbance of the effects of dopamine could cause hypertension with suppression of plasma renin activity and/or salt-sensitivity. 8945755: These results indicate that picrotoxin affects interactions between GABA neurons and DA system in rat brain to induce hypertension during an epileptic attack. 9370048: The subsequent low level of brain dopamine induces hypertension. 9760022: Catecholamines, dopamine and the renal kallikrein-kinin system may participate in the pathogenesis of hypertension. 10205244: The uncoupling of the D1 receptor in both rats (previously described) and humans (described here) suggests that this mechanism may be involved in the pathogenesis of hypertension; the uncoupling may be due to ligand-independent phosphorylation of the D1 receptor in hypertension. 15171362: [Involvement of dopamine receptor in the pathogenesis of hypertension and hypertensive target-organ damage]. 18547994: Disruption of either the endothelin B receptor (ETB) or D(3) dopamine receptor gene in mice produces hypertension. 25368031: Disruption of the D4 dopamine receptor gene in mice produces hypertension that is associated with increased renal angiotensin type 1 (AT1) receptor expression. 32293069: Acute renal depletion of sorting nexin 1 (SNX1) in mice results in blunted natriuretic response and hypertension due to impaired dopamine D 5 receptor (D 5 R) activity. 32349533: FUTURE DIRECTIONS: Identifying the mechanisms of renal dopamine receptors in the regulation of oxidative stress and their contribution to the pathogenesis of hypertension remains an important research focus. Increased understanding of the role of reciprocal regulation between renal dopamine receptors and oxidative stress in the regulation of blood pressure may give us novel insights into the pathogenesis of hypertension and provide a new treatment strategy for hypertension. 36672619: Deletion of any of the five dopamine receptors may lead to salt-sensitive hypertension. 3699195: [Role of renal dopamine receptor in the pathogenesis of hypertension after sodium loading]. 6723774: These results further suggest that cyclo(leucyl-glycine) interacts with brain dopamine receptors, and that brain dopamine receptors may be involved in the etiology of hypertension. 8130121: We have proposed the dopamine receptor gene as one candidate in the pathogenesis of hypertension. 8262273: However, it is plausible that the impairment of dopamine generation and/or the defective responses of a dopamine receptor might induce sodium retention and hypertension. Since dopamine is one of the important endogenous hypotensive and natriuretic substances, it is speculated that impaired dopamine generation and/or the disturbance of the effects of dopamine could cause hypertension with suppression of plasma renin activity and/or salt-sensitivity. 8433803: More importantly, up-regulation of D1 and D2 dopamine receptors in the striatum of young prehypertensive spontaneously hypertensive rats suggests that dopamine may be involved in the pathogenesis of hypertension in this strain of genetically hypertensive rats. 9719042: Subsequently, it may be possible to use a therapeutic approach to correct the defect in dopamine receptor gene causing the hypertension. 11447838: We have hypothesized that AD results from a progressive dysfunction of APP. There are two pieces of supporting data for this: first, APP is overexpressed in Down's syndrome, which leads to AD-like neuropathology by the age of 40 in virtually all affected individuals; secondly, specific point mutations in APP cause some forms of familial AD. 11755021: Results support the hypothesis that in a group of persons at risk for AD because of DS, olfactory impairment is greater in older individuals, suggesting progressive impairment over time. 15834031: OBJECTIVE: Down's syndrome (DS) is the most frequent genetic cause of Alzheimer-type dementia. 18676989: Enlarged early endosomes in the neurons of young Down syndrome (DS) and pre-Alzheimer's disease (AD) brains suggest that a disturbance in endocytosis is one of the earliest hallmarks of AD pathogenesis in both conditions. 19509306: Regulator of calcineurin 1 (RCAN1), a gene identified from the critical region of Down syndrome, has been implied in pathogenesis of Alzheimer's disease (AD). 21944886: Transfer of the amyloid beta and/or of beta-amyloid precursor protein of the fetus with trisomy 21 to the maternal blood stream and its possible contribution to the pathogenesis of the maternal Alzheimer's Disease. The evidence that is derived from several sources--genetic, among them--suggests that the Abeta participates in the pathogenesis of Alzheimer's Disease (AD). 24888381: The amyloid precursor protein gene is on chromosome 21, and so is over-expressed in Down syndrome, leading to amyloid beta (Abeta) over-production, a major upstream pathway leading to Alzheimer disease (AD). 24962069: Individuals with Down syndrome (DS) are at increased risk of developing AD in adulthood as a result of chromosome 21 trisomy and triplication of the amyloid precursor protein (APP) gene. 2534160: These results indicate that neither the normal aging processes, Alzheimer's disease, nor the increased in vitro lipid peroxidation reported in fetuses with Down's syndrome result from a gross lack of alpha-tocopherol, or cause a significant depletion of the vitamin. 2563716: A lot of recent molecular genetic experiments and many neuropathological analogies of Alzheimer's dementia and Down's syndrome indicate a damage on the chromosome 21 as possible cause of Alzheimer's dementia. 27867340: DS is also the most frequent genetic cause of Alzheimer's disease (AD), and ~50% of those with DS will develop AD-related dementia. 34182407: This early detection of tau can help characterize the tau accumulation phase during preclinical Alzheimer's disease progression in Down syndrome and suggests that there may be a relatively narrow window after Abeta accumulation begins to prevent the downstream cascade of events that leads to Alzheimer's disease. 35596914: Correlating Alzheimer's disease biomarkers in Down syndrome and cognitive function scores while considering the effect of psychosocial risk factors helps us identify the mechanisms leading to Alzheimer's disease at an early age. 9732570: This article, the first of two parts, considers the link between Down's syndrome and Alzheimer's disease and how this link has been a significant factor with regards to research into the aetiology of Alzheimer's disease. 10445667: Seventeen male Sprague-Dawley rats were given L-NAME (60 mg/kg/day) in drinking water for 6 weeks to induce hypertension, and then treated with amlodipine (L-NAME + A, 5 mg/kg/day, n = 9), or a vehicle (L-NAME + V, n = 8) for 4 weeks. 10701821: Fifteen male Sprague-Dawley rats were given L-NAME (60 mg/ kg/day) in drinking water for 6 weeks to induce hypertension, and then treated with imidapril (L-NAME-I, n = 8, 1 mg/kg/day, subdepressor dose), or a vehicle (L-NAME-V, n = 7) for 4 weeks. 10858026: A 1% sodium chloride solution was used as drinking water to induce hypertension. 11448615: Effect of sucrose addition to drinking water, that induces hypertension in the rats, on liver microsomal Delta9 and Delta5-desaturase activities. 15602793: Chronic inhibition of nitric oxide synthase induced by N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (50 or 75 mg.kg(-1) x day(-1)) in drinking water for 6 weeks caused a sustained hypertension, comparable in the two groups. 15644486: Rats were maintained for 2 wk on 8.0% NaCl chow with NG-nitro-L-arginine methyl ester (L-NAME) in the drinking water (12.5 mg/l) to induce hypertension and accelerate the onset of renal disease. 16793027: In this study, adult Wistar rats were subjected to the same hypoxic regimes and given the nitric oxide synthase (NOS) inhibitor N(6)-nitro-L-arginine methyl ester (L-NAME) in drinking water (NLN, IHLN and CHLN regimes) to induce hypertension. 16940562: Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (C<F10<F60). 17898042: Substitution of chromosome 20 from the BN to the FHH attenuated the development of l-NAME-induced hypertension, normalized plasma renin activity, and decreased plasma creatinine in male rats. Male and female rats of each of the parental and consomic strains were maintained for 2 wk on high-salt (8.0% NaCl) chow with N(G)-nitro-l-arginine methyl ester (l-NAME) in the drinking water (12.5 mg/l) to induce hypertension and renal disease. 18287667: This chapter describes the detailed methods that utilize the drinking water of rats to develop models of nitric oxide synthase (NOS) inhibition-induced, guanosine triphosphate cyclohydrolase (GTPCH) inhibition-induced, and glucocorticoid-induced hypertension. 26432844: Depressor effect of chymase inhibitor in mice with high salt-induced moderate hypertension. The aim of the present study was to determine whether long-term high salt intake in the drinking water induces hypertension in wild-type (WT) mice and whether a chymase inhibitor or other antihypertensive drugs could reverse the increase of blood pressure. 27386147: In this study, we evaluated the anti-cataractogenic effect of cinnamaldehyde (CA), a natural organic compound, in rats with fructose-induced hypertension. For six weeks, the normal group received a suspension of 0.5% carboxy methyl cellulose (10 mL/kg/day, p.o.) while five other groups received a 10% (w/v) fructose solution in their drinking water to induce hypertension. 27683016: Sodium is an integral part of water, and its excessive amount in drinking water causes high blood pressure and hypertension. 28455132: These data suggest that GME had a protective effect against l-NAME-induced hypertension and cardiovascular remodeling via suppressing p47phox NADPH oxidase subunit and iNOS protein expression resulting in enhancing NO bioavailability. Male Sprague-Dawley rats were given 40mg/kg/day of l-NAME in drinking water to induce hypertension, and were simultaneously treated with GME at a dose of 200mg/kg/day. Nomega-Nitro-l-arginine methyl ester (l-NAME)-induced hypertension and cardiovascular remodeling are associated with oxidative stress and inflammation. GME prevented the development of hypertension and cardiovascular remodeling induced by l-NAME with reduced oxidative stress and inflammation. 33748480: Background: Based on the cross-sectional and cohort studies, exposure to As via drinking water can cause hypertension. 35555082: Gut microbiota depletion with antibiotics enhances fructose induced salt-sensitive hypertension in normal rats. INTRODUCTION-: We reported that 20% fructose in drinking water induced salt-sensitive hypertension in normal rats. CONCLUSION: - Chronic antibiotic treatment induced gut microbiota depletion and enhanced fructose induced salt-sensitive hypertension in normal rats, an effect that was associated with decreased plasma beta-hydroxy-butyrate, lactate and insulin. The contribution of the gut microbiota to fructose induced salt-sensitive hypertension or renal function has not been studied. Aim- We hypothesized that gut microbiota depletion with antibiotics (ABX) would change fructose induced salt-sensitive hypertension, renal excretory function and plasma levels of bacterial metabolites (lactate, beta-hydroxy-butyrate). 35556816: These results suggested that the overexpression of S1PR1 in the renal medulla attenuates sodium retention by the inhibition of ENaC function in the DOCA-induced SS-HTN. The mice were then implanted with the silastic DOCA sheet subcuntaneously and 1% NaCl drinking water to induce salt-sensitive hypertension (SS-HTN). 38148348: The goal of the study are to define the energy metabolic profile in heart failure induced by obesity and hypertension in aged female mice, and to attempt to lessen the severity of heart failure by stimulating myocardial glucose oxidation. The primary energy metabolic change in heart failure induced by obesity and hypertension in aged female mice is a dramatic decrease in glucose oxidation. 13-Month-old C57BL/6 female mice were subjected to 10 weeks of a 60% high-fat diet (HFD) with 0.5 g/L of Nomega-nitro-L-arginine methyl ester (L-NAME) administered via drinking water to induce obesity and hypertension. 6847256: One percent salt, 1 ppm cadmium, or 1 ppm cadmium plus 1 ppm lead in drinking water caused similar mild hypertension in rats. 7119901: Long-term exposure to cadmium in drinking water can induce hypertension in rats. There were other (non-cadmium) differences between the stock and rye diets and between the remainder of our experimental conditions and those used by other investigators, presumably explaining the failure of some others to induce hypertension with cadmium. 10809426: PATIENTS AND METHODS: Our study evaluates ecNOS gene status and NO metabolites in kidney transplanted patients under chronic CsA treatment with CsA-induced hypertension. BACKGROUND: CsA-induced endothelial dysfunction and CsA-induced hypertension have been attributed to CsA effects on the endothelial-derived factors controlling vasomotor tone, but the mechanisms responsible are unclear. 11112045: Cyclosporin-induced endothelial dysfunction and hypertension: are nitric oxide system abnormality and oxidative stress involved? While the mechanism(s) responsible are unclear, CsA-induced endothelial dysfunction and CsA-induced hypertension have been attributed to the CsA effect on the endothelial-derived factors controlling vasomotor tone. Our study evaluates endothelial nitric oxide synthase (ecNOS) gene status (PCR analysis) and plasma levels of NO metabolites (ELISA) in kidney and heart transplant patients under chronic CsA treatment with CsA-induced hypertension. 11347860: However, CsA has an important side effect, producing renal vasoconstriction and systemic hypertension. 11349731: RESULTS: CsA-induced hypertension and nephrotoxicity were associated with myocardial infarcts and vasculopathy of the coronary arteries. 12227681: Oxidative stress and TGFbeta in kidney-transplanted patients with cyclosporin-induced hypertension. In conclusion, carvedilol reduces the oxidative stress and corrects the altered cellular signaling mediated by oxidative stress in CsA-induced post-transplant hypertension. 15483783: CONCLUSION: Body hydration status was more sensitive to dietary salt fluctuations during CsA treatment than without CsA, and a high-sodium diet seemed to enhance the CsA-induced hypertension side effect. 1549860: These findings suggest the potential of dietary EPO and F to offset nephrotoxic effects of CsA administration, and suggest that EPO may also be useful in countering CsA-induced hypertension. 16612258: RESULTS: CsA induced severe hypertension, cardiac hypertrophy, endothelial dysfunction, and pronounced albuminuria. 17821861: The results suggest that losartan is safer compared to other antihypertensives for the treatment of CSA induced hypertension. 17954158: The present study sought to evaluate the prevention and reversion effects of isosorbide-5-mononitrate (Is-5-Mn) on the development of hypertension (HT) and on the underlying vascular and platelet morphofunctional disturbances, using an animal model of cyclosporine (CsA)-induced HT. Our data suggested that Is-5-Mn therapy may be a valid choice to prevent the morphofunctional changes associated with CsA-induced HT, when used as a preventive therapy. Dual effect of nitrate therapy for cyclosporine-induced hypertension on vascular and platelet morphofunctional markers; an animal model. 2056124: These findings may help in the understanding of CSA-induced hypertension and vasculopathy. 2112669: Although the mechanism of cyclosporin (CsA)-induced hypertension is unknown, it has been shown to inhibit prostacyclin (PGI2) production directly, which may be a factor. Decrease in cyclosporin-mediated prostacyclin production in renal versus carotid arteries: a mechanism for cyclosporin-induced hypertension. 21170880: Aside from this, there is evidence suggesting the possible involvement of free radicals during the development of CsA-induced hypertension. In the collecting duct, CsA may cause hypertension by stimulating the epithelial Na+ channel (ENaC) through a pathway associated with inhibition of ABCA1 and consequent elevation of cholesterol in the cells. 22226938: The hypertensive effect of CSA disappeared in rats pretreated intracisternally (i.c.) with N(omega)-nitro-l-arginine methyl ester (L-NAME, nonselective NOS inhibitor), N(5)-(1-iminoethyl)-l-ornithine (L-NIO, selective eNOS inhibitor), N(omega)-propyl-l-arginine (NPLA, selective nNOS inhibitor), or 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ, guanylate cyclase inhibitor), suggesting the importance of central eNOS/nNOS/GC cascade in CSA-induced hypertension. 2405549: Cyclosporine-induced hypertension in sheep. We have previously shown that administration of intravenous CsA to sheep for 5 days at 12 mg/kg/day produces a hypertension that is resistance mediated and independent of nephrotoxicity. 24942911: Experimental models of CsA-induced hypertension have shown an increase in renal NKCC2. 25280976: BACKGROUND: Cyclosporine (CsA) is frequently responsible for hypertension in bone marrow transplant children. CONCLUSIONS: Because lacidipine appears to have no effect on CsA exposure, it may be the best option among CCBs for treating high blood pressure caused by CsA in children. 31222723: As ABCA1 can be blocked by cyclosporine A, these results suggest further investigation of the possible use of statins to treat CsA-induced hypertension. 3154381: Further improvement in medium-term results can be anticipated as a result of reducing CsA-induced nephrotoxicity and hypertension as a result of triple therapy and adjusting the components of that therapy to the individual needs of particular patients. 3576678: The data are consistent with the hypothesis that CsA induces nephrotoxicity and de novo hypertension through a contractile effect on vascular smooth muscle. 9468460: Cyclosporine-induced hypertension and decline in renal function in healthy volunteers. Thus, the present study confirms and extends earlier observations that renal dysfunction and sodium retention are not the initiating events in CsA-induced hypertension. 9690215: However, CsA can cause nephrotoxicity and hypertension (HTN). Depressed renal and vascular nitric oxide synthase expression in cyclosporine-induced hypertension. These observations suggest that CsA-induced HTN may be, in part, related to impaired NO production. This study was designed to test the hypothesis that CsA-induced HTN is related to depressed nitric oxide (NO) production. 9723371: ecNOS overexpression in CsA-treated renal transplant patients: implications for CsA-induced hypertension. 9749227: In view of two main mechanismes implicated in CsA-induced hypertension the most logical therapeutic approach would be to use diuretics and calcium inhibitors. 11979537: Renal artery thrombosis or embolus is a rare condition that may lead to hypertension and renal failure. 13451997: Successful treatment by nephrectomy of hypertension resulting from aorticorenal embolus. 15707852: Selective pulmonary vasodilators attenuate acute pulmonary embolism (APE)-induced pulmonary hypertension. 16253237: Hemodynamic effects of combined sildenafil and L-arginine during acute pulmonary embolism-induced pulmonary hypertension. 16304337: STUDY OBJECTIVES: To evaluate the effects of L-arginine on acute pulmonary embolism (APE)-induced pulmonary hypertension and increases in lung matrix metalloproteinase (MMP)-2 and MMP-9 activities. 16504213: Sildenafil attenuates acute pulmonary embolism (APE)-induced pulmonary hypertension. These results show that the combined administration of 1microMol kg(-1) of DETA-NO and sildenafil is not advantageous compared with sildenafil alone, thus suggesting that sildenafil alone produced maximum attenuation of APE-induced pulmonary hypertension, as far as the NO-cGMP pathway is concerned. 16650492: BACKGROUND: Matrix metalloproteinases (MMPs) modulate vascular contractility and may affect acute pulmonary embolism (APE)-induced pulmonary hypertension. CONCLUSIONS: Our study shows that doxycycline attenuates APE-induced pulmonary hypertension, and indicates that MMP-9 has a role in APE-induced pulmonary hypertension. 17133179: Here, we evaluate the effects of atorvastatin pretreatment on APE-induced pulmonary hypertension, 24-hr mortality rate, and changes in plasma and lung MMP-2 and MMP-9 activities. OBJECTIVE: Matrix metalloproteinases (MMPs) have been implicated in the pathophysiology of acute pulmonary embolism (APE)-induced pulmonary hypertension. 1890982: Large-vessel cerebral arterial disease (intimal hyperplasia with superimposed thrombosis) has clearly been established as the most important cause of stroke in SCD, and considerable evidence suggests that pulmonary arterial thrombosis/embolism is a major cause of pulmonary infarction and hypertension. 20804854: In conclusion, although iNOS-derived NO may play a key role in APE-induced oxidative stress, our results suggest that the iNOS inhibitor S-methylisothiourea neither attenuates APE-induced pulmonary hypertension, nor enhances the beneficial hemodynamic effects produced by sildenafil. 21964667: APE-induced pulmonary hypertension is aggravated by active pulmonary vasoconstriction. 5305688: Sympathetic nerve activity during hypertension produced by vertebral embolism. 7157602: [Surgical treatment of mitral valve defect and hypertension as a result of inveterated embolism of the renal artery]. 10526135: These data imply that excitation of the AC can activate many nuclei controlling emotion and stress via CRF and SP, and excessive activities of these nuclei may be the neural basis of hypertension induced by prolonged emotional stress. The purpose of the present study is to analyze the possible neural basis of hypertension induced by prolonged emotional stress. 16946584: The AHA angiotensin system is also responsible for hypertension induced by emotional stress and central Na(+) increases. 1874436: [Brain adrenoreceptors in rats with inherited arterial hypertension due to emotional stress]. 18769977: We describe a 65-year-old woman with a history of hypertension and smoking who presented with an acute episode of chest pain precipitated by severe emotional stress. 1950: In tranquillizing doses the preparation has an antihypertensive effect and prevents the development of a long-term tonic hypertension due to emotional stress. 21029000: Genetic control of the corticosterone level at rest and under emotional stress in ISIAH rats with inherited stress-induced arterial hypertension. 21797992: CONCLUSIONS: This study do not support previous hypothesis that emotional stress may be a cause of hypertension. 2945340: Hypertension, decrease of respiratory rate and increase of Hildebrandt index were observed as a result of PES, ethanol consumption, and especially under PES during ethanol consumption. 564519: The role of experimental emotional stress in the genesis of arterial hypertension was studied. 572925: Investigation of the role of prolonged emotional stress in the genesis of hypercholesteremia and hypertension. 942865: [The role of prolonged emotional stress in the genesis of hypercholesterolemia and hypertension]. 9622022: These results indicate that both CRF and SP in the above mentioned nuclei may play important roles in hypertension induced by prolonged emotional stress. 11566943: In other animal models, such as the deoxycorticosterone acetate (DOCA)-salt rat, hypertension develops as the result of an induced hormonal imbalance. 12442092: Pheochromocytoma, hypercorticism, primary aldosteronism or glucocorticoid-remediable aldosteronism can be present or diagnosed at any term and may cause severe hypertension. Hypertension may be pregnancy-induced, essential or secondary to endocrine disorders. 12635375: [Our experience in the surgical treatment of the arterial hypertension due to endocrine disturbances]. This study is trying to expose our experience in the surgical treatment for adrenal tumors which produce arterial hypertension, experience gained over a period of 25 years. 1737549: [Hypertension caused by endocrine disorders]. 2332685: [Hypertension due to endocrinologic disorders]. 25893613: This indicates the importance of endocrine disorders in the aetiology of hypertension. 26098187: [Arterial hypertension secondary to endocrine disorders]. 31655779: Even if in a majority of cases hypertension is essential, possible secondary causes, which can be related to endocrine disorders, must be detected and correctly managed. 33079272: RECENT FINDINGS: More than 15 endocrine disorders with varying rates of prevalence can cause hypertension. 34918071: Primary aldosteronism (PA) is an endocrine related condition leading to arterial hypertension due to inappropriately high and unregulated aldosterone concentration. 36329530: Hypertension can be primary (primary hypertension, PHT), or secondary to endocrine disorders (endocrine hypertension, EHT), such as Cushing's syndrome (CS), primary aldosteronism (PA), and pheochromocytoma/paraganglioma (PPGL). 7941161: In both groups the above hormonal abnormalities followed the pattern of progressive hyperkinetic syndrome running with an inadequate fall in peripheral vascular resistance responsible for arterial hypertension in these patients. 8571747: High blood pressure is due to endocrine disorders in only a small fraction of hypertensive patients. 15727865: beta-Secretase is an important protease in the pathogenesis of Alzheimer's disease. 16293708: As an essential protease in the generation of amyloid beta, gamma-secretase is believed to play an important role in the pathogenesis of Alzheimer's disease. 17098871: Rare familial forms of Alzheimer's disease (AD) are thought to be caused by elevated proteolytic production of the Abeta42 peptide from the beta-amyloid-precursor protein (APP). 19544621: Growing evidence suggests a causative role for intracellular accumulation of amyloid precursor protein (APP) and its proteolytic products in the pathogenesis of AD. Mitochondrial dysfunction is one of the key characteristics of AD pathogenesis. 21331224: Amyloid Precursor Protein (APP) and its proteolytic product amyloid beta (Abeta) are critical in the pathogenesis of Alzheimer's Disease (AD). 21354962: Ubiquitin ligase was an important protease in the pathogenesis of Alzheimer's Disease (AD). 22464639: DESIGN: Sixty female Sprague Dawley rats were divided into four groups n=15, (1) normal control group (con), (2) group underwent surgery to remove ovaries (ovx control group), (3) ovx group received aluminum chloride in a dose of 17 mg/kg daily for 2 months to induce AD (AD group), (4) AD group treated with alpha-chymotrypcin (alpha-ch) at dose (8.1 unit/rat/day) which is equivalent to the recommended human dose (alpha-ch-treated group) for three months. CONCLUSION: This study revealed that alpha-chymotrypcin significantly ameliorates the neuroinflammation characterizing Alzheimer's disease in ovariectomized rats due to it's proteolytic activity as well as it's anti-inflammatory effect. 25528641: The amyloid precursor protein (APP) and its proteolytic cleavage product Abeta are widely believed to be central to the etiology of Alzheimer's disease (AD). 28826672: Delta-secretase, a lysosomal asparagine endopeptidase (AEP), simultaneously cleaves both APP and tau, controlling the onset of pathogenesis of Alzheimer's disease (AD). 8773762: The imbalance of an extracellular protease system may participate in the pathogenesis of Alzheimer's disease. 10461686: It is further suggested that hyperinsulinemia is more important than endothelial dysfunction as a cause of hypertension in fructose-fed rats. 10949060: Consequently, endothelial dysfunction has been implicated as an important event in the pathogenesis of atherosclerosis, coronary vasoconstriction, hypertension, and myocardial ischaemia. 11498459: Endothelial dysfunction is considered an intermediate phenotype in the pathogenesis of hypertension and atherosclerosis. 11532102: Endothelial dysfunction may predispose the patient to accelerated atherosclerosis and may be involved in the pathogenesis of hypertension in end-stage renal failure. 11872361: Insulin resistance and associated hyperinsulinemia have been observed in effort as well as vasospastic angina pectoris (VSAP), atherothrombotic cerebral infarction, and in ASO without obesity, HT, or diabetes, suggesting the resistance resulting from endothelial dysfunction. 11955849: BACKGROUND: Endothelial dysfunction is an early stage in the development of coronary atherosclerosis and has been implicated in the pathogenesis of hypertension and cardiomyopathy. 12022241: Therefore, the decrease in FMD observed in severe hypertension may be caused by endothelial dysfunction as well as by structural vascular changes, suggesting difficulties in interpreting FMD solely as a measure of endothelial dysfunction in hypertensive patients with left ventricular hypertrophy. 12510414: CONCLUSIONS: The significant elevation of the SBI and DBI in normotensives with ED is an evidence convincing that a dysfunctional endothelium is responsible for vasopressant effects that cause a paraphysiological status of \pre-hypertension\. 12629100: Disorders of the lipoprotein metabolism are a major cause of endothelial dysfunction that may result in hypertension and proteinuria, clinical hallmarks of preeclampsia (PE). 12877071: There are several mechanisms about high blood pressure induced by insulin resistance in type 2 diabetes. High blood pressure was partially caused by the endothelial dysfunction. 12877075: In this review, we present the possibility that endothelial dysfunction causes hypertension in diabetes mellitus. It is unclear that endothelial dysfunction is a cause or consequence of hypertension. 15992627: They also have aortic complications such as aneurysm and dissection, which result from a diffuse arteriopathy and continued hypertension that may be caused by underlying endothelial dysfunction. 16733240: Several possible mechanisms linking insulin resistance and compensatory hyperinsulinemia with hypertension have been described, such as renal sodium reabsorption enhancement, sympathetic nervous system activation, and blunted insulin-mediated vasodilation caused by endothelial dysfunction. 17438881: Endothelial dysfunction is an important factor leading to atherosclerosis, hypertension and heart failure. 17569300: INTRODUCTION: It is generally thought that development of hypertension in preeclampsia (PE) is due to generalized endothelial dysfunction and/or results from an imbalance in the production and/or action of vasoactive factors, resulting in higher cytosolic Ca2+ concentration which in turn leads to vasoconstriction and decreased blood pressure perfusion in organs, including the fetoplacental unit. 17937587: These antiangiogenic factors produce systemic endothelial dysfunction, resulting in hypertension, proteinuria, and the other systemic manifestations of preeclampsia. 18520719: RECENT FINDINGS: Many of the cardiovascular complications associated with both aging and hypertension are attributable, in part, to endothelial dysfunction, particularly vasomotor dysregulation. 18823739: VED has been associated in the pathogenesis of hypertension, atherosclerosis, coronary artery diseases, diabetes mellitus and nephropathy. 18938721: Inflammatory status is involved in the pathophysiology of several cardiovascular disorders and in the genesis of high blood pressure. C reactive protein participates during inflammation activating the first component of complement with disorganization of the phospholipidic array of the endothelial sarcolemmal membrane and the consequent endothelial dysfunction related to the genesis of high blood pressure. 19304127: Endothelial dysfunction has been implicated as an important event in the pathogenesis of arteriosclerosis, coronary vasoconstriction, hypertension, and myocardial ischemia. 19770776: These data suggest that inflammation and endothelial dysfunction may play a role in the cause of hypertension. 20455988: INTRODUCTION: Atrial fibrillation (AF) has been shown to be associated with activation of the renin-angiotensin-aldosterone system, endothelial dysfunction, and increased sympathetic activity, all of which could lead to hypertension (HTN). 20885365: The results from animal studies and clinical observations support renal microvascular and tubulointerstitial injury being the key to uric acid-induced hypertension. The identification of conceivable biological mechanisms by which uric acid could cause high blood pressure has led to new insights about therapeutic modalities that may control high blood pressure and cardiovascular outcomes. Associations with other systemic derangements, including endothelial dysfunction, low-level systemic inflammation, sympathetic overactivity and insulin resistance, render uric acid to a complex but potentially direct causal role in the pathogenesis of hypertension. 21266263: These anti-angiogenic factors produce systemic endothelial dysfunction, resulting in hypertension, proteinuria, and the other systemic manifestations of preeclampsia. 21306413: Endothelial dysfunction plays a critical role in the development and progression or pathogenesis of hypertension. 21668772: OBJECTIVE: Pre-eclampsia is diagnosed by hypertension and proteinuria, probably caused by endothelial dysfunction, resulting in symptoms including oedema, inflammation and altered metabolism. 23024479: Conditions like hypertension, atherosclerosis and diabetes are known to be the result of endothelial dysfunction which could begin early in the life of an individual. 23220708: High systolic blood pressure caused by endothelial dysfunction is a comorbidity of metabolic syndrome that is mediated by local inflammatory signals. 23261267: INTRODUCTION: Pre-eclampsia is a serious complication of pregnancy, characterized by severe endothelial dysfunction resulting in hypertension, proteinuria and maternal end-organ damage. 23796541: BACKGROUND: The spectrum of cardiovascular toxicity by cyclosporine (CsA) includes hypertension, accelerated atherosclerosis, and thrombotic microangiopathy, all of which are the result of endothelial cell dysfunction. 24394658: Several cardiovascular risk factors including, hypercholesterolaemia and hypertension, lead to diseased blood vessels due to endothelial cell dysfunction. 24738065: This brief review was focused on the participation of endothelial dysfunction, individual endothelium-derived factors, and their mechanisms of action in the development of high BP in the most frequently used rodent experimental models of arterial hypertension, including nitric oxide deficient models, spontaneous (pre)hypertension, stress-induced hypertension, and selected pharmacological and diet-induced models. 24943896: Several of the other compounds can activate the Nrf2 signaling pathway that increases the expression of antioxidant enzymes, thereby decreasing oxidative stress and associated problems such as endothelial dysfunction that leads to hypertension as well as decreasing generalized inflammation that can lead to problems such as atherosclerosis. 25051774: The main pathogenetic mechanism is endothelial dysfunction, leading to hypertension, diabetes, congestive heart failure. 25547341: Endothelial dysfunction in humans attenuates activity-dependent vasodilation, resulting in exercise-induced hypertension in otherwise normotensive individuals. 26645289: Magnetic resonance tomography was employed to verify endothelial dysfunction of renal arteries in Wistar and OXYS rats under conditions of induced arterial hypertension. 27425399: In the vasculature, TRPV4 is a regulator of vessel tone and is implicated in hypertension and diabetes due to endothelial dysfunction. 27837398: PURPOSE OF REVIEW: Hypertension is either a cause or a consequence of the endothelial dysfunction and a major risk factor for cardiovascular disease (CVD). 27884224: This article updates recent literature with a focus on the function of insulin resistance, obesity, and renin angiotensin aldosterone system-mediated oxidative stress on endothelial dysfunction and the pathogenesis of hypertension. 29084442: Inflammation and endothelial dysfunction may play an important role in the multifactorial pathogenesis of hypertension. 29540166: BACKGROUND: Preeclampsia and gestational hypertensive disorders are thought to occur due to endothelial cell dysfunction and abnormal placentation, triggered by angiogenesis-related factors yet undetermined. 30075114: Endothelial cells play a key role in the regulation of blood pressure; however, a Mendelian form of hypertension that is primarily due to endothelial dysfunction has not yet been described. Insights obtained from the study of rare Mendelian forms of hypertension have been invaluable in elucidating the mechanisms causing primary hypertension and development of antihypertensive therapies. 30354446: Fibrosis is a common consequence of inflammation- and oxidative stress-related endothelial dysfunction in aging, hypertension, diabetes mellitus, obesity, ischemia, and organ injury. 31852420: Background The role of platelets in the development of vascular inflammation and endothelial dysfunction in the pathogenesis of hypertension is well established at this time. 31911124: In preeclampsia, endothelial dysfunction is a major contributor to aberrant gasotransmitter signaling, resulting in hypertension after 20 weeks gestation. 32010369: At present, it is widely used in dealing with hypertension due to endothelial dysfunction. 32149110: In cooperation, it contributes to chronic oxidative stress and endothelial dysfunction, which might lead to hypertension and atherosclerosis. 32294029: Oxidative stress is often associated with cardiovascular diseases and, when it affects vessels, it induces endothelial dysfunction, which, in turn, could precipitate atherosclerosis and hypertension. 33333432: It is characterized by imbalances in angiogenesis, inflammation and endothelial dysfunction which cause the development of hypertension and proteinuria, sometimes progressing into a multisystem disorder. 33433680: Two major obstetric diseases, preeclampsia (PE), a pregnancy-induced endothelial dysfunction leading to hypertension and proteinuria, and intra-uterine growth-restriction (IUGR), a failure of the fetus to acquire its normal growth, are generally triggered by placental dysfunction. 35665261: Mitochondrial dynamics and reactive oxygen species production have been associated with endothelial dysfunction, which in turn causes the development of atherosclerosis, hypertension, and even pulmonary hypertension, including pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. 35789679: Among the clinical consequences of endothelial dysfunction are arterial hypertension, macro- and microangiopathy, and microalbuminuria. 36409370: Hypertension remains the main cause of cardiovascular complications leading to increased mortality. Endothelial dysfunction as a factor leading to arterial hypertension. 37217298: Endothelial dysfunction can lead to hypertension by impairing vasodilatation and promoting vasoconstriction. 38039843: PE is a clinical syndrome characterized by hypertension secondary to systemic inflammation, endothelial dysfunction, and syncytiotrophoblast stress leading to hypertension and multiorgan dysfunction. 38146722: Our findings support previous research regarding the involvement of endothelial dysfunction and a higher sodium level in the pathogenesis of IDH. 9435319: The vascular pathophysiology of preeclampsia, a hypertensive disorder unique to human pregnancy, has been postulated to be due to endothelial dysfunction, primarily manifest as deficient nitric oxide (NO) synthesis. 9453325: In conclusion, endothelial dysfunction seems to be independent from the degree of vascular structural alterations and from the etiology of hypertension, and it is probably more linked to the hemodynamic load. 10024341: We investigated the involvement of actions mediated by endothelin-A (ETA) and endothelin-B (ETB) receptors in the pathogenesis of deoxycorticosterone acetate (DOCA)-salt-induced hypertension in rats. Different contributions of endothelin-A and endothelin-B receptors in the pathogenesis of deoxycorticosterone acetate-salt-induced hypertension in rats. 10684006: These results suggest that the increased ET and the change of NOS may play a role in the pathogenesis of hypertension and atherosclerosis. 12409981: Collectively, the results suggest that RAS plays a more important role than the endothelin system in the pathogenesis of arterial hypertension as well as left ventricular hypertrophy and fibrosis in GC-A gene-disrupted mice. 12514388: CONCLUSIONS: Long-term EPO treatment might have impaired flap survival because of direct or prostaglandin-mediated vasoconstriction, endothelin-induced hypertension, increased peripheral vascular resistance, hyperviscosity, and increased thrombosis. 12631344: Data also suggest that dysfunction of the renal ET system may be important in the pathogenesis of hypertension. 1455261: [Role of endothelin in the pathogenesis of rat experimental hypertension produced by aorta narrowing and saline uptake]. 14582451: Endothelins (ETs) are a family of potent peptidic vasoconstrictors that have been implicated in the pathogenesis of many cardiovascular disorders such as hypertension, myocardial infarction, congestive heart failure, atherosclerosis and restenosis. 15171363: [Involvement of endothelin in the pathogenesis of hypertension and hypertensive target-organ damage]. 15838279: Endothelin represents a necessary intermediate of angiotensin II-induced resistance artery remodeling in hypertension. 15879484: Concomitant antagonism of endothelial and vascular smooth muscle cell ETB receptors for endothelin induces hypertension in the hamster. 1592449: These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. Salt-dependency of endothelin-induced, chronic hypertension in conscious rats. 1592467: Captopril prevents chronic hypertension produced by infusion of endothelin-1 in rats. These results indicate that endothelin-induced hypertension may involve stimulation of the renin-angiotensin system but not an increase in circulating angiotensin II concentration. 16323976: Endothelin and reactive oxygen species have been identified as important mediators in the pathogenesis of hypertension and associated end-organ damage. 17200683: Although the effects of ET on vascular function and growth are well-recognized, the role of ET and its receptors in the regulation of blood pressure and in the pathogenesis of hypertension is not clearly established. 18056787: These findings provide support for roles for leptin and the ET system in the pathogenesis of obesity-associated hypertension. 18784261: CD-specific knockout (KO) of ET-1 causes hypertension, CD-specific KO of the ETA receptor does not alter BP, while CD-specific KO of the ETB receptor increases BP to a lesser extent than CD ET-1 KO. Combined knockout of collecting duct endothelin A and B receptors causes hypertension and sodium retention. 2174284: [Role of endothelin in the pathogenesis of experimental hypertension in rats]. 2190924: Chronic hypertension produced by infusion of endothelin in rats. These results indicate that elevated blood levels of endothelin could produce a maintained hypertension without sodium or water retention and that the hemodynamic basis for the increased mean arterial pressure is similar to that seen in most other forms of experimental and clinical hypertension. 23070275: This review will discuss what is currently known about the endothelin system, the role of ET-1 in the pathogenesis of hypertension and kidney disease, and summarize literature on the therapeutic potential of endothelin system antagonism. 24119223: Data from experimental studies support the hypothesis that exogenous administration of testosterone may induce the activation of the renin-angiotensin system (RAS), the production of endothelin and the regulation of anti- or/and proinflammatory cytokines involved in the pathogenesis of hypertension and kidney damage. 2508983: Intravenous administration of endothelin (0.03-0.3 nmol kg-1) resulted in a dose-dependent transient hypotension followed by a long-lasting hypertension and inhibition of platelet aggregation. 26598884: In addition, inappropriate suppression or activation of the renin angiotensin system (RAS) and/or activation of the sympathetic nervous system (SNS) leading to marked increases in oxidative stress and endothelin production are implicated in the etiology of hypertension that has its origins in fetal life. 2689821: Endothelin (5 nmol/kg, i.v.) caused a transient hypotension followed by a lasting hypertension in rats. 31326653: The Reduced Uterine Perfusion Pressure (RUPP) model results in hypertension and fetal growth restriction in a pregnant rat due to placental ischemia caused by mechanical obstruction of blood flow to uterus and placenta. We hypothesized that complement activation following placental ischemia stimulates the endothelin pathway to cause hypertension and impair fetal growth. 31593221: In this study, our aim was to determine the efficacy of selective ETA versus dual ETA/B receptor blockade for the prevention of angiogenesis inhibitor-induced hypertension and albuminuria. TRANSLATIONAL PERSPECTIVE: The endothelin (ET) system is implicated in the pathogenesis of angiogenesis inhibitor-induced hypertension and renal injury. Here we demonstrate that the development of angiogenesis inhibitor-induced hypertension and albuminuria is solely dependent on the ETA receptor and that an upregulation in PGI2 plays a previously unidentified role in the deleterious effects of angiogenesis inhibitors. 31809283: We found information regarding the role of the brain-gut--bone marrow axis, the brain-gut--kidney axis, the high-salt diet, short-chain fatty acids (SCFAs), neurotransitters, such as serotonin, dopamine and norepinephrine, nitric oxide, endothelin and steroids in modulating gut microbiota and in contributing to the pathogenesis of hypertension. 7509977: Chronic pathophysiologic circulating endothelin levels produce hypertension in conscious dogs. 7777724: The characterization of endothelin and the nitric oxide (NO)-arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. 9072354: These data showed that endothelins may not exert an important role on the pathogenesis of hypertension. 9690046: The endothelins are 21-amino-acid peptides which may play a role in the pathogenesis of hypertension. 9736265: A role for endothelin in the pathogenesis of hypertension: fact or fiction? 9883706: Cyclosporin-induced hypertension is a major complication of immunosuppression in transplant recipients but its pathophysiology is only partly understood. We examined the effects of: (1) nitric oxide enhancement with L-arginine administration and antagonism with N-nitro-L-arginine; and (2) chronic endothelin receptor blockade with the non-peptide endothelin receptor antagonist, bosentan, in two animal models of cyclosporin-induced hypertension. These results support the roles of both increased endothelin synthesis and decreased nitric oxide activity in the pathogenesis of cyclosporin A-induced hypertension. 10198379: The present data demonstrate that intracerebroventricular and intra-arterial administration of very low doses of ET-1 produces hypertension in conscious trout. 10499377: Cyclosporin A employed in treatment of organ allograft rejection, is associated with hypertension possibly due to endothelin-1. 10844136: Endothelin-1 has vasoconstrictor and mitogenic properties and may contribute to the pathogenesis of hypertension by enhancing vasoconstrictor mechanisms. 11078349: We suggest that the lower ET-1-induced hypertension and hindlimb vasoconstrictions observed in female rats may be responsible for the lower risk of developing coronary heart disease in premenopausal women. 11078355: Adenovirus gene transfer of endothelin-1 (ET-1) in rats causes a transient elevation of plasma ET-1 levels, leading to systemic hypertension. 11078375: In this study, we determined plasma ET-1 levels and the expression of ET-1 mRNA in tissues of rats rendered hypertensive using distinct mechanisms: deoxycorticosterone acetate (DOCA)-salt hypertension: N(G)-nitro-L-arginine-methyl ester- (L-NAME) induced hypertension; and spontaneously hypertensive rats (SHR-SP). Whether ET-1 could be a primary cause of hypertension or a secondary factor associated with hypertension, however, remains unknown. Recent studies revealed important roles for endothelin-1 (ET-1) in the pathogenesis of hypertension. 11206720: Even in group F60, ET-1-induced hypertension was blocked incompletely. 12193127: These results suggest that ET-1 and angiotensin-II are probably involved in the mechanism that leads to hypertension since the effect of these hormones is probably not compensated by kinins in B(2)KO mice. Mice with disruption of the kinin B(2) receptor (B(2)KO mice) are sensitive to salt-rich diets, which causes hypertension. 12352314: Pretreatment with FR-139317 inhibited the magnitude of ET-1-induced hypertension and increased the duration of the depressor action of ET-1. 12425483: BACKGROUND: Endothelin-1 (ET-1) is a strong vasoconstrictive peptide that is involved in the pathogenesis of arterial hypertension. 12574005: Enalapril attenuates endothelin-1-induced hypertension via increased kinin survival. 12605017: Relationship between eicosanoids and endothelin-1 in the pathogenesis of erythropoietin-induced hypertension in uremic rats. Recent studies suggest a possible link between recombinant human erythropoietin (rhEPO)-induced hypertension and endothelium-derived vasoconstrictor autocoids. These results suggest that endothelium-derived vasoconstrictor autacoids (TXA and ET-1) are involved in the pathogenesis of rhEPO-induced hypertension in uremic rats. The current study was designed to evaluate the role of eicosanoids such as thromboxane (TX) A and prostacyclin (PGI ) and of endothelin-1 (ET-1) and the relationship between these vasoactive substances in rhEPO-induced hypertension in uremic rats. 15302986: The combined effects of the elevations in circulating ET-1 and Ang II, as well as the associated ROS production, may contribute to the development of hypertension induced by chronic ET-1 infusion. The ET-1-induced hypertension was prevented by simultaneous treatment with a new AT1 receptor antagonist, olmesartan (0.01% in chow, 117+/-5 mmHg, n =7), or hydralazine (15 mg/kg/day in drinking water, 118+/-4 mmHg, n=6). 15314687: Collecting duct-specific knockout of endothelin-1 causes hypertension and sodium retention. 15471983: These results argue against the hypothesis that increased venomotor tone in DOCA-salt hypertension is caused by increased ET-1 concentration around splanchnic venous smooth muscle cells. 15738350: We reported previously that simulating sleep apnea in rats by exposing them 7 hours per day to intermittent hypoxia/hypercapnia (IH) elevates plasma endothelin-1 and causes hypertension, which is reversed by an endothelin-1 antagonist. Augmented endothelin vasoconstriction in intermittent hypoxia-induced hypertension. We hypothesized that in this model of sleep apnea-induced hypertension, vascular sensitivity to endothelin-1 is increased in combination with the elevated plasma endothelin-1 to cause the endothelin-1-dependent hypertension. 15928212: Collecting duct (CD)-specific knockout (KO) of endothelin-1 (ET-1) causes hypertension, impaired ability to excrete a Na load, and enhanced CD sensitivity to the hydrosmotic effects of vasopressin (AVP). 17028040: It has been hypothesized that the increased rate of production and/or release of ET-1 from the vascular endothelium may contribute to the pathogenesis of hypertension. 17130675: Our results indicated that endothelin-1 plays a key role in the FK506-induced change in vascular reactivity to noradrenaline in renal vascular beds and drug-induced hypertension in the rats. 1725422: This is the most likely cause of intracisternal ET-1-induced hypertension. Endothelin-1-induced hypertension: a consequence of medullary ischemia? 18516095: Renal collecting duct (CD)-specific knockout of endothelin-1 (ET-1) causes hypertension and impaired Na excretion. 18784261: CD-specific knockout (KO) of ET-1 causes hypertension, CD-specific KO of the ETA receptor does not alter BP, while CD-specific KO of the ETB receptor increases BP to a lesser extent than CD ET-1 KO. Combined knockout of collecting duct endothelin A and B receptors causes hypertension and sodium retention. 2069564: These data suggest that intracisternally administered big ET-1 is converted to ET-1 and that the generated ET-1 produces cerebral vasospasm and hypertension. 2139584: Infusion of endothelin-1 at the higher rate (120 pmol h-1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. 21818684: Endothelin-1 (ET-1) is produced in unusually large amounts by the renal collecting duct and acts locally to control renal salt and water excretion and arterial pressure; disorders of collecting duct ET-1 activity can cause marked hypertension. 21870722: CONCLUSIONS: Chronic exposure to complex stress conditions in rats with endothelin-1-induced hypertension determined a decrease of plasma cortisol levels, effect correlated with elevated blood pressure and decrease in the number and phagocytic function of peripheral neutrophils. AIM: to investigate the influence of some stress factors in endothelin-1-induced hypertension. 22046801: CONCLUSIONS: In this animal model of endothelin-1-induced hypertension the blood pressure increased significantly under chronic exposure to stress, reaching the highest values when associating stress and experimentally induced dyslipidemia. 22759779: CONCLUSIONS: Based on both in-vivo and in-vitro data, we have shown a potential causal association between Arg(972) IRS-1 and elevated plasma ET-1 level in hypertensives, which may account for the aggravated hypertension observed in hypertensives with heterozygous Arg(972) IRS-1. 23912930: Endothelin-1 (ET-1) is a potent vasoconstrictor that is implicated in the pathogenesis of hypertension, including the hypertension that is often associated with chronic kidney disease (CKD) and the metabolic syndrome. 29311252: Results are compatible with a significant role of reduced renal medullary NO bioavailability in VEGF inhibitor-induced hypertension. The present study was designed to test the hypothesis that VEGF receptor inhibitor treatment leads to hypertension through decreased renal medullary formation of NO and endothelin-1. In the renal medulla, inhibition of NO formation by local L-NAME or by impaired endothelin-1 leads to hypertension. 32337867: Research on (ET-1) has demonstrated that elevated ET-1 levels in autosomal dominant polycystic kidney disease leads to systemic hypertension. 32980622: 17-Hydroxyprogesterone caproate improves hypertension and renal endothelin-1 in response to sFlt-1 induced hypertension in pregnant rats. 34575135: The information presented includes basic concepts on the role of ET-1 in the pathogenesis of HTN without going into detailed analyses, which allows it to be used by a wide range of specialists. 7509986: Further study is required to elucidate whether this is entirely caused by a direct effect of ET-1 on smooth-muscle cell mitogenesis or is also by the hemodynamic effects of ET-1-induced hypertension, or an effect of another mediator released in response to the ET-1 (e.g., angiotensin II). 7721437: Indirect evidence has implicated endothelin-1 in the pathogenesis of hypertension. 8781542: These findings support a potential role for ET-1 in the pathogenesis of coronary atherosclerosis and hypertension evoked by TXA2. 9002526: Finally, impaired renal clearance of ET-1 may cause hypertension in patients with end-stage renal disease. 9403586: ET-1 produced a sustained hypertension and PD 155080 (56.4 micromol/kg [25mg/kg] BID PO) normalized blood pressure (BP) during the 5 days of drug administration. 9767170: Little is yet known, however, why deficiency of ET-1, which was originally found as a potent vasoconstrictor, led to higher AP in these mice. 10651647: Since SPs are composed predominantly of Abeta1-42, which is more amyloidogenic in vitro, the enzymes involved in generating Abeta1-42 may be particularly important to the pathogenesis of AD. 11032903: To define the enzymes involved in the etiology of Alzheimer's disease, we compared in mouse and human brain the mRNA levels and cellular localization of the ubiquitous beta-amyloid precursor protein (beta-APP) with those of the putative alpha-secretases ADAM10 and ADAM17 and the beta-secretases BACE and BACE2. 15275956: The PGF(2 alpha), an enzymatic product of arachidonic acid, may affect the pathogenesis of AD. 15665036: Each of the genotypes (Tg ABAD, Tg mAPP and Tg mAPP/ABAD mice, and non-TG littermates) displayed normal reproductive fitness, development and lifespan (1) These findings link ABAD-induced oxidant stress to critical aspects of Alzheimer's disease (AD)-associated cellular dysfunction, suggesting a pivotal role for this enzyme in the pathogenesis of AD. 15917100: Any change in the fine balance between these enzymes and their substrate may contribute to the etio-pathogenesis of AD. 18565755: In order to access beta-secretase (BACE1), and enzyme strongly implicated in the cause of Alzheimer's disease, inhibitors must possess sufficient lipophilicity to traverse two lipid bilayers. 19321181: Statins inhibit HMG-CoA reductase, the enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis thus inserting itself into the pathogenesis of AD. 19579178: This enzyme is pivotal in the generation of beta-amyloid (A beta), a neurotoxic endogenous peptide believed to be involved in the pathogenesis of Alzheimer's disease (AD). 20066010: Since these secretases mediate proteolytic processing of numerous proteins, little success has been achieved to treat AD by secretase inhibitors because of inevitable undesired side effects. Dysregulation of beta-site APP-cleaving enzyme (BACE) and/or gamma-secretase leads to anomalous production of amyloid-beta peptide (Abeta) and contributes to the etiology of Alzheimer's disease (AD). 23410524: In addition to MAO inhibition, PLZ also inhibits primary amine oxidase (PrAO), an enzyme implicated in the etiology of Alzheimer's disease, diabetes and cardiovascular disease. 26940238: The CYP17A1 gene encodes cytochrome P450c17alpha, an enzyme that catalyzes the formation of sex hormones, which have been linked to the pathogenesis of Alzheimer's disease (AD). 27784218: Uleine Disrupts Key Enzymatic and Non-Enzymatic Biomarkers that Leads to Alzheimer's Disease. 29303784: Acetylcholinesterase (AChE) is an enzyme that metabolises the ACh at synaptic cleft resulting in Alzheimer's disease. 29851073: ?-Secretase is the enzyme that generates various forms of A?, such as A?40 and A?42, the latter being an aggregation-prone toxic peptide that is involved in the pathogenesis of AD. 31353736: AChE is an important therapeutic target because excessive activity of this enzyme is a causative factor of neurodegenerative diseases such as dementia and Alzheimer's. 32239935: Compounds 1 - 9 were found to exhibit potent inhibitory activity in the 1.0 * 10 -3 to 2.2 MUM range against acetylcholinesterase, an enzyme directly involved in the etiology of Alzheimer's disease and senile dementia. 34263703: The molecular docking analysis reveals that the studied molecule under interest can act as a potent inhibitor against the amyloid beta-protein (Abeta) enzyme, which causes the Alzheimer's disease. 35013923: In Silico Molecular Docking Approach Against Enzymes Causing Alzheimer's Disease Using Borassus flabellifer Linn. 37148523: Since the activity of dopamine b hydroxylase (DbetaH) is reduced in the hippocampus and neocortex in the brain, changes in the physiological status of dopamine have been reported in Alzheimer's disease (AD) induced by this enzyme. 1033105: 2) TLP-607 slightly hypertension induced by dopamine, adrenaline and noradrenaline, but had no effect on hypotension induced by acetylcholine and histamine. 10957659: Of the 13 nonsurvival cases, maximal epinephrine-induced hypertension sustained over 15 minutes (peak systolic blood pressure > 210-250 mm Hg) was tolerated without leakage in a subgroup of five animals (100%). 11069044: Mean values for Evans-blue dye were found to be 0.28 +/- 0.04 microg/g tissue in control animals and 1.0 +/- 0.2 microg tissue after adrenaline-induced acute hypertension (p < .01). Influence of antioxidants on blood-brain barrier permeability during adrenaline-induced hypertension. The rats supplemented with nontoxic doses of sodium selenite in drinking water for three months or vitamin E was given intraperitoneally before adrenaline-induced acute hypertension. The results show that antioxidants did not influence the blood-brain barrier breakdown during adrenaline-induced acute hypertension. 11097543: In contrast, epinephrine produced severe hypertension and tachycardia. 11375836: Epinephrine in concentrations of 1:100,000 and 1:200,000 causes significant hypertension. 11529687: The interrelationship between the breakdown of the blood-brain barrier according to the Evans-blue passage and an abrupt increase in blood pressure (DeltaP) was studied in rats subjected to adrenaline-induced acute hypertension and also pentylenetetrazol-induced seizures. 11983199: Acute adrenaline induced hypertension in diabetes leads to a significant decrease of NOx concentrations in comparison with the controls, adrenaline-only administered and STZ-only administered rats. AIM: To examine the plasma nitrate/nitrite (NOx-two end products of the nitric oxide metabolism) and endothelin (ET) concentrations, and response to acute adrenaline induced hypertension in diabetic rats. 12487093: Adrenaline-induced hypertension was used to destroy the BBB, which was evaluated using triphenyltetrazolium (TTC) staining of the brain slices just after giving adrenaline for 30 s. 12879669: Over a specific dose range, systemic hypertension induced by adrenaline, noradrenaline and dopamine did not significantly increase cerebral blood flow under 2% isoflurane anaesthesia. 1309718: Experimental data support four important concepts: 1) epinephrine stimulates prejunctional beta 2-adrenergic receptors that facilitate norepinephrine release from sympathetic nerve endings; 2) epinephrine can be converted into a cotransmitter by neuronal uptake and on subsequent release augment the simultaneous discharge of norepinephrine; 3) exogenous epinephrine can induce sustained hypertension in rats; and 4) there is a period of critical sensitivity to endogenous epinephrine in a genetic model of rat hypertension. 13317317: [Demonstration of the difference of mechanism of hypertension produced by carotid occlusion and of hypertension produced by adrenalin injection]. 13404042: [Effects of heparin on the velocity of circulation and on hypertension produced by adrenalin and noradrenalin]. 14561528: Our previous publication has stressed the benefits of losartan, an angiotensin II receptor blocker, on the permeability of blood-brain barrier (BBB) and blood pressure during L-NAME-induced hypertension. Epinephrine-induced acute hypertension in diabetic hypertensive rats increased the content of EB dye dramatically in cerebellum and diencephalon (p < 0.01) and slightly in both cerebral cortex (p < 0.05). 14967192: Surgical pain stress increased blood-brain barrier permeabiliy in comparison to acute adrenalin-induced hypertension (p < 0.01). 1513750: Our results showed that the extravasation of Evans blue albumin was most pronounced in the brains of hypothermic rats compared to normothermic rats after adrenaline-induced acute hypertension. During adrenaline-induced acute hypertension the mean arterial blood pressure increased in both normothermic and hypothermic animals. Blood-brain barrier lesions were present in 40% of normothermic rats, and 60% of hypothermic rats after adrenaline-induced hypertension. Mean value for Evans blue dye in the whole brain was found to be 0.530 +/- 0.202 mg% in the normothermic rats and 0.752 +/- 0.256 mg% in the hypothermic rats during adrenaline-induced hypertension. 15195355: We tested the effect of nifedipine, a calcium entry blocker, on the cerebrovascular permeability for proteins in adrenalin-induced acute hypertension. Protection of blood-brain barrier breakdown by nifedipine in adrenaline-induced acute hypertension. 1526884: The rate of TMPA entry into perilymph was increased by epinephrine-induced hypertension or by simultaneous administration of histamine and prostaglandin E2. 1973355: Acute hypertension was induced using infusions of epinephrine during the control period and later propranolol (1.5 mg/kg) plus atropine (0.2 mg/kg). Effects of muscarinic and beta-adrenergic blockade on the aortic elastic response to epinephrine induced acute hypertension in conscious dogs. 1983053: By subcutaneous insertion of osmotic minipumps leading to continuous infusion of l-adrenaline, we were able to induce hypertension in normotensive Wistar-Kyoto strain (WKY) rats which was shown to be completely reversible by application of the non-selective beta-adrenoceptor antagonist carvedilol. 20850911: Compounds 18, 20 and 21 were found to possess a high hypotensive effect through their expected alpha(1)-blocking activity like the clinically used drug prazosin but with advantageous of being did not cause reflex tachycardia and having prolonged duration of action when tested in adrenaline-induced hypertension in anaesthetized rats. 21286460: We have experienced epinephrine-induced cardiovascular crisis, with severe hypertension, tachycardia, and cardiac arrest after subcutaneous infiltration of a 2% lidocaine and 1 : 200,000 epinephrine solution in a patient with an asymptomatic subarachnoid hemorrhage. 22557134: An experimental evaluation of the effect of rudraksha (elaeocarpus ganitrus roxb) in adrenaline and nicotine induced hypertension. Elaeocarpus ganitrus (Roxb) reduces adrenaline induced hypertension and also normal blood pressure; but it is not effective in nicotine induced hypertension. 23785438: These tumors release excessive epinephrine and norepinephrine resulting in hypertension and cardiovascular crises for which surgery is the only definitive treatment. 23977929: Arterial injection of adrenaline causing severe hypertension during emergency gastroscopy. 25013797: Compounds 7-Chloro-3-(4-(3-(4-chlorophenyl)-4,5- dihydroisoxazol-5-yl)phenyl)-2-p-tolylquinazolin-4(3H)-one (23) and 7-Chloro-3-(4-(3-(4-chlorophenyl)-4,5-dihydroisoxazol-5-yl)phenyl)-2-(4-methoxyphenyl)quinazolin-4(3H)-one (24) exhibited potent antihypertensive activity through their anticipated alpha 1-adrenergic receptor blocking property similar to its clinically used analogue, prazosin, without affecting heart rate with prolonged duration of action when tested in adrenaline induced hypertension in anaesthetized rats. 25517550: Furthermore, in the chlorpromazine and propranolol-pretreated rats, modest hypertension was induced by adrenaline, but hypotension and tachycardia were not significantly shown. 2801151: Regional cerebral blood flow in acute hypertension induced by adrenaline, noradrenaline and phenylephrine in the conscious rat. 2873235: Treatment with epinephrine resulted in hypertension. 2922776: After a mild injury, induced moderate hypertension (121-140 mm Hg) improved spinal cord blood flow significantly, whereas hypotension decreased it in a linear fashion. Even extreme hypertension (161-180 mm Hg) induced by adrenaline did not significantly increase spinal cord blood flow at T1 but caused hyperemia at C6 due to loss of autoregulation. 3227933: Because chronic infusions of adrenalin (A) produce hypertension in rats, it has been suggested that A is a mediator of stress-induced hypertension. 3380853: The results shown that chronic alcohol protects the blood brain barrier permeability against hypertension due to adrenalin. 3414376: To determine whether such temporary exposure of the brain parenchyma to plasma constituents may lead to permanent morphological alterations, acute hypertension was induced by i.v. adrenaline in conscious rates given Evan's blue and horseradish peroxidase as tracers. Adrenaline-induced hypertension: morphological consequences of the blood-brain barrier disturbance. 3963479: Local anesthetic solutions containing epinephrine produce tachycardia and hypertension when given intravenously and may identify intravenous placement. 4056685: Atropine treatment in vivo revealed vagal cardio-inhibitory tone in some animals and always blocked the reflex bradycardia seen during adrenaline induced hypertension. 4222921: [Action of calcium ions on adrenalin-induced arterial hypertension in rats]. 43064: Acute hypertension was induced by adrenaline, noradrenaline or angiotensin in awake unrestrained rats with chronic indwelling catheters in a jugular vein and in the aorta. Blood-brain barrier to albumin in awake rats in acute hypertension induced by adrenaline, noradrenaline or angiotensin. 43065: Rats, neonatally sympathectomized by 6-hydroxydopamine, had significantly increased extravasation of 125I serum albumin in the brain after adrenaline-induced hypertension than nonsympathectomized rats. 5509006: [Determination of adrenaline and noradrenaline in the urine of patients suffering from hypertension with special reference to the genesis of hypertension]. 5914258: Their discharge was inhibited during hypertension caused by injections of adrenaline and during inflation of the lungs, but was increased during tracheal occlusion, stimulation of peripheral chemoreceptors and irritation of the larynx. They were activated during hypertension due to adrenaline and often by tracheal occlusion, chemoreceptor stimulation, laryngeal irritation and lung inflation. 5975131: [The antagonistic action of lactic acid on adrenalin and noradrenalin-induced hypertension]. 6111172: Rats were subjected to adrenaline-induced acute hypertension during either the day or night. The blood-brain barrier in adrenaline-induced hypertension. 6121402: The phenothiazine dixyrazine (5 mg . kg-1 i.v.) had minimal, transient hypotensive effects but significantly reduced the leakage of 125I labelled serum albumin in conscious rats subjected to acute hypertension provoked by i.v. adrenaline or bicuculline. 6138461: Both alpha 1- and alpha 2-adrenoceptor blocking agent also significantly inhibited the hypertension induced by noradrenaline. This hypertensive effect was suppressed by an alpha 2-adrenoceptor blocking agent when an alpha 1-adrenoceptor blocking was responsible for the reversal of adrenaline-induced hypertension, and conversely. In fact, only a significant decrease of the noradrenaline-induced hypertension was observed after each alpha-blocker. In anaesthetized dog, the adrenaline induced hypertension is reversed by both alpha 1- and alpha 2-adrenoceptor blocking agents such as AR-C 239 and yohimbine. 6160347: Adrenaline-induced hypertension in rats. 6167799: Nicergoline slightly attenuated the pressor responses of dogs to noradrenaline and tyramine and, in addition, reversed the hypertension induced by adrenaline and dimethylphenylpiperazinium. 6499237: Adrenaline was infused intravenously into conscious dogs to test whether chronically elevated plasma levels can produce arterial hypertension. These results are therefore not in accord with the hypothesis that increased plasma levels of adrenaline may cause hypertension by activation of pre-junctional beta-adrenoceptors. 6693517: Interrelationship between the breakdown of the blood-brain barrier (BBB) to Evans blue and elevations in the regional cerebral blood flow (rCBF) was studied in rabbits subjected to adrenaline- or metaraminol-induced systemic hypertension and also in bicuculline-induced seizures. 6747660: In rabbits subjected to bicuculline (BC)- or pentylenetetrazole (PTZ)-seizures of 3 or 20 min duration or to adrenaline-induced hypertension, specific gravity (SG) was measured bilaterally in 15 regional brain areas in order to detect possible associations between the regionally limited blood-brain barrier openings due to these insults (see Nitsch and Klatzo 1983) and the presence of brain edema. 7318322: Adrenaline-induced hypertension in rats. 7376807: Acute hypertension was induced by adrenaline or bicuculline in rats mechanically ventilated with 70% nitrous oxide in oxygen, in unrestrained rats breathing the same gas mixture, and in conscious unrestrained rats breathing air. 7440898: This suppression of adrenal nerve activity preceded the hypertension induced by epinephrine. 7783978: During adrenaline-induced acute arterial hypertension the mean arterial blood pressure increased in both non-diabetic and diabetic animals. From these results it was suggested that the extravasation of Evans blue albumin is more pronounced in the brains of diabetic rats in comparison with non-diabetic rats after adrenaline-induced acute hypertension, which is indicative of changes in BBB permeability due to diabetes mellitus. Changes in BBB permeability were observed in 52% of the non-diabetic rats, and in 72% of the diabetic rats after adrenaline-induced acute arterial hypertension. 7802751: Inadvertent epinephrine injection induced ventricular dysrhythmias, hypertension, hypotension and pulmonary oedema. 8109997: During epinephrine-induced hypertension, there were major pressure drops between a4 and a3, and between a3 and a2. Under angiotensin II (A II)-induced hypertension, the pressure of all arteriolar vessels increased roughly in proportion to the increase in mean arterial blood pressure. 8221694: Arteriolar pressure in each segment both under normotension and under hypertension induced by angiotensin II, epinephrine, or methoxamine was measured using a microocclusion technique. 8252896: MEASUREMENTS AND MAIN RESULTS: Epinephrine administered during uncompromised hemodynamics led to hypertension, bradycardia, and decreased cardiac output that were unaffected by arterial pH values between 6.9 and 7.6. 8577804: 2 mg% in the normothermic rats and 0.40 +/- 0.2 mg% in the mild hyperthermic rats during adrenaline-induced hypertension (p < 0.05). During adrenaline-induced acute hypertension the mean arterial blood pressure increased in both normothermic and mild hyperthermic animals. Our results show that the extravasation of Evans blue albumin was less pronounced in the brains of mild hyperthermic rats compared to normothermic rats after adrenaline-induced acute hypertension. 8867715: Although high dose epinephrine treatment led to a significantly higher blood pressure during early reperfusion, rapidly changing heterogeneities of early brain recovery were observed in both groups. 8874308: High-dose epinephrine resulted in severe tachycardia and hypertension immediately after resuscitation and in a higher mortality rate immediately after resuscitation. 9187777: PURPOSE: Detection of intravascular injection of local anaesthetic during placement of regional blocks in children by using epinephrine-induced tachycardia or hypertension may produce false positive and false negative findings. 10146863: Depletion of iron stores, hypertension, increased blood coagulability and reduced dialyser efficiency resulting from epoetin treatment may all add a small additional component to the true cost. 10213636: Mechanism of erythropoietin-induced hypertension. Several mechanisms have been considered in the pathogenesis of EPO-induced hypertension. 11028413: [Erythropoietin-induced hypertension]. 11590249: Many potential reasons for erythropoietin-induced hypertension in uraemic patients have been postulated, including increased blood viscosity as haematocrit rises, a reversal of hypoxic vasodilatation, increased blood volume that is not compensated by haemodialysis, ultrafiltration and impaired nitric oxide synthesis, preventing vascular relaxation in response to increased blood viscosity. 11675943: Variables estimated to be associated with Epo-induced hypertension were the T allele, gender (male), and the degree of increase in Ht, in descending order. These results suggest that the AGT T235 variant may be the primary gene responsible for the development of Epo-induced hypertension. The association of the angiotensinogen (AGT) gene variation at codon 235, the T235 variant, with hypertension induced by erythropoietin (Epo) was investigated in patients with progressive renal disease requiring treatment for renal anemia with Epo. 11702579: 4--Neuroendocrine activation, including the sympathetic nervous system, renin-angiotensin-aldosterone system, atrial natriuretic peptide and erythropoietin, which may result in nycturia, nocturnal hypotension and diurnal hypertension. 1325627: Serotonergic mechanism of erythropoietin-induced hypertension. 17022600: [Erythropoietin-induced hypertension]. 19218474: The possible mechanisms of Epo-induced hypertension are examined with in vivo animal and in vitro data, as well as pathophysiological human studies in both normal subjects and CKD patients. Arterial hypertension induced by erythropoietin and erythropoiesis-stimulating agents (ESA). 29228345: Mechanisms and mediators of hypertension induced by erythropoietin and related molecules. Animal studies show the primary importance of chronic kidney disease in the genesis of EPO-induced hypertension. EPO-induced hypertension, at least in part, appears to be independent of an increase in hemoglobin, because experiments show that hemoglobin may be increased by EPO without an increase in blood pressure (BP) by simply treating the animals with EPO-binding protein and that treatment with EPO in the setting of iron deficiency may not increase hemoglobin but may still increase BP. Preclinical studies show deranged regulation of the nitric oxide, endothelins and porstanoids and the sympathoadrenal and renin-angiotensin pathways as causes of EPO-induced hypertension. Human studies suggest that EPO administration is also associated with increased responsiveness to catecholamines and angiotensin II on vascular tissue; in addition, hypoxia-induced vasodilation may be impaired in those with EPO-induced hypertension. However, experimental data are not consistent across studies and better mechanistic designs are needed, especially in patients with chronic kidney disease, to dissect the precise mechanism of EPO-induced hypertension. The purpose and focus of this review is to critically evaluate the mechanisms of EPO-induced hypertension. 33628672: We have explored the pathogenesis of erythropoietin-induced hypertension and discussed some ways to prevent and treat this condition. Also, an attempt has been made to find out the role of blood viscosity in erythropoietin-induced hypertension. Erythropoietin-Induced Hypertension: A Review of Pathogenesis, Treatment, and Role of Blood Viscosity. We mainly studied clinical trials that unraveled the mechanism of hypertension caused by erythropoietin. 7740514: It is concluded that serotonin may play a role in the development of hypertension caused by rHuEPO. The aim of this study was to investigate the mechanism of erythropoietin-induced hypertension in respect to its action on blood serotonergic system. 8252582: CONCLUSIONS: One mechanism of erythropoietin induced hypertension may be an increase in [Ca2+]i in vascular smooth muscle cells. 8290018: Is the intracellular calcium-mediated pathway involved in erythropoietin-induced hypertension? 8302467: Erythropoietin-induced hypertension without raising haematocrit. 8559495: BACKGROUND: In a retrospective study, antiplatelet therapy has been shown to be associated with a decreased incidence of erythropoietin-induced hypertension. 8575115: Uraemia is necessary for erythropoietin-induced hypertension in rats. 8677211: [Arterial hypertension induced by erythropoietin]. 8967402: In this study, to reveal the mechanism of EPO-induced hypertension, we examined the acute effect of EPO on blood pressure (BP) and renal hemodynamics in genetically hypertensive rats, and we also tested the effect of BQ-123, an endothelin ETA-receptor blocker, on EPO-induced changes in hemodynamics. Erythropoietin (EPO) has been reported to induce hypertension in hemodialysis patients with family history of hypertension. 9421942: Erythropoietin-induced hypertension. 9774370: We recently demonstrated that EPO-induced hypertension is hematocrit independent and accompanied by elevated cytosolic [Ca2+]i and nitric oxide (NO) resistance. Concurrent administration of felodipine abrogated EPO-induced hypertension, normalized resting and stimulated [Ca2+]i, and increased NOx excretion and eNOS and iNOS proteins. Nitric oxide metabolism in erythropoietin-induced hypertension: effect of calcium channel blockade. Long-term administration of erythropoietin (EPO) frequently causes hypertension in humans and animals with chronic renal failure (CRF). 10082505: We have recently shown that erythropoietin (EPO)-induced hypertension is unrelated to the rise in hematocrit and is marked by elevated cytosolic [Ca+2] and nitric oxide (NO) resistance. 10213636: Mechanism of erythropoietin-induced hypertension. Several mechanisms have been considered in the pathogenesis of EPO-induced hypertension. 10225477: Patients were divided into two groups, one of which received antiplatelet therapy and the other did not, and a comparison was made between them with respect to the incidence of EPO-induced hypertension. 10803695: We investigated to see whether an altered role of nitric oxide (NO) system is involved in erythropoietin (EPO)-induced hypertension in chronic renal failure (CRF). 11016796: There was no difference in the rate of Ht increase between patients with and without Epo-induced hypertension. The objective of the present study was to investigate whether circulating AM is involved in erythropoietin (Epo)-induced hypertension in patients with renal anemia due to progressive renal disease. It is too early yet to claim that there is no AM-mediated mechanism in Epo-induced hypertension. However, the present study does not support the notion that circulating AM is associated with the pathogenesis of Epo-induced hypertension. In response to treatment with Epo, a rise in mean blood pressure of >10 mmHg (Epo-induced hypertension) was found in 22% (12/54 cases) of the patients enrolled. 11313825: Moreover, the uremic rats showed Epo-induced hypertension, which is the major side-effect of recombinant human Epo. 11496057: Contrary to the original view, erythropoietin-induced hypertension is not due to amelioration of anemia, because a similar rise in blood pressure occurs, despite persistent anemia, in erythropoietin-treated iron-deficient animals and humans. 11675943: Variables estimated to be associated with Epo-induced hypertension were the T allele, gender (male), and the degree of increase in Ht, in descending order. These results suggest that the AGT T235 variant may be the primary gene responsible for the development of Epo-induced hypertension. The association of the angiotensinogen (AGT) gene variation at codon 235, the T235 variant, with hypertension induced by erythropoietin (Epo) was investigated in patients with progressive renal disease requiring treatment for renal anemia with Epo. 12558321: However, the mechanism of the r-HuEPO induced hypertension has not been fully elucidated. The results suggest that an inhibitory effect of r-HuEPO on NO production might be, at least in part, related to the r-HuEPO induced hypertension in this case. We report a case of r-HuEPO induced hypertension in an anephric patient. It is well known that chronic administration of r-HuEPO often causes hypertension in dialysis patients. A case of erythropoietin induced hypertension in a bilaterally nephrectomized patient. 12911161: Increased endothelin: nitric oxide ratio is associated with erythropoietin-induced hypertension in hemodialysis patients. These results suggest that an increase in ET-1/NOx ratio in blood, probably occurring in vascular endothelial cells, may be associated with rHuEPO-induced hypertension in HD patients. 16049546: Cyclooxygenase inhibition with acetylsalicylic acid unmasks a role for prostacyclin in erythropoietin-induced hypertension in uremic rats. We previously reported that thromboxane (TX)A2 synthesis and receptor blockade prevented recombinant human erythropoietin (rhEPO)-induced hypertension in chronic renal failure rats. Cyclooxygenase inhibition had no effect on rhEPO-induced hypertension owing, in part, to simultaneous inhibition of both TXA2 and its vasodilatory counterpart PGI2 synthesis, whereas the vascular ET-1 overproduction was maintained. 17385001: In this context, the present study addressed whether or not HBP measured in the morning could be useful to predict EPO-induced hypertension. Most studies regarding EPO-induced hypertension have involved evaluation using office/clinic BP (OBP). The development of EPO-induced hypertension was effectively predicted by HBP in the morning (from 62% to 72% before and after EPO treatment; P = 0.0031 by Wilcoxon's analysis), but not by OBP (from 42% to 47% before and after treatment; P = 0.1399). BACKGROUND: Correction of anemia by erythropoietin (EPO) is often associated with a rise in blood pressure (BP; EPO-induced hypertension). 17548719: Can Epo-induced hypertension be eliminated? Thus, Epo-bp and anti-Epo-bp antibodies eliminate Epo-induced hypertension without affecting hematocrit and blood volume. 1794212: To investigate the mechanisms of hypertension induced by recombinant human erythropoietin (rHuEPO) in patients on hemodialysis (HD), mean blood pressure (MBP), plasma renin activity (PRA), whole blood viscosity, blood volume (BV), cardiac index (CI) and total peripheral resistance index (TPRI) were measured before and after treatment with rHuEPO for 3 months in 9 patients on HD. Mechanisms of hypertension induced by erythropoietin in patients on hemodialysis. 18506108: However, since CCB use was strongly associated not only with rHuEPO dose but also with systolic blood pressure and the use of alpha-blockers and ARB, these findings might be caused by erythropoietin (EPO)-induced hypertension. 19218474: The possible mechanisms of Epo-induced hypertension are examined with in vivo animal and in vitro data, as well as pathophysiological human studies in both normal subjects and CKD patients. Arterial hypertension induced by erythropoietin and erythropoiesis-stimulating agents (ESA). 19458615: Endothelial nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) contribute to erythropoietin (EPO)-induced hypertension, a major adverse reaction associated with EPO therapy. Hypertension induced by erythropoietin has a correlation with truncated erythropoietin receptor mRNA in endothelial progenitor cells of hemodialysis patients. To investigate the mechanism of EPO-induced hypertension, we examined circulating endothelial progenitor cells (EPCs) taken from 56 hemodialysis (HD) patients. A truncated form of EPOR acts as a dominant negative regulator of EPO signaling, leading to hypertension. 21690481: The underlying mechanisms of EPO-induced hypertension still remain to be determined. 24463938: Erythropoietin-induced hypertension and vascular injury in mice overexpressing human endothelin-1: exercise attenuated hypertension, oxidative stress, inflammation and immune response. 27667620: Venesection for epo- induced hypertension. 29228345: Mechanisms and mediators of hypertension induced by erythropoietin and related molecules. Animal studies show the primary importance of chronic kidney disease in the genesis of EPO-induced hypertension. EPO-induced hypertension, at least in part, appears to be independent of an increase in hemoglobin, because experiments show that hemoglobin may be increased by EPO without an increase in blood pressure (BP) by simply treating the animals with EPO-binding protein and that treatment with EPO in the setting of iron deficiency may not increase hemoglobin but may still increase BP. Preclinical studies show deranged regulation of the nitric oxide, endothelins and porstanoids and the sympathoadrenal and renin-angiotensin pathways as causes of EPO-induced hypertension. Human studies suggest that EPO administration is also associated with increased responsiveness to catecholamines and angiotensin II on vascular tissue; in addition, hypoxia-induced vasodilation may be impaired in those with EPO-induced hypertension. However, experimental data are not consistent across studies and better mechanistic designs are needed, especially in patients with chronic kidney disease, to dissect the precise mechanism of EPO-induced hypertension. The purpose and focus of this review is to critically evaluate the mechanisms of EPO-induced hypertension. 7618043: Improvement of erythropoietin-induced hypertension in hemodialysis patients changing the administration route. 7652230: Erythropoietin-induced hypertension is easily controlled by drugs, but also by low dose of erythropoietin. Pathogenesis of erythropoietin-induced hypertension is ill known. Subcutaneous administration of erythropoietin is an approach to avoid the induction of hypertension. 8077802: Is erythropoietin-induced hypertension a phenomenon due to the intracellular Ca++ mobilisation? 8377279: [Effect of human recombinant erythropoietin (Epo) on cellular Ca2+, Na+, and K+ regulation of vascular smooth muscle cells grown in vitro--a new insight into the pathogenesis of Epo induced hypertension]. 8507814: Erythropoietin (EPO)-induced hypertension is a common complication of EPO usage. 8556836: Changes in diurnal blood pressure variation and red cell and plasma volumes in patients with renal failure who develop erythropoietin-induced hypertension. RCV did not differ between the patient group developing EPO-induced hypertension (EpHT, n = 11) and the group with no change in BP (NC, n = 13) either before or after treatment. These results suggest that EPO-induced hypertension is associated with increased daytime vasoconstriction and greater hemoconcentration due to lower plasma volume. 8731114: Given the transient nature of the rise in its plasma concentration, endogenous EPO does not appear to play a role in the genesis of the observed systemic HTN. Sustained systemic arterial hypertension induced by extended hypobaric hypoxia. Thus, prolonged hypobaric hypoxia leads to a severe hematocrit-independent systemic hypertension (HTN) that persists long after the restoration of normoxia. 8735172: Evidence for the involvement of endothelial cells in the pathogenesis or erythropoietin-induced hypertension, and for endothelial cell damage in patients with chronic renal failure, has emerged and appears to be of major concern. 8760088: We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO. 8773347: The mechanism of erythropoietin-induced hypertension in dialysis patients is unclear. 8788598: Erythropoietin (rHuEPO)-induced hypertension represents a clinical problem in hemodialysis units. 8967402: In this study, to reveal the mechanism of EPO-induced hypertension, we examined the acute effect of EPO on blood pressure (BP) and renal hemodynamics in genetically hypertensive rats, and we also tested the effect of BQ-123, an endothelin ETA-receptor blocker, on EPO-induced changes in hemodynamics. Erythropoietin (EPO) has been reported to induce hypertension in hemodialysis patients with family history of hypertension. 9056686: The mechanisms, however, by which EPO may cause hypertension are still unclear. 9113497: To assess the role of altered cellular calcium metabolism, resting platelet cytosolic calcium was measured in 12 previously normotensive patients with end-stage renal disease before and after 12 weeks of EPO-therapy, after 12 weeks of combined antihypertensive pharmacotherapy of EPO-induced hypertension, and after 12 weeks of concurrent administration of EPO and indomethacin. The results of the present study suggest that EPO-induced hypertension might be related to altered cellular calcium homeostasis. Antihypertensive therapy of EPO-induced hypertension resulted in a reduction of blood pressure and a reduction of platelet calcium to near normal levels (128 +/- 6 nmol/l). Hypertension induced by recombinant human erythropoietin (rHU-EPO) can be prevented by indomethacin. Patients with EPO-induced hypertension showed a significant raise in platelet calcium by comparison with calcium levels prior to EPO (179 +/- 15 vs 120 +/- 8 nmol/l), and there was a positive correlation between their blood pressure and platelet calcium levels (r = 0.9, p < 0.001). 9189856: This observation suggests that EPO-induced hypertension in this model is not mediated by an increased circulating ET level. Erythropoietin-induced hypertension in rat is not mediated by alterations of plasma endothelin, vasopressin, or atrial natriuretic peptide levels. Clinical studies intended to discern the possible role of endothelin (ET) in the pathogenesis of EPO-induced hypertension have produced contradictory results. 9305323: Erythropoietin causes hypertension, and hypertensive encephalopathy has been associated with its use. 9774370: We recently demonstrated that EPO-induced hypertension is hematocrit independent and accompanied by elevated cytosolic [Ca2+]i and nitric oxide (NO) resistance. Concurrent administration of felodipine abrogated EPO-induced hypertension, normalized resting and stimulated [Ca2+]i, and increased NOx excretion and eNOS and iNOS proteins. Nitric oxide metabolism in erythropoietin-induced hypertension: effect of calcium channel blockade. Long-term administration of erythropoietin (EPO) frequently causes hypertension in humans and animals with chronic renal failure (CRF). 10028946: Essential hypertension and congestive heart failure (CHF) are examples of cardiovascular disorders that may cause renal failure, although sometimes a primary kidney defect may lead to hypertension. 1005044: Repeated hypertensive pregnancies after eclampsia are often a sign of latent essential hypertension and may precipitate prematurely a chronic hypertension that is in the making. 11391990: It is well known that the pathogenesis of essential hypertension is multi-factorial, and that the environmental and genetic factors and their interaction play important roles on pathogenesis of hypertension. 15010711: It also concentrates on essential hypertension and does not deal with the diagnosis and management of secondary causes of hypertension. 24522943: In contrast to adults, where acute HTN is most likely due to uncontrolled primary HTN, children and adolescents with acute HTN are more likely to have secondary HTN. 25621304: Five themes emerged: 1) Accuracy of blood pressure measurement and hypertension diagnosis, 2) Shift in the epidemiology of pediatric hypertension from secondary to primary hypertension, 3) Patient characteristics considered in the decision to initiate workup, 4) Obesity-centered choice of diagnostic tests and lifestyle modifications, and 5) Variable threshold for initiating antihypertensive pharmacotherapy vs. referral to hypertension specialists. 30277729: Primary hypertension is now the most common cause of hypertension in children and adolescents. 32336227: Metabolites and Hypertension: Insights into Hypertension as a Metabolic Disorder: 2019 Harriet Dustan Award.For over 100 years, essential hypertension has been researched from different perspectives ranging from genetics, physiology, and immunology to more recent ones encompassing microbiology (microbiota) as a previously underappreciated field of study contributing to the cause of hypertension. 32880744: Extracellular Vesicles in Essential Hypertension: Hidden Messengers.PURPOSE OF REVIEW: Hypertension affects about half of all Americans, yet in the vast majority of cases, the factors causing the hypertension cannot be clearly delineated. 34342483: Most cases of hypertension are because of essential hypertension, however 5% - 15% of cases can be a result of a secondary cause. 3551600: Although there is much circumstantial and some direct clinical evidence suggesting that a high consumption of salt predisposes patients to the development of essential hypertension, the mechanism by which such consumption causes high blood pressure is not clear. 36374635: Primary HTN is now the predominant cause of HTN among the pediatric population in the United States, especially among adolescents. 38572182: Pheochromocytoma and paraganglioma (PPGL) are chromaffin cell tumors that produce, store, and secrete catecholamines, leading to HT and other adrenergic manifestations. Even though primary HT, obesity, and preeclampsia are the main causes of HT in this period, other less familiar conditions must be considered during the investigation. 6184557: Thus, we propose the membrane theory of essential hypertension--that membrane abnormalities lead to hypertension. 7496558: This review identifies some of the changes in platelet structure and function in essential hypertension and their role in the pathogenesis of hypertensive vascular disease. 8381929: However, the hypertension prevalence rates in the GN patients significantly exceeded those seen in the corresponding age/sex bands in the general UK population and varied considerably between GN subtypes; thus hypertension in patients with GN and 'near normal' renal function is not solely due to essential hypertension. 8806984: The results indicate a lack of association between ACE I/D polymorphism and essential hypertension in this Greek population, suggesting that other genes must contribute to the pathogenesis of hypertension. 9747906: INHIBITING THE SYMPATHETIC SYSTEM: As the clinical consequences of sympathetic nervous activation in essential hypertension appear to go beyond that of hypertension pathogenesis, extending to a causal influence in atherosclerosis development, cardiovascular hypertrophy and cardiac arrhythmias, it is possible that, of all antihypertensive drugs, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk. 1028554: In addition, estrogen may trigger high blood pressure and increase some blood clotting. 10385681: Regulation of human COMT gene expression may be important in the pathophysiology of various human disorders including estrogen-induced cancers, Parkinson's disease, depression, and hypertension. 11058906: This finding may be important clinically with regards to the treatment of many neuropsychiatric disorders and in the pathophysiology of various human disorders including estrogen-induced cancers, Parkinson's disease, depression and hypertension. 17022598: [Estrogen-induced hypertension]. 17642147: This suggests that the lower level of estrogens is not only one factor in the etiology of hypertension in women in this period. 185040: Estrogenic compounds are the most important group of drugs that can induce hypertension. Other drugs may cause hypertension. 21293310: RESULTS: The surgical loss of ovarian hormones, particularly estrogen, led to exacerbated hypertension, impaired myocardial relaxation, diminished diastolic compliance, increased perivascular fibrosis, and increased relative wall thickness. 22688265: However, controversial benefit of hormone replacement therapy in postmenopausal women raises the hypothesis that the loss of endogenous estrogens alters genetic susceptibility determinants per se, resulting in hypertension mechanisms beyond correction by hormone replacement. 24786446: There are several proposed mechanisms for the development of hypertension that are unique to women and pertain to the aging-related elevated risk for hypertension resulting from falling estrogen levels during menopause. 26419930: However, long-term supplement of estrogen may cause uterine hyperplasia and hypertension leading to a high risk of endometrial cancer and breast cancer. 28746172: Sex- and age-specific variances in the prevalence of hypertension are partly induced by estrogen. 30485368: BACKGROUND: The menstrual cycle is regulated by reproductive hormones such as estrogen which has been implicated in the pathogenesis of hypertension and is associated with obesity. 306034: [Hypertension due to hormonal contraceptives and estrogens (author's transl)]. 3814904: The role of the sympathetic nervous system in oestrogen-induced hypertension in rats. 4289438: Estrogen-induced arterial hypertension in the hibernating male toad, Bufo arenarum Hensel. 4325189: Should high blood pressure or hypertension occur, the drugs must be stopped even if the estrogen-induced hypertension is reversible after cessation of the medication. 6393087: Most studies on hypertension caused by OCs were performed with pills containing 50-100 mc of estrogens and 1-4 mg of gestagen. A literature review is presented to show that oral contraceptives (OCs) can cause arterial hypertension in women. Estrogens appear to dominate in the pathogenesis of hypertension caused by OCs. 6838497: This study investigates whether qualitative rather than quantitative differences in renin substrate were associated with estrogen induction of hypertension by comparing the plasma concentration of high molecular weight renin substrate (HMS) in 18 healthy normotensive, nonpregnant women aged 35-50 taking no medication; 20 normotensive subjects receiving estrogens as oral contraceptives (OCs) or ethinyl estradiol (EE) 50 mcg; and 5 women on OCs or EE 50 mcg who became hypertensive on estrogen therapy. 7047019: Since both estrogen and progestogen seem to be responsible in the etiology of hypertension the lowest possible dosage of OC should be chosen. 7105645: Developing the most effective therapeutic approach to estrogen induced hypertension, when withdrawal of the estrogen source is not feasible, would be enhanced by a clear understanding of the mechanisms by which the hypertension occurs. 7946157: Transgenic rats carrying the mouse Ren-2 gene (Ren-2d)27 provide a unique model to study the interplay between the renin-angiotensin system and estrogen in the pathogenesis of hypertension. 7956510: In conclusion, the alteration of function of endothelium may play an important role in the modulation of estrogen-induced mild hypertension. 963965: Estrogen-induced hypertension. 10535697: High D2O concentrations can reduce salt- and ethanol-induced hypertension in rats and protect mice from gamma irradation. 11265132: [Effects of ethanol on the nervous and vascular systems: the mechanisms of alcohol-induced hypertension]. The effects of ethanol on the nervous and vascular systems in relation to the mechanisms of alcohol-induced hypertension proposed so far are reviewed here. More detailed and integrated mechanisms for alcohol-induced hypertension, which is not a homogeneous disease, remain to be clarified. 8) The difference in the genetic polymorphism of acetaldehyde dehydrogenase among Japanese people may not be directly related to development of alcohol-induced hypertension. 7) Long-term heavy drinking often results in the development of insulin resistance and glucose intolerance, which in turn triggers hypertension. 11342802: The mechanisms by which consumption of alcohol leads to hypertension and perhaps renal disease are unknown. 11468026: Ethanol has been reported to cause hypertension, the mechanism of which is unknown. 11740147: CONCLUSIONS: These results reveal that alcohol is able to induce hypertension and provide evidence that alcohol inhibits the transcriptions of both 11beta-HSD2 and CYP11B2 in the vasculature, leading to lower aldosterone and higher corticosterone production in vessels, and increased vasoconstrictor responses to norepinephrine. 12377357: Roles of tyrosine kinase-, 1-phosphatidylinositol 3-kinase-, and mitogen-activated protein kinase-signaling pathways in ethanol-induced contractions of rat aortic smooth muscle: possible relation to alcohol-induced hypertension. 1321191: These findings are discussed in the context of ethanol-induced hypertension in humans and possible genetic variations in central nervous, cardiac and vascular effects. 15683747: The data suggested that ethanol induces hypertension at higher doses by depleting NO and antioxidants and increasing oxidative tissue injury in rats. The dose response of ethanol-induced hypertension and associated oxidative stress response has not been well established. 16078602: [Alcohol-induced arterial hypertension and genetic polymorphism of alcohol-metabolizing enzymes]. 1635234: [Possible mechanisms of alcohol-induced hypertension]. 16425420: AIM: To study the role of hepatic sinusoidal capillarization and perisinusoidal fibrosis in rats with alcohol-induced portal hypertension and to discuss the pathological mechanisms of alcohol-induced hepatic portal hypertension. Pathological mechanisms of alcohol-induced hepatic portal hypertension in early stage fibrosis rat model. 16467407: CONCLUSIONS: Physical training attenuates the chronic ethanol-induced hypertension via reduction of body weight, clearance of ethanol, and augmentation of the aortic endothelial relaxation response in rats. 16487260: Alcohol-induced hypertension is well recognized with clear evidence for a direct pressor effect of chronic alcohol consumption provided by a number of intervention studies in humans. The mechanism of alcohol-induced hypertension is not clearly understood. 16718371: Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model. 17019839: Vasoconstriction effects and modification of smooth muscles are well established factors of alcohol-induced hypertension. 1737652: These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity. 17519114: Vascular endothelial oxidative stress in alcohol-induced hypertension. 17519555: CONCLUSION: Hypertension caused by chronic ethanol treatment as well as L-NAME administration could be associated with the reduction of APN and APA activity. 17531597: Alcohol-induced hypertension--just how much of a cardiovascular risk factor? 17917312: In conclusion, we found that a large percentage of the hypertensives in a general Japanese male population had alcohol-induced hypertension. The proportion of individuals with alcohol-induced hypertension among total hypertensives in a general Japanese population: NIPPON DATA90. 18093048: The threshold amount of alcohol consumption determined in this study provides valuable information for preventing alcohol-induced hypertension. 1844546: The implications of these results in the pathogenesis of alcohol-induced hypertension are discussed in light of our previous studies on spontaneously hypertensive and normotensive rats which demonstrated a correlation between cardiac free magnesium levels and blood pressure. 1872991: The present study investigated the role of the sympathetic nervous system in the development of ethanol-induced hypertension (EIH) in the rat. Role of the sympathetic nervous system in ethanol-induced hypertension in rats. 19641713: CONCLUSIONS: The duration of alcohol ingestion is important in the induction of hypertension and the associated NO and antioxidant depletion, and oxidative tissue injury. The time response of alcohol-induced hypertension and associated tissue oxidative stress response has not been fully explored. 20193752: The aim of this study was to evaluate the protective effect of Allanblackia floribunda aqueous extract on alcohol- and sugar-induced hypertension in rats. CONCLUSION: These results demonstrate that the aqueous extract of Allanblackia floribunda can prevent alcohol- and sugar-induced hypertension and oxidative stress in rats. 2045140: High blood pressure due to alcohol. 21327566: However, the contribution of alcohol-induced hypertension to stroke morbidity and mortality may be greater than observed, because the effects of different drinking patterns have not been separately investigated. 22227471: SIGNIFICANCE: Folic acid intake improves the hypertension provoked by alcohol by increasing the aldosterone clearance, drastically reducing the serum levels of this hormone and thus its hypertensor effect. 2291843: Alcohol increases blood pressure in both hypertensive and normotensive subjects and alcohol induced hypertension enhances the risk of both hemorrhagic and ischaemic strokes. 2330733: [Alcohol-induced hypertension]. Genesis and therapeutic consequences of alcohol-induced hypertension are discussed. 23492672: Both confounder-adjusted multivariable and IV analyses suggested that a greater alcohol consumption among those who drank any alcohol resulted in a higher BP [mean difference in SBP per doubling of alcohol consumption among drinkers: 0.76 mmHg (95% CI: 0.63, 0.90) from multivariable analyses and 0.94 mmHg (-3.03, 4.69) from IV analyses; P-value for difference in these results = 0.95]. 24490573: CONCLUSION: The long-term administration of DOG can relieve alcohol-induced hypertension, while alleviating general signs, liver and kidney injuries and abnormal blood fat biochemical indexes. METHOD: The alcohol-induced hypertension rat model was established by feeding alcohol drink to normal rats (the alcohol volume fraction increases from 5% to 22%). OBJECTIVE: To observe the effect of Dendrobium officinale granule (DOG) on symptoms, blood pressure and serum biochemical indexes of long-term-alcohol-induced hypertension rats. [Effect of Dendrobium officinale granule on long-term-alcohol-induced hypertension rats]. 24891935: For the prevention of alcohol-induced hypertension is to reduce the amount of alcohol intake. Loss of relaxation due to inflammation and oxidative injury of the endothelium by angiotensin II leading to inhibition of endothelium-dependent nitric oxide production is the major contributors of the alcohol-induced hypertension. Alcohol-induced hypertension: Mechanism and prevention. 24944758: Support for the concept of ethanol as a cause of hypertension derives from several epidemiologic studies demonstrating that in the general population, increased blood pressure is significantly correlated with ethanol consumption. Possible mechanisms underlying ethanol-induced hypertension were proposed based on clinical and experimental observations. 25161923: This study was designed to investigate the effect of the chemo-profiled hydroethanolic leaf extract of Byrsocarpus coccineus in ethanol- and sucrose-induced hypertension. Ameliorative Effect of Hydroethanolic Leaf Extract of Byrsocarpus coccineus in Alcohol- and Sucrose-Induced Hypertension in Rats. 2540763: Blood ethanol level and physiologic measurements during ethanol-induced hypertension. 25519078: CONCLUSION: Current results suggest that the aqueous extract used in this study possess antihypertensive activity against ethanol and sucrose induced hypertension in rats by the improvement of biochemical and oxidative status, and by protecting liver, kidney and vascular endothelium against damages induced by chronic consumption of ethanol and sucrose. BACKGROUND: The present study was designed to evaluate the effects of the aqueous extract obtained from the mixture of fresh leaf of Persea americana, stems and fresh leaf of Cymbopogon citratus, fruits of Citrus medica and honey on ethanol and sucrose induced hypertension in rats. 2563915: Other factors, such as cations, may be more important than alcohol in the pathogenesis of hypertension in this group. 25801625: Studies focusing on molecular mechanisms showed a link between overproduction of ROS in the vasculature and ethanol-induced hypertension. 26135944: Alcohol-induced hypertension: an important healthcare target in Belgium. 26142527: Our results suggested an important role of intra and extra cellular electrolytes in both stress and ethanol-induced hypertension. 2698711: More than 60 gr daily of ethanol may be an important factor in the etiology of high blood pressure. 2728563: The alcoholic cardiomyopathy, which is the result of toxicity of alcohol, but also of alcohol-induced hypertension, coronary sclerosis and toxic destroyed nervous system, is demonstrated with a the keep of case. 27382085: RESULTS: Apocynin (10 mg/kg/day, i.p.) prevented ethanol-induced hypertension. AIMS: Investigate the role of NADPH oxidase on ethanol-induced hypertension and vascular oxidative stress. NADPH Oxidase Plays a Role on Ethanol-Induced Hypertension and Reactive Oxygen Species Generation in the Vasculature. SHORT SUMMARY: The key findings of our study are that ethanol-induced hypertension is mediated by NADPH oxidase. This mechanism is involved in vascular dysfunction and hypertension induced by ethanol. 27722988: The major finding of our study is that NAD(P)H oxidase-derived ROS play a role on ethanol-induced hypertension and endothelial dysfunction in resistance arteries. Reactive oxygen species derived from NAD(P)H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries. 28797835: The major finding of our study is that TNFR1 contributes to ethanol-induced hypertension and oxidative stress in the vasculature. We evaluated the contribution of tumor necrosis factor-alpha receptor 1 (TNFR1) to ethanol-induced hypertension and vascular oxidative stress and the possible role of perivascular adipose tissue (PVAT) in such responses. 28954635: Recommendations to handle alcohol-induced hypertension in primary healthcare settings were derived at the conference, and their degree of evidence was graded. Towards new recommendations to reduce the burden of alcohol-induced hypertension in the European Union. 2919378: The article presents the case history of a 28 year-old male with alcohol-induced hypertension and extreme hypercholesterolemia (36 mmol/l) and hypertriglyceridemia (76 mmol/l). [Alcohol-induced hyperlipemia. Hypertension and extreme hypercholesterolemia/hypertriglyceridemia in a patient with hidden alcohol abuse]. 3012594: These results may support a role for the vasoconstrictive hormone AII in the etiology of alcohol-induced hypertension. 30723512: (Poaceae) Aqueous Extract on Ethanol-Induced Hypertension in Wistar Rat. 30893362: Evidence suggests that ethanol-induced hypertension is associated with increased cardiovascular responsiveness to vasopressors in vivo and enhanced reactivity of isolated arteries to vasopressors ex vivo. 3208835: We also examined the effect of chronic ethanol consumption on the phenylephrine response and the effect of ethanol in vitro on that response during the development of ethanol-induced hypertension. 3296839: Since the chronic effects of ethanol on the cardiovascular system appear to be pivotal in the etiology of hypertension, coronary heart disease, and strokelike events, it is important to elucidate and understand the effects of chronic ethanol abuse and its mechanism(s) of action on the peripheral and cerebral blood vessels. 3301352: Finally, the available evidence suggests that alcohol induced hypertension will indeed lead to the usual hypertensive sequelae. 3596770: Ethanol-induced hypertension involves impairment of baroreceptors. 3670129: The ability of alcohol to elevate r-a activity may be seen as a contributing factor to alcohol-induced hypertension because angiotensin is a potent pressor agent. 3793941: Interactive roles of monovalent and divalent cations in pathogenesis of hypertension caused by alcohol. 3999153: Alcohol-induced hypertension: mechanisms, complications, and clinical implications. 6116043: Alcohol-induced hypertension. 6140440: The mechanism of alcohol-induced hypertension is uncertain and is more likely to be due to an effect of alcohol rather than to the pressor response produced by alcohol withdrawal. 6400431: Such mv. reactions as observed may be considered as a potential contributive pathogenic factor in ethanol-induced cardiomyopathies and hypertension. 6847023: A method for distinguishing alcohol-induced from non-alcohol-induced hypertension in drinkers is needed. These preliminary findings suggest that presumed alcohol-induced hypertension is as harmful as other forms of hypertension. 7032823: The mechanism behind the increased plasma renin level as well as the possible role of the renin--angiotensin system in alcohol-induced hypertension remain unsettled. 7231303: Role of alcohol in the aetiology of hypertension. 7432285: Role of alcohol in the aetiology of hypertension. 7554412: It is possible, therefore, that alcohol does not so much cause hypertension, but rather a rapidly reversible rise in blood pressure which does not cause cardiovascular damage. 7585279: Ethanol- and threonine-induced hypertension in rats: a common mechanism. CONCLUSION: These results suggest that acetaldehyde may be a common cause of both ethanol- and threonine-induced hypertension. 7599760: Elevated intracellular free calcium (Ca2+) has been proposed as a mechanism of alcohol-induced hypertension from animal experimental studies, but this has not been confirmed in man. 7805788: This pressor action of ethanol in the fetal circulation may contribute to the pathogenesis of the fetal alcohol syndrome as well as represent an underlying mechanism of ethanol-induced hypertension. 7847586: Role of magnesium and calcium in alcohol-induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31P-NMR, spectroscopy and a unique magnesium ion-selective electrode. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free Mg2+ ([Mg2+]i), which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca2+) overload. 8281480: Deuterium oxide normalizes blood pressure and elevated cytosolic calcium in rats with ethanol-induced hypertension. This study examined the effect of 10% deuterium oxide (D2O) in drinking water on systolic blood pressure, platelet cytosolic free calcium, aortic calcium uptake and renal vascular changes in rats with ethanol-induced hypertension. 8447725: Ethanol induced hypertension in rats: reversibility and role of intracellular cytosolic calcium. 8542680: Changes in membrane fluidity have been proposed to contribute to the pathogenesis of ethanol-induced hypertension possibly through changes in membrane lipid patterns, but reports are inconsistent. Altered membrane function is a potential mechanism involved in ethanol-induced hypertension. 8805006: During our work on molecular influences of lifestyle factors on hypertension, the question arose to what extent cellular and molecular events could be involved in alcohol-induced hypertension. 8833231: N-acetyl cysteine attenuates ethanol induced hypertension in rats. 8868036: Mechanisms of alcohol induced hypertension are still unclear. 8903667: Is an increased waist : hip ratio the cause of alcohol-induced hypertension? 8948319: Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. 1071589: Clipping of one renal artery with removal of the other kidney produced severe hypertension with no significant changes in exchangeable sodium or plasma renin levels. 1192616: Hypertension induced by renal artery partial constriction and removal of the other kidney is also associated with reduction of interstitial space compliance; a sudden rise in interstitial space compliance may be the primary factor in the course of events that leads to the rapid fall in blood pressure which occurs when the constriction is removed from the renal artery. 15796940: Failure to recognize cystic PCC before resection may lead to uncontrollable hypertension in the operating room, with potentially serious consequences. 17478757: CONCLUSIONS: Complete removal of FKBP12 and 12.6 from endothelial RyRs induces an intracellular Ca2+ leak which may contribute to the pathogenesis of endothelial dysfunction and hypertension caused by rapamycin or FK506. 1773523: In some ways, these results resemble a well recognized model of hypertension produced by the removal of 70-80% of renal mass plus excess salt consumption (RRM-salt). 18340683: A U shaped trend of hypertension in patients on PD has been recently demonstrated as a result of a steadily increased blood pressure partly attributed to fluid retention resulting from lower sodium removal with time. 18638735: This review examines prevention and treatment of delayed cerebral vasospasm after aneurysm haemorrhage, with emphasis on techniques for removal of cisternal blood, fluid loading and induced hypertension, and calcium antagonists. 20829519: However, there has been concern regarding reduced sodium removal leading to hypertension and resulting in a faster decline in residual renal function (RRF). 2276579: Removal of endothelium or pathological situations that can induce endothelial dysfunction (atherosclerosis, diabetes, hypertension or subarachnoid hemorrhage) cause increases on the vascular contractility elicited by agonists (noradrenaline, serotonin, EDCFs, etc.). 2350475: In the patients studied, surgical or medical elimination of the mechanism responsible for the hypertension when the patients were below the age of 40 reduced diastolic blood pressure 1 to 2 years later to below 90 mm Hg in 24 of 25 patients. We have analyzed the effect of age on the response of the blood pressure to the removal of the cause of hypertension in groups of patients with primary aldosteronism, renovascular hypertension, Cushing's syndrome and hypothyroid hypertension. 2704162: In addition to liquidation of the fistula for removal of the cause of biliary hypertension, choledochoenteroanastomosis was established in 4 patients and various manipulations on the papilla were performed in 16 patients. 2861663: Amelioration or cure of hypertension, hypercortisolism, diarrhea with steatorrhea, and massive proteinuria resulted from excision of a pheochromocytoma that contained immunoreactive ACTH, VIP, and somatostatin. 28698257: Removal of TGF-beta or blocking its signaling before hypertension induction accelerated hypertension progression, whereas supplementation of TGF-beta1 substantially suppressed neuroinflammation, kidney norepinephrine level, and blood pressure. 30248339: These results indicate that hypertension induced by the surgical removal of one kidney and partial ligation of the other renal artery method in WHHL rabbits may not only enhance the development of atherosclerosis but also destabilize the plaques, increasing cardiac death. 3387186: Reversibility of the depression of endothelium-dependent relaxation was investigated on aorta from renovascular hypertensive rats in which blood pressure was normalized by removal of the stenotic kidney three months after induction of hypertension. 573441: Removal of the clip 6, 13 or 24 days after the induction of the hypertension was followed by a rapid decrease in blood pressure. 6470917: In six ewes hypertension was induced by surgical removal of one kidney and reduction of arterial blood flow to the remaining kidney (one-kidney renovascular hypertension). 7037635: Thus, sustained inhibition of the renin-angiotensin system did not modify the correction of hypertension produced by removal of the constricting clip, and the response to surgical correction did not appear to be entirely mediated by changes in the activity of the renin-angiotensin system, particularly in the chronic stage. 9746518: Vascular diseases such as hypertension have also been attributed to changes in vascular smooth muscle function as a consequence of altered Ca2+ removal. 10094144: Numerous lines of evidence suggest that some of the neurotoxicity associated with Alzheimer's disease (AD) is due to proteolytic fragments of the amyloid precursor protein (APP). 10928985: Numerous lines of evidence indicate that some of the neurotoxicity associated with Alzheimer's disease (AD) is due to proteolytic fragments of the amyloid precursor protein (APP). 12507755: Amyloid peptide (Abeta) is a 40/42-residue proteolytic fragment of a precursor protein (APP), implicated in the pathogenesis of Alzheimer's disease. 12708616: The regulated intramembrane proteolysis of the amyloid precursor protein (APP) that results in the generation of a toxic 40 to 42 amino acid fragment, Abeta, and a C-terminal intracellular fragment stands central in the pathogenesis of Alzheimer's disease. 1438289: The peptide comprising the carboxyl-terminal 100 amino acids of the beta-amyloid precursor protein (beta APP) has been shown to aggregate into amyloid-like fibrils in vitro and to be neurotoxic, suggesting that this fragment may play a role in the etiology of Alzheimer disease. 15145073: Micromolar concentrations of beta-amyloid (Abeta), a 40/42-amino-acid-long proteolytic fragment (Abeta(1-40/42)) of the amyloid precursor protein, was shown previously to play a crucial role in pathogenesis of Alzheimer's disease. 15821343: Several lines of evidence suggest that some of the neurotoxicity in Alzheimer's disease (AD) is attributed to proteolytic fragments of amyloid precursor protein (APP) and beta-amyloid (Abeta) may not be the sole active component involved in the pathogenesis of AD. 16087241: It is a fragment of the presynaptic protein alpha-synuclein and, as such, it is implicated in the aetiologies of both Alzheimer's (AD) and Parkinson's (PD) disease. 16480887: These findings provide the first evidence that APP-betaCTF can accumulate in the axons of OA-treated neurons, and may suggest that APP-betaCTF is involved in the pathogenesis of AD. 16820299: Amyloid-beta peptide (Abeta), a proteolytic fragment generated from the amyloid precursor protein, has been implicated as the toxic molecule involved in the pathogenesis of Alzheimer's disease. 17714184: However, an increased level of APP intracellular domain was also observed, highlighting the need to increase our knowledge about the relevance of this fragment in Alzheimer's disease pathogenesis. 19733011: We propose that the electrical activity of neurons causes a structural destabilization of the fragments, which could lead to fibril formation, and thereby contributes to the pathogenesis of Alzheimer's Disease. 19901559: Surprisingly, a recent report suggests that PrP is a receptor for toxic oligomeric species of a-beta, a pathogenic fragment of the amyloid precursor protein, and likely contributes to disease pathogenesis of Alzheimer disease. 20412390: These apoE4 fragments have been hypothesized to be involved in the pathogenesis of AD, although the mechanism is not clear. 21960299: While physiological function(s) of APP still remain a matter of debate, consensus exists that the proteolytic processing of this protein represents a critical event in the life of neurons and that abnormalities in this process are instrumental in Alzheimer's disease (AD) pathogenesis. Understanding neuron-specific mechanisms of APP processing would help illuminating the physiological roles of APP-derived proteolytic fragments and provide novel insights on AD pathogenesis. 23517619: Processing of beta-amyloid precursor protein (APP) by beta- and gamma-secretases in neurons produces amyloid-beta (Abeta), whose excess accumulation leads to Alzheimer's disease (AD). Knowledge on subcellular trafficking pathways of APP and its fragments is important for the understanding of AD pathogenesis. 25150572: Although full-length APP has been thoroughly studied, the role of the cleavage fragments especially the N-terminal fragments (N-APPs) in Alzheimer's disease pathogenesis was still elusive. 27697033: It has been demonstrated that recombinant antibody fragments may neutralize toxic extra- and intracellular misfolded proteins involved in the pathogenesis of AD, PD, DLB, FTD, HD or TSEs and may target toxic immune cells participating in the pathogenesis of MS. 29848690: One of the most active fragments of the pathological \endogen\ substrate responsible for AD was investigated in the presence of amyloid-beta fragment on the reversal of multidrug resistance and apoptosis induction on multidrug-resistant tumor cells in model experiments. 31649526: The amyloid beta (Abeta)-peptide, its amyloid precursor protein (APP) and the intermediate APP-c-terminal fragments (APP-CTFs) are all important players in AD pathogenesis. 7588622: Due to the capacity of these cells to secrete and accumulate intracellular amyloid fragments, we hypothesize that in the pathogenesis of AD there is a positive feed-back loop where neurons are both producers and victims of amyloid, leading to neuronal degeneration and dementia. 8687017: There is mounting evidence that at least some of the neurotoxicity associated with AD is due to fragments from APP. Excessive amyloidogenic pathway of APP processing may be the final common pathway involved in the pathogenesis of AD. 8780033: There is mounting evidence that at least some of the neurotoxicity associated with Alzheimer's disease (AD) is due to proteolytic fragments of the beta-amyloid precursor protein (beta APP). 8888112: Synthetic peptides homologous to beta A and its fragments contribute to investigate the mechanisms of beta A deposit formation and the role played by beta A in AD pathogenesis. 8954102: Our finding that PHF-like structures assemble from a MAP-2 fragment raises new questions about MAP-2's role in the etiology of Alzheimer's Disease. 9219695: Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 (PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease. 9312066: Fractionation studies revealed that the C-terminal fragment generated by expression of the Alzheimer mutations, like C100, partitioned into membrane fractions and was particularly enriched in synaptosomes. 9358827: The aim of the present study was: (i) to investigate the conditions determining the toxicity of Al and A beta 25-35; and (ii) to assess whether melatonin could attenuate the damage done by both aluminium and the amyloid fragment, thus suggesting a pathway for the aetiology of AD. 9875721: Numerous lines of evidence suggest that some of the neurotoxicity associated with Alzheimer's disease (AD) is due to proteolytic fragments of the amyloid precursor protein (APP). 10976051: Epidemiological studies have indicated that susceptibility of human adults to hypertension and cardiovascular disease may result from intrauterine growth restriction and low birth weight induced by maternal undernutrition. 11118401: Outcome measures were the recurrence of hypertensive disorders, and poor pregnancy outcome due to intrauterine death growth retardation, intrauterine death, placental abruption, hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome, eclampsia, or premature birth. 11877360: However, it is not clear whether it is fetal growth restriction or the accelerated postnatal growth that often follows it that leads to higher blood pressure. 1524554: Intrinsic fetal anomalies such as chromosomal abnormalities, primary growth failure syndromes, congenital infections and congenital anomalies are of equal importance with maternal disorders, in particular chronic use of alcohol, tobacco and narcotics, and pregnancy complications like hypertension and pre-eclampsia, in causing fetal growth retardation. 17476289: We examined whether intrauterine growth restriction or the subsequent catch-up postnatal weight gain leads to higher blood pressure in early life to confirm that size at birth and early postnatal growth rates appear to be important determinants of blood pressure changes in early life. 18384844: The renin-angiotensin system has been reported to play a role in IUGR-induced hypertension. 18704113: CONCLUSION: For those born in the first half of the twentieth century, the association between low birth weight and adult hypertension is due to poor fetal growth and not due to preterm birth. 20219873: Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. 25550341: Enhanced vascular responsiveness to angiotensin II is observed, and blockade of the renin-angiotensin system abolishes hypertension in adult growth-restricted rats, suggesting that the renin-angiotensin system contributes to intrauterine growth restriction-induced hypertension. 26781277: Elevated maternal testosterone levels are shown to cause fetal growth restriction, eventually culminating in sex-specific adult-onset hypertension that is more pronounced in males than in females. 27658996: This review highlights the fact that hypertension is likely to be a legacy of preterm birth due to IUGR and failure to meet nutritional needs in early infancy when fed formula instead of breastfeeding or human milk. 27899104: The aim of this study was to demonstrate that IUGR-induced HT and CRD are linked to the magnitude of nephron number reduction, independently on its cause. 32046425: We hypothesized that maternal genetic risk for FGR may similarly affect fetal kidney development, leading to adult onset hypertension. 32880745: Moreover, preterm birth and IUGR are known to cause upregulation of the postnatal renin-angiotensin system, resulting in hypertension. 35638239: Prematurity increases the risk of adulthood hypertension while intrauterine growth restriction may even lead to hypertension during childhood. 36053356: Biomarkers currently used in routine clinical care do not allow early postnatal prediction of higher blood pressure or worse kidney function due to IUGR, so further studies are needed. 1011591: [Surgical treatment of vasorenal hypertension caused by fibromuscular dysplasia of the renal arteries]. 1156158: One hundred thirteen patients (106 women, seven men), 18 to 64 years in age, with hypertension as a consequence of renal artery fibrodysplasia underwent operation during a 13-year period. 1251005: Renal venography was performed in a patient suffereing from hypertension due to fibromuscular dysplasia of the renal artery. 1285968: The vasorenal genesis of hypertension was caused by fibromuscular dysplasia (FMD) of the renal arteries in 61 patients, unspecific aortoarteritis (UAA) in 39, hypoplasia of the abdominal aorta, kidneys, and renal arteries in 22 patients, supernumerary renal arteries were found in 7 patients. 14314048: HYPERTENSION CAUSED BY FIBROMUSCULAR DYSPLASIA OF THE RENAL ARTERIES. 15476494: Pretransplant evaluation of the donors may include an angiography to evaluate the renal arteries, and failure to recognize renal arterial stenosis, particularly fibromuscular dysplasia, by noninvasive methods may eventually lead to hypertension and ischemic renal failure. 15920452: Retrospective follow-up for 7.0+/-4.7 years of 69 consecutive patients (age 44+/-13 years) treated for hypertension due to FMD, 59 patients underwent PTRA and eight patients surgery. 159354: Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. 16475187: Fibromuscular dysplasia (FMD) leading to renal artery stenosis and hypertension is one of the most common treatable causes of secondary hypertension. 17117900: The mean age was 13.9 +/- 3.73 years, with 26.4 +/- 35.2 months of known hypertension, mean systolic blood pressure 191.1 +/- 30.6 mmHg, mean diastolic blood pressure 135.3 +/- 21.2 mmHg and 69% due to fibromuscular dysplasia. 17200897: FMD of the renal arteries is one of the leading causes of curable hypertension. 17672905: CASE PRESENTATION: In this report, we present a relatively uncommon case of renovascular hypertension in a 35-year-old female with a history of intractable hypertension as a result of fibromuscular dysplasia involving an accessory renal artery. BACKGROUND: Renovascular hypertension is defined as hypertension caused by renal artery stenosis. 19733990: These suggested that the renal infarctions due to fibromuscular dysplasia caused systemic hypertension. 20591148: Therefore, hypertension secondary to fibromuscular dysplasia is the most common cause of curable hypertension. 20979950: Our findings suggest that it is therefore necessary to consider FMD with aneurysmal formation as a possible cause of hypertension and renal hemorrhage in infants. 22286647: Fibromuscular dysplasia (FMD) involves small- and medium-sized arteries, being a well-known cause of hypertension in young Caucasian women, when renal arteries are involved. 24649423: The treatment of choice of hypertension due to FMD is percutaneous renal angioplasty (PTRA). Renal artery stenosis (RAS) from fibromuscular dysplasia (FMD) is an uncommon cause of hypertension that affects mostly women. 26222531: A 25-year-old man underwent an autotransplantation of his right kidney because of fibromuscular dysplasia-induced renal artery stenosis and subsequent hypertension. 26417194: The second case reports a 17-year-old man who presented with arterial hypertension caused by FMD of the left renal artery and was subsequently successfully treated by angioplasty. 27504335: This case highlights that FMD should be kept in mind as a rare cause of resistant hypertension in young males; although it is most common in young females. Resistant Hypertension due to Fibromuscular Dysplasia in a Young Male: A Rare Case Report. 27792790: FMD is often an underdiagnosed cause of hypertension and stroke, has higher prevalence in females (~80%) but its pathophysiology is unclear. 27827286: [Hypertension due to fibromuscular dysplasia: look for additional disease sites]. 29528871: Although FMD can result in hypertension and serious vascular complications, there is no proof that it can alter LV regardless of FMD type and its extent. 2978967: We conclude that PTA is the treatment of choice for children with hypertension due to fibromuscular dysplasia and should be attempted for stenosis of the transplanted renal artery. 29883369: FMD can lead to hypertension, arterial dissections, subarachnoid haemorrhage, stroke or mesenteric ischemia. 29889158: These differences may explain the often more severe clinical presentation and higher success rate of revascularization in unifocal FMD, but also suggest that the pathophysiological mechanisms leading to hypertension may differ between these two disease entities. 3072442: Atherosclerosis, aorto-arteritis and fibromuscular dysplasia are the most common causes of vasorenal hypertension. 32914075: Introduction: Renal artery fibromuscular dysplasia is generally considered a contraindication of kidney transplantation, since fibromuscular dysplasia occasionally induces hypertension or renal insufficiency in the recipient and/or donor. 36027404: CONCLUSIONS: Renovascular hypertension is responsible for less than 1% of all cases of hypertension and, when present, it is usually caused by atherosclerotic disease or fibromuscular dysplasia. 37586716: CASE REPORT: In this report, we present an uncommon case of renovascular hypertension in a 21-year-old non-white female with a 3-year history of hypertension secondary to fibromuscular dysplasia involving bilateral renal arteries. Fibromuscular dysplasia is a rare cause of hypertension that can easily be missed. 5533112: [Some features of fibromuscular dysplasia of the renal artery leading to vasorenal hypertension]. 6723113: Scleroembolization for treatment of hypertension caused by intrarenal arterial fibrodysplasia. 7057321: Spontaneous reversal of hypertension caused by fibromuscular dysplasia. 7089815: A case of severe hypertension due to fibromuscular dysplasia of the renal artery in a young adult woman is described. 7213086: Stenosis of the abdominal aorta due to fibromuscular dysplasia caused hypertension of the coarctation genesis. 7830849: A young female presented with hypertension and oliguric renal insufficiency caused by fibromuscular dysplasia of the renal arteries. 786426: A young man was discovered to have symptomless hypertension, which subsequently proved to be caused by fibromuscular dysplasia of the renal arteries. 8114966: [Hypertension caused by arterial fibromuscular dysplasia]. 8152504: [Hypertension caused by arterial fibromuscular dysplasia]. 9489789: We report on 4 of 9 sibs with a syndrome of stenosis of the renal arteries and chronic hypertension, variable stenosis or occlusion of cerebral, abdominal and probably coronary arteries due to suspected fibromuscular dysplasia, congenital cardiac abnormalities, brachydactyly and syndactyly of the hands and feet, and increased bone fragility consistent with a mild form of osteogenesis imperfecta. 1105838: Renal artery stenosis with resultant hypertension may occur secondary to stenosis at the anastomosis, atherosclerotic plaque formation or intimal fibrosis of the renal artery. 1320231: In advanced hypertension the observed reduction in tissue kallikrein was probably secondary to a loss of distal tubular mass, as a result of tubular atrophy and fibrosis. 17650360: In portopulmonary hypertension, cirrhosis and portal hypertension lead to pulmonary arterial hypertension, and portopulmonary hypertension has been considered a contraindication for transplantation. 18306572: We report a case of noncirrhotic portal fibrosis (NCPF) leading to PPHT which is exceedingly rare with only very few cases reported in the literature. 19949639: BACKGROUND AND OBJECTIVES: Hypertension develops as a result of cardiac hypertrophy and fibrosis or as a result of exchange of the extracellular matrix. 20491346: Liver failure, which often results from cirrhosis, may lead to the hepatopulmonary syndrome and portopulmonary hypertension. 24982243: Vascular extracellular matrix (ECM) remodelling, which is the result of disruption in the balance of ECM synthesis and degradation, induces vessel fibrosis and thereby leads to hypertension. 24993609: In our study, cardiac function, dimensions and histological determination of the fibrosis of rats with two-kidney, one-clip induced hypertension and sham-operated rats were assessed using an echocardiography system and Masson's trichrome. 28128707: Damping ratio and liver stiffness vary differently with respect to cause of portal hypertension (ie, congestion- or cirrhosis-induced hypertension). 37064881: Methods: A lung fibrosis-induced PH mouse model was constructed using a single intratracheal instillation of bleomycin (BLM), after which DON was administered daily. 3880603: The hypertension was due to long-standing cirrhosis in 4 patients; the other 3 patients had prehepatic hypertension due to thrombosis involving the portal vein in 1 and the splenoportal confluence in 2. 440360: Nonsurgical treatment of severe hypertension due to renal-artery intimal fibroplasia by percutaneous transluminal angioplasty. 4569532: Perirenal fibrosis as a cause of uremia and hypertension in human transplanted kidneys. 5936970: Hypertension due to subadventitial fibrosis of the renal artery. 8450041: Disproportionate collagen accumulation without histological evidence of fibrosis was noted within 1 wk after hypertension induction. 10232545: Many patients now undergo empirical hyperdynamic vasospasm therapy with hypervolemia, induced hypertension, and nimodipine. 10805462: Hypertension due to hypervolemia may also play a role in the development of HAS. 19112833: The hypertension in HD patients is caused by excess extracellular fluid volume (ECV) on the other hand hypertension resistant to normalization of ECV may result from the accelerated activity of the systemic and local--vascular renin-angiotensin-aldosteron system (RAAS). 19153263: Volume excess is thought to be important in the pathogenesis of hypertension among hemodialysis patients. 19528362: Although volume excess causes hypertension, whether it also affects circadian patterns of arterial pressures among hemodialysis patients remains unknown. 19700514: Elucidating the factors responsible for DOCA-salt hypertension will be helpful in understanding the causes of hypertension resulting from hypervolaemia, hyperaldosteronism and high salt intake. 21330484: BACKGROUND AND OBJECTIVES: Hypervolemia is an important and modifiable cause of hypertension. 21629259: The induction of hypertension, hypervolemia, and hemodilution is advocated for vasospasm, but it is unclear whether hemodilution confers any benefit. 22843460: MATERIAL AND METHODS: Fifty eight patients who had aneurysm clipping and were admitted to the neurointensive care unit were treated with normovolemia and induced hypertension (n=35) or hypervolemia supported with induced hypertension (n=23) targeting a mean arterial pressure of 110-130 mm Hg and central venous pressure of 8-12 mm Hg. This study is designed to see the difference of moderate or aggressive hypervolemia supported with induced hypertension in symptomatic vasospasm detected with transcranial Doppler ultrasonography (TCD) measurements. 22951101: Hypervolemia is thought to be a major cause of hypertension, and diuretics are useful to improve blood pressure control in CKD. 23154648: BACKGROUND/AIMS: Obesity and hypervolemic status are the main causes of hypertension in patients with chronic kidney disease (CKD). 2360460: Symptomatic ischaemia developed in 25 patients, however, in 15 of them it was fully reversible, due to the possibility of aggressive antivasospastic treatment (hypervolaemia, induced arterial hypertension). 3276753: Systemic arterial hypertension was noted in nearly all patients and is likely to be the result of hypervolemia secondary to cyclosporine-induced sodium retention. 32920540: Together, C. benthamiana extract might be useful in the management of hypertension due to volume overload in the cardiovascular system. 33819385: Because in either case the hypertension was associated with loss of water, and thus with hypo- rather than hypervolemia, the authors argue, that this concept of pathogenesis of hypertension is antipodal to the classic view that relies on hypervolemia due to sodium retention. 34618758: Emerging clinical evidence also suggests potential harmful impact of historic empiric treatments for SAH-associated vasospasm, such as prophylactic induction of hypertension, hypervolemia, and hemodilution (triple H therapy). 6387428: These observations do not support the concept that hypervolemia may represent the initial event leading to high blood pressure in essential hypertension; in contrast, changes in blood volume appear to reflect variations in blood pressure. 10093929: Role of free radicals and metal ions in the pathogenesis of Alzheimer's disease. 10462121: The ability of homogenates from Alzheimer and control brains to inhibit formation of thiobarbituric acid reactive products (TBAR) induced by free radicals was compared. 16447689: Short-term study mostly involved of newly evaluated assay methods for important substances such as the second level in the cell life span in the variation of lipid metabolite of cardiovascular diseases based on atherosclerosis, Alzheimer disease, and their evaluation by homogeneous assay of HDL-C, LDL-C, enzymatic assay for choline relating metabolites, and lipoperoxide as the results of free radical reactions. 19361273: Mitochondrial dysfunction, which is closely related to intracellular calcium overload and excessive free radicals, is an important cause of Alzheimer's disease (AD). 20648652: The oxidative stress observed in brains of subjects with AD and MCI may be due, either fully or in part, to increased free radicals mediated by amyloid-beta peptide (Abeta). 23326794: BACKGROUND: Alzheimer's disease is a neurodegenerative disease appearing as a result of free radicals and oxidative stress. 26606243: Previous studies in Down's syndrome (DS) and Alzheimer's disease (AD) suggested that the accumulation of protein oxidative damage results from the increased free radical production, mainly related to metabolic alterations, mitochondrial degeneration and amyloid-beta deposition, and aberrant activity of protein degradative systems. 27796744: Genistein has been mainly focused because of its potential on amelioration of Abeta-induced impairment and its antioxidant capacity to scavenge the free radicals produced in AD. 33781589: In particular, Fe 2+ has been hypothesized to produce free radicals that induce oxidative damage and eventually cause Alzheimer's disease (AD). 35538829: RESULTS: Findings suggested that channels of free radicals, such as transition metal accumulation, and genetic factors are mainly accountable for the redox imbalance that assist to understand better the pathogenesis of AD and incorporate new therapeutic approaches. Here we reviewed some of the key findings that have shown the function of Abeta peptide, oxidative stress, free radical damage Triggering Receptors Expressed on Myeloid Cells 2 (TREM2), Nitric Oxide (NO), and gut microbiota in the aetiology of AD. 38527587: This may lead to iron accumulation in the brain and the catalysis of free radicals that damage cerebral neurons and eventually lead to Alzheimer's disease (AD). 7643122: Recent studies revealed that A beta can be neurotoxic by a mechanism involving free radical production and loss of cellular ion homeostasis, thus implicating A beta as a key factor in the pathogenesis of AD. 7866588: Substantial evidence has accumulated implicating metals and free radicals in the pathogenesis of the major neurodegenerative disorders (Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis). 8239316: Free radicals in the genesis of Alzheimer's disease. 8847550: We present evidence to support the premise that many of the pathological correlates of Alzheimer's disease are precipitated by free radical- and oxidative stress-induced mechanisms. 9298634: Alzheimer's disease (AD) and vascular dementia (VaD) share several features such as overactivation of microglial cells, damage induced by free radicals, glutamate and calcium overload. 11438492: Dysfunction of the nitrergic pathway has been shown to cause LES hypertension and impaired relaxation in achalasia. 12770924: This review focuses on the dysfunction of the intrinsic brain renin-angiotensin system (RAS) in the pathogenesis of hypertension. 16037123: In hypertension, increased peripheral vascular resistance results from vascular dysfunction with or without structural changes (vessel wall remodeling and/or microvascular rarefaction). 17124432: Neuronal NE reuptake may be impaired in individuals with renal disease and/or hypertension due to dysfunction of the NE transporter. 18072654: Lower urinary tract dysfunction can lead to renal failure, owing to chronic infection and hypertension resulting from incomplete bladder drainage. 18212443: Chronic allograft dysfunction is the main cause of post transplant hypertension. 18320579: RhoA is involved in many cellular and physiological aspects, and a dysfunction of the G(12/13)-Rho pathway can lead to hypertension, cardiovascular diseases, stroke, impaired wound healing and immune cell functions, cancer progression and metastasis, or asthma. 19118493: Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. 19704105: The cardiac angiotensin II system may play a role in the pathogenesis of cardiac remodeling and dysfunction induced by a combination of hypertension and exaggerated BPV. 19794106: The LPS-induced dysfunction of renal D1 receptors alters salt handling and causes hypertension in rats during salt overload. 20021066: Vascular dysfunction, therefore, is the major contributor for the pathogenesis of hypertension, atherogenesis, thrombosis, and stroke. 212619: Hypertension induced by adrenocortical dysfunction--hypertension in 17 alpha-hydroxylase deficiency and metopirone-induced hypertension. 22321236: CONCLUSION: Prenatal lipopolysaccharide exposure results vascular renin-angiotensin system dysfunction, which may play an important role on the pathogenesis of hypertension development in offspring rats. 23401751: The conclusion made here is that hypertension in SHR produces important variations in cerebrospinal fluid proteins that could be due to a choroid plexus dysfunction and this fact supports the close connection between hypertension and blood to cerebrospinal fluid barrier disruption. 23841815: This variation could thus hypothetically cause dysfunction of endothelium and lead to hypertension. 23846908: Growing evidence exists linking mtDNA, its mutations, and mitochondrial dysfunction to the pathogenesis of hypertension. 24023697: Blood pressure increases with age, and dysfunction of the dopamine D3 receptor has been implicated in the pathogenesis of hypertension. 24046802: Portopulmonary hypertension after orthotopic liver transplantation is a complication that carries high mortality due to cardiopulmonary dysfunction. 24266989: Two porcine models of IAH that cause abdominal compartment syndrome [ACS] with organ dysfunction were created. Temporal differences in the development of organ dysfunction based on two different approaches to induce experimental intra-abdominal hypertension in swine. 24285249: These data support the hypothesis that a dysfunction of purinergic neurotransmission and enhanced sympathetic activity are contributing factors in the pathogenesis of hypertension. 24745173: Oxidative stress induces inflammation, proliferation and migration of vascular smooth muscle cells, may regulate apoptosis and the function of the cells of vascular wall, finally leading to dysfunction of endothelium, media and adventitia, leading to cardiovascular diseases such as atherosclerosis, hypertension or heart failure. 24828834: CONCLUSIONS: Our results suggest that baroreflex dysfunction impairs cardiac function, and increases pulmonary artery pressure, supporting a role for baroreflex dysfunction in the pathogenesis of hypertensive cardiac disease. 25104455: Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension. 25288640: These animals also have allowed us to dismiss etiological connections between hypertension and metabolic disease and, most importantly, identify pathophysiological programs that cooperate in the development and consolidation of hypertensive states caused by local vascular tone dysfunctions. 25411145: There are anatomical and physiological evidences that the ventrolateral (VL) region of the medulla plays an important role in blood pressure regulation and that dysfunction at this level may generate hypertension (HT). 25432379: Endothelial injury or dysfunction leads to multiple cardiovascular diseases, such as atherosclerosis, myocardial infarction, stroke, hypertension and peripheral vascular disease. 25483714: This review outlines that defects of the connexin 40 protein leads to hypertension because of dysfunction of renin secreting cells of the kidney. 25533905: These results suggest that in utero high-fat diet exposure causes hypertension and glucose intolerance resulting from mesenteric adipose tissue dysfunction in offspring, independently of maternal obesity. 25882860: The current review focuses on recent advances on the molecular mechanisms and consequences of eNOS dysfunction in hypertension, and potential novel therapeutic strategies restoring eNOS function to treat hypertension. 26521150: Hypertension in Plin1-/- mice might occur as a deleterious consequence of PVAT dysfunction. 26781276: Low-Salt Diet and Circadian Dysfunction Synergize to Induce Angiotensin II-Dependent Hypertension in Mice. 26828852: To examine the involvement of RAAS in modulation of salt taste sensitivity, we utilized aldosterone/NaCl-treated rats as a well-established model of salt-sensitive hypertension caused by RAAS dysfunction. 27268036: On the other hand, dysfunction of pericytes could participate in the pathogenesis of cardiovascular disease, such as arterial hypertension, fibro-calcific cardiovascular remodeling, myocardial edema and post-ischemic coronary no-reflow. 27872234: Here, we attempted to determine whether the impairment of EDH in hypertension is attributable to the dysfunction of TRPV4 and S/IKCa, using isolated superior mesenteric arteries of 20-week-old stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched Wistar-Kyoto (WKY) rats. 28200062: Activation of the innate immune system, inflammation, and subsequent adaptive immune system response causing end-organ injury and dysfunction ultimately leads to hypertension and its associated sequelae including coronary artery disease, heart failure, stroke, and chronic kidney disease. 28255983: KEY POINTS: Dysfunctions in CNS regulation of arterial blood pressure lead to an increase in sympathetic nerve activity that participates in the pathogenesis of hypertension. 28259969: The A4401G mutation was reported to cause the mitochondrial dysfunction responsible for hypertension. 2831079: With the current knowledge of both calcium homeostasis and the function and properties of cellular Ca2+-target proteins/signal transduction systems, a dysfunction of cellular calcium metabolism is considered in relation to the pathogenesis of hypertension. 2835965: With the current knowledge of both calcium homeostasis and the function and properties of cellular Ca2+-target proteins/signal transduction systems, a dysfunction of cellular calcium metabolism is considered in relation to the pathogenesis of hypertension. 28541412: BACKGROUND: Animal researches reported that the dysfunction of profilin1 (PFN1) was involved in the physiological arterial stiffness and vascular remodeling linking to the etiology of hypertension (HT). 28560821: KEY POINTS: Carotid body dysfunction is recognized as a cause of hypertension in a number of cardiorespiratory diseases states and has therefore been identified as a potential therapeutic target. 28594709: OBJECTIVES: African-Americans have a higher prevalence of hypertension compared with whites, possibly due to elevated oxidative stress and subsequent vascular dysfunction. 29455823: Repair of tetralogy of Fallot with atrioventricular septal defect may be associated with hemodynamic challenges in the postoperative period particularly as left atrial hypertension secondary to left atrioventricular valve dysfunction may exacerbate pulmonary regurgitation and augment low cardiac output. 29859399: Hypertension results due to dysfunction of different metabolic pathways leading to the increased risk of cerebral ischemia, atherosclerosis, cardiovascular and inflammatory disorders. 31244220: Malfunction of SMCs can lead to hypertension, asthma, and erectile dysfunction, among other disorders. 3160767: These results support the hypothesis that immunological dysfunction plays an important role in the aetiology of spontaneous hypertension. 3465908: These results support the hypothesis that immunological dysfunction and enhanced sympathetic activity cause spontaneous hypertension. In the present study the combined role of enhanced sympathetic activity and immunological dysfunction in the pathogenesis of hypertension in the SHR was investigated. 34964013: These cellular and tissue remodeling is the fertile soil for the development of age-associated structural and functional disorders in the cardiovascular and cerebrovascular systems in the pathogenesis of obesity, type II diabetes, hypertension, atherosclerosis, heart dysfunction, and cognitive decline. 451873: Hypotension and hypertension as consequences of baroreceptor dysfunction following carotid endarterectomy. 8142921: These findings collectively suggest that studies of the vasodilatory and antihypertensive effects of these plant-derived drugs on the regulation of cytosolic Ca2+ in vascular smooth muscle are consistent with the current hypothesis of Ca2+ dysfunction as an important etiological factor for the pathogenesis of hypertension. 8587282: However, the complex nature of post-transplant hypertension has made it difficult to discern if its occurrence is the cause or the consequence of chronic allograft dysfunction. 8588722: OBJECTIVES: Arterial hypertension due to renovascular dysfunction is uncommon in children. 9174380: Functional disturbance of this dilatory pathway may be highly significant for the pathophysiology and pathogenesis of arterial hypertension. 941839: Malfunction of viscosity-receptors (viscoreceptors) as the cause of hypertension. 10737603: These results support the hypothesis that cathepsin D links lysosomal dysfunction to the etiology of Alzheimer's disease and suggest a new approach to treating the disease. 10790719: Decreased melatonin production with malfunction of REM sleep is proposed to be a cause of sudden infant death syndrome and Alzheimer's disease, because the loss of the antioxidant function of melatonin allows brain injury to occur. 11447838: We have hypothesized that AD results from a progressive dysfunction of APP. There are two pieces of supporting data for this: first, APP is overexpressed in Down's syndrome, which leads to AD-like neuropathology by the age of 40 in virtually all affected individuals; secondly, specific point mutations in APP cause some forms of familial AD. 12387703: Neuronal cell dysfunction and cell death due to oxidative stress may causally contribute to the pathogenesis of progressive neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, as well as acute syndromes of neurodegeneration, such as ischaemic and haemorrhagic stroke. 12453672: This raises a question whether Alzheimer's dementia is secondary to vascular dysfunction in the central nervous system (CNS) and, therefore, the neurodegeneration that follows is a consequence of inadequate cerebral blood flow, altered brain metabolism and failure in physiological functions of brain endothelium which represents a site at the blood-brain barrier (BBB). 12476348: Studies of the pathogenic actions of mutations in presenilins and amyloid precursor protein that cause early-onset familial AD have established central roles for perturbed cellular calcium homeostasis and oxidative stress in the neurodegenerative process. The clinical presentation of patients with AD is dominated by cognitive deficits and emotional disturbances that result from dysfunction and degeneration of neurons in the limbic system and cerebral cortex. 1453480: Finally, disfunction of the lysosomal system may play a role in the pathogenesis of Alzheimer's disease. 14689635: This adaptation in Alzheimer's disease may be caused by dysfunction of the mechanism in adaptation of a quickly recovering central process. 15639790: Selective dysfunction of mGlu II receptors may also lead to abnormal protein phosphorylation (i.e., tau phosphorylation), culminating in neurodegenerative disorders (i.e., Alzheimer disease). 15781969: Phospho-beta-catenin accumulation in Alzheimer's disease and in aggresomes attributable to proteasome dysfunction. Accumulation of cytoplasmic inclusion bodies in many neurodegenerative diseases, including Alzheimer's disease (AD), might result from dysfunction of the ubiquitin-proteasome system. 15847115: CONCLUSIONS: Spectrophotometric enzymatic analyses of respiratory complexes in brain homogenates do not support the primary contribution of mitochondrial RC dysfunction in the pathogenesis of AD. 16002400: Synaptic dysfunction is one of the earliest events in the pathogenesis of Alzheimer disease (AD). 16078048: Since mitochondrial dysfunction has been proposed as an underlying cause of AD and a specific haplogroup was found to affect AD susceptibility in Caucasians, we investigated whether inherited mitochondrial haplogroups affect risk of developing AD dementia in Ohio and Indiana Amish communities. 16178023: There is strong evidence from genetics and transgenic mouse models that mitochondrial dysfunction results in neurodegeneration and may contribute to the pathogenesis of Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, hereditary spastic paraplegia, and cerebellar degenerations. 16569229: BACKGROUND: Alzheimer's disease is a neurodegenerative disorder characterized by a progressive cognitive impairment, the consequence of neuronal dysfunction and ultimately the death of neurons. 16814428: A pathological feature of Alzheimer's disease (AD) is an area-specific neuronal loss that may be caused by excitotoxicity-related synaptic dysfunction. 17168642: Today, we know that Abeta-degrading proteases are critical regulators of brain Abeta levels in vivo, with evidence accumulating that their dysfunction may play a role in the etiology of AD. 17512984: Oxidative stress, bioenergetic failure and mitochondrial dysfunction are all implicated in the etiology of neurodegenerative diseases such as Alzheimer's disease (AD). 17558294: Tau is an axonal microtubule-associated protein, whose dysfunction causes neurodegenerative diseases such as Alzheimer's disease and other tauopathies. 17678440: Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer's disease. 17696767: This article discusses critical issues of mitochondria causing dysfunction in aging and AD and discusses the strategies to protect neurons caused by mitochondrial dysfunction. 1776729: As elucidation of the reasons behind amyloid deposition must shed some light on the pathogenesis of AD, we review the current state of knowledge on the nature of the AD amyloid protein, its origin, and its formation. At the cellular level, Alzheimer's disease (AD) must be the result of neuronal dysfunction and degeneration leading to a reduction in synaptic density. 17786024: Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer disease. 17911214: Growing evidence suggests that mitochondrial dysfunction is one of the key intracellular lesions associated with the pathogenesis of Alzheimer's disease (AD). 17959149: Our results provide a template for the design of curcuminoid-based synthetic small-molecule fold catalysts that accelerate the folding of ER-processed proteins; this assumes significance given that nitrosative stress and dysfunction of the ER-resident oxidoreductase protein disulfide isomerise due to S-nitrosylation are factors associated with the pathogenesis of Alzheimer's and Parkinson's diseases. 17986027: The epidemiological finding of an increased risk of dementia in patients with diabetes mellitus has raised the hypothesis that a dysfunction of the insulin receptors plays a role in the pathogenesis of Alzheimer's disease (AD). 18322383: Structural and functional genomics studies demonstrate that genomic factors, probably induced by environmental factors, cerebrovascular dysfunction, and epigenetic phenomena, might be responsible for AD pathogenesis leading to premature neuronal death. 18641892: In Alzheimer's disease, pathological and neuroimaging data indicate that apathy is likely due to a dysfunction of the medial prefrontal cortex. 18949251: BACKGROUND: Subjects with Alzheimer's disease (AD) have elevated cortisol levels as a result of hypothalamic-pituitary-adrenal (HPA) axis dysfunction. 19182481: When AD or DLB patients walk with incongruent visual information, they may increase their postural sway or instability, because of their executive dysfunction. 19389700: Caspase-cleaved tau expression induces mitochondrial dysfunction in immortalized cortical neurons: implications for the pathogenesis of Alzheimer disease. 19417214: Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal injury in the pathogenesis of Alzheimer's disease. 19496804: There is strong evidence that beta-amyloid (Abeta) causes oxidative stress and induces mitochondrial dysfunction in the pathogenesis of Alzheimer's disease. 19519498: However, there is growing evidence that early stages of AD may be due to neuronal network dysfunction produced by the actions of soluble forms of Abeta. 19544621: Growing evidence suggests a causative role for intracellular accumulation of amyloid precursor protein (APP) and its proteolytic products in the pathogenesis of AD. Mitochondrial dysfunction is one of the key characteristics of AD pathogenesis. 19682326: The current clinical criteria for diagnosis of AD are focused mostly on cognitive deficits produced by dysfunction of hippocampal and high-order neocortical areas, whereas noncognitive, behavioural and psychological symptoms of dementia such as disturbances in mood, emotion, appetite, and wake-sleep cycle, confusion, agitation and depression have been less considered. 19853658: Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer's disease. 19907182: BACKGROUND/AIM: The contribution of mitochondrial dysfunction and oxidative stress to the pathogenesis of Alzheimer's disease (AD) has previously been described. 20016833: Whether mitochondrial dysfunctions are merely a consequence of AD pathology, or are early seminal events in AD pathogenesis remains to be determined. 20061648: Although increasing evidence supports a role for mitochondrial dysfunction in the pathogenesis of AD, there have been few studies that simultaneously evaluate changes in multiple mitochondrial proteins. 20107079: Alzheimer's disease (AD) is attributable to synapse dysfunction and loss, but the nature and progression of the presynaptic structural and functional changes in AD are essentially unknown. 20127811: Recent studies suggest that synaptic dysfunction is one of the earliest events in the pathogenesis of AD. 20463402: Increasing evidence is implicating mitochondrial dysfunction as a central factor in the etiology of Alzheimer's disease (AD). 20512543: Cognitive impairment symptoms of AD are induced by limbic system dysfunction, and an early-stage AD brain without dementia has the potential for atrophy in the hippocampal region. 20553766: The dysfunction and loss of basal forebrain cholinergic neurons and their cortical projections are among the earliest pathological events in the pathogenesis of Alzheimer's disease (AD). 20555132: Although mitochondrial dysfunction and the resultant oxidative stress are believed to play a major role in the pathogenesis of both early- and late-onset AD, it is conceivable that the altered physiological state of the cells leading to sporadic AD could involve additional mechanisms. 20661404: Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of Alzheimer's disease. 20730022: Studies in mice expressing both human amyloid precursor protein and human tau have provided clear evidence that amyloid-beta and tau interact in the pathogenesis of AD. A defined effort must be made to develop therapies that directly address the impact of tau dysfunction in the pathogenesis of AD. 20840064: We also cover the recent findings on cellular and animal models that highlight mitochondrial dysfunction as a fundamental mechanism in AD pathogenesis. 21046564: The case for blood-brain barrier dysfunction in the pathogenesis of Alzheimer's disease. 21112383: Chronic mild cerebrovascular dysfunction as a cause for Alzheimer's disease? This review proposes the hypothesis that a chronic mild longlasting cerebrovascular dysfunction could initiate a cascade of events leading to AD. 21143177: Dysfunction of one or more of these proteins is hypothesized to contribute to the pathogenesis of Alzheimer's disease (AD). 21244356: Mitochondrial dysfunction has been widely implicated in the etiology of Alzheimer's disease (AD). 21336338: The analyses of the similarities and differences of these dysfunctional pathways provide insights into understanding the dynamics of AD progression in six brain regions from a network perspective, which will further shed light on the pathogenesis of AD. 21450370: Mitochondrial dysfunction is likely a significant contributing factor to Alzheimer disease pathogenesis, and both amyloid peptide (Abeta) and pathological forms of tau may contribute to this impairment. 21514369: Especially in the context that mitochondrial dysfunction is an early and prominent characteristic of Alzheimer's pathogenesis, EMF treatment could have profound value in the disease's prevention and treatment through intervention at the mitochondrial level. 2165009: The hypothesis that the symptomatology of Alzheimer's disease is attributable to cholinergic dysfunction is supported by postmortem studies that have demonstrated reduced choline acetyltransferase (ChAT) activity across all areas of cerebral cortex and diminished numbers of perikarya in the basal forebrain nucleus basalis of Meynert. 22024748: Primary lysosomal dysfunction causes cargo-specific deficits of axonal transport leading to Alzheimer-like neuritic dystrophy. 22391273: Mitochondrial dysfunction is considered a major causative factor in Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). 22539855: Alzheimer's disease (AD) in the early stages is characterized by memory impairment, which may be attributable to synaptic dysfunction. Oxidative stress, mitochondrial dysfunction, and Ca2+ dysregulation are key factors in the pathogenesis of AD, but the causal relationship between these factors and synaptic dysfunction is not clearly understood. 22751174: The evidence that neurovascular dysfunction is an integral part of Alzheimer's disease (AD) pathogenesis has continued to emerge in the last decade. 22833458: From mitochondrial dysfunction to amyloid beta formation: novel insights into the pathogenesis of Alzheimer's disease. Furthermore, there is cumulating evidence that Abeta formation impairs mitochondrial function and that mitochondrial dysfunction is an early event in the pathogenesis of AD. 22914888: Several lines of evidence point to synaptic dysfunction as a cause of AD and that synapse loss is a pathological correlate associated with cognitive decline. 22922216: The recognition that G(1)/S checkpoint dysfunctions in Alzheimer's disease (AD) has opened a novel avenue for better understanding the pathogenesis of AD, as well as for searching for new biomarkers for early diagnosis of AD. 22961084: Our data indicate that insulin dysfunction in NOD mice leads to AD-like tau hyperphosphorylation in the brain, with molecular mechanisms likely involving a deregulation of PP2A. 22995655: Mitochondrial dysfunction and synaptic damage have been described as early events in Alzheimer's disease (AD) pathogenesis. 23107435: Increasing evidence demonstrates that amyloid beta (Abeta) elicits mitochondrial dysfunction and oxidative stress, which contributes to the pathogenesis of Alzheimer's disease (AD). 23126372: Thus, deficiency in mural vascular cells may contribute to disrupted vascular barrier properties and resultant neuronal dysfunction during AD pathogenesis. 23151073: Oxidative damage and mitochondrial dysfunction have been also implicated in the pathogenesis of AD, but the question as to whether they are involved in the onset and progression of the pathology or rather represent a consequence of neurodegeneration is still debated. Vascular factors and mitochondrial dysfunction: a central role in the pathogenesis of Alzheimer's disease. 23382999: Abnormal mitochondrial motility and mitochondrial dysfunction within axons are critical for amyloid beta (Abeta)-induced synaptic stress and the loss of synapses relevant to the pathogenesis of Alzheimer's disease (AD). 23494712: The dysfunction of the Neurovascular Unit (NVU) has been proposed to be causative in AD development, due to an impaired clearance of Abeta from the brain. 23756733: Their dysfunction may cause various life-threatening disorders, such as Parkinson's, Alzheimer's, and cardiovascular diseases. 23948929: Dysfunction of this signaling process may underlie glia-based aspects of AD pathogenesis. 24171818: Here, we provide an overview of current research focused on the relevance of autophagic/lysosomal dysfunction in AD pathogenesis as well as potential therapeutic targets aimed at restoring autophagic/lysosomal pathway function. 24252187: As such, NVU/BBB dysfunction, associated to irregularities in cerebral blood flow (CBF), has been proposed to contribute in the pathogenesis of Alzheimer's disease (AD), mainly by impairing cerebral Abeta clearance. 24450113: Currently, AD is believed to begin with synaptic dysfunction caused by soluble Abeta oligomers, playing a more important role in the etiology of AD than insoluble Abeta ibrils ('oligomer hypothesis'). 24512632: Dysfunction of retromer is a risk factor for the pathogenesis of Parkinson's disease (PD) and Alzheimer's disease (AD), both neuro-degeneration disorders. 24610177: Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer's disease (AD). 24664866: The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons (lipids, proteins, and nucleic acids) can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, inflammation, and beta-amyloid (Abeta) peptides. 24684730: Synaptic dysfunction and synapse loss are key features of Alzheimer's pathogenesis. 24713000: Together, our results support the role of tau and calcineurin as two intermediate signaling molecules between Abeta initiation and eventual synaptic dysfunction early in AD pathogenesis. 24728903: Human studies show that besides loss of cognition/learning ability, neuropsychological symptoms such as anxiety and seizures are seen as high as 70 and 17 % respectively in AD patients, suggesting dysfunction of GABAergic neurotransmission contributes to pathogenesis of AD. 24902900: Evidence indicates that nitrosative stress and mitochondrial dysfunction participate in the pathogenesis of Alzheimer's disease (AD). 25045655: Since synaptic dysfunction and degeneration are early events during the pathogenesis of AD, we aim to investigate the effects of testosterone on oligomeric Abeta-induced synaptic changes. 25062013: Soluble oligomeric amyloid beta (oAbeta) causes synaptic dysfunction and neuronal cell death, which are involved in the pathogenesis of Alzheimer's disease (AD). 25106114: Alzheimer's disease (AD) has historically been considered to arise due to the specific dysfunction and pathology of neurons in brain areas related to cognition. 25322927: BACKGROUND: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer's disease (AD) pathogenesis remain elusive. 25400096: Although it is well documented that soluble beta amyloid (Abeta) oligomers are critical factors in the pathogenesis of Alzheimer's disease (AD) by causing synaptic dysfunction and neuronal death, the primary mechanisms by which Abeta oligomers trigger neurodegeneration are not entirely understood. 25465240: Olfactory dysfunction is a recognized risk factor for the pathogenesis of Alzheimer's disease (AD), while the mechanisms are still not clear. 25511446: Although pathological hallmarks of AD are senile plaques, neurofibrillary tangles, and neuronal degeneration which are associated with increased oxidative stress, synaptic loss is an early event in the pathogenesis of AD. Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies. 25531259: This review explores the potential role of mitochondrial epigenetic dysfunction in Alzheimer's disease etiology and discusses some technical issues pertinent to the study of these processes. 25533203: INTRODUCTION: Synaptic dysfunction is an early event in Alzheimer's disease (AD) pathogenesis and directly related to cognitive impairment. 25688079: Despite widespread recognition of the significance of vascular dysfunction in Alzheimer's disease aetiology and progression, much uncertainty still surrounds the mechanism underlying Alzheimer's disease vascular injury. 26075247: Diabetes is associated with various nervous disorders, such as cognitive deficits, depression, and Alzheimer's disease, and that may be caused by neural stem cell dysfunction. 26126792: Dysfunction of protein transport contributes to pathogenesis of AD and other neurodegenerative diseases. 26186010: Additionally, oxidative damage and the dysfunction of the antioxidant system play important roles in the pathogenesis of osteoporosis and AD. 26311408: Vascular dysfunction in the pathogenesis of Alzheimer's disease--A review of endothelium-mediated mechanisms and ensuing vicious circles. This study reviews the current literature of in vitro and ex vivo studies on endothelium-mediated mechanisms underlying vascular dysfunction in AD pathogenesis, with the aim of presenting a comprehensive overview of the complex network of causative relationships. 26359500: Thus, this study suggests that GAPDH aggregates accelerate Abeta amyloidogenesis, subsequently leading to mitochondrial dysfunction and neuronal cell death in the pathogenesis of AD. Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by loss of neurons and formation of pathological extracellular deposits induced by amyloid-beta peptide (Abeta). 26380416: [THE ROLE OF beta-AMYLOID AND MITOCHONDRIAL DYSFUNCTION IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE]. 26440450: In Alzheimer's disease (AD), the deposition of beta-amyloid (Abeta) is hypothesized to result in a series of secondary neurodegenerative processes, leading ultimately to synaptic dysfunction and neuronal loss. 26500157: This study demonstrates for the first time mitochondrial dysfunction in transgenic mice with a mutation within the Abeta peptide (the Arctic APP mutation), and confirms previous studies suggesting that mitochondrial dysfunction and oxidative stress is an early event in the pathogenesis of Alzheimer disease. 26601965: Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most widespread neurological disorders (NDs) characterized by degeneration of cognitive and motor functions due to malfunction and loss of neurons in the central nervous system (CNS). 26647379: This multi-sensor system measured mitochondrial parameters in the brain of transgenic mice that model Alzheimer's disease (AD), because mitochondrial dysfunction is believed to be a primary event in the pathogenesis of AD. 26829765: Characterizing the early NVU damage and identifying biomarkers of neurovascular dysfunction may provide a fresh insight into Alzheimer pathogenesis and open opportunities for pediatric neuroprotection. 26869037: Mounting evidence has implicated autophagic dysfunction in the pathogenesis of several major neurodegenerative disorders, such as Parkinson's disease, Alzheimer's disease and Huntington's disease, where deficient elimination of abnormal and toxic protein aggregates promotes cellular stress, failure and death. 26949964: Alzheimer's disease (AD) and Parkinson's disease (PD) are such kind of killer CDs that occur due to dysfunction of cholinergic and dopaminergic neurons. 26976084: Its dysfunction and aggregation into insoluble paired helical filaments is involved in the pathogenesis of Alzheimer's disease (AD), constituting, together with accumulated beta-amyloid (Abeta) peptides, a hallmark of the disease. 27073745: Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized by cognitive impairment and dementia, resulting from progressive synaptic dysfunction, loss and neuronal cell death. 27340665: Cellular dysfunctions involving specific subcellular compartments, such as mitochondria and endoplasmic reticulum (ER), are emerging as crucial players in the pathogenesis of AD, as well as increased oxidative stress and dysregulation of calcium homeostasis. 27439966: It is well known that cognitive deficit of AD is caused by synaptic dysfunction. 27556379: On the other hand, experimental findings and human observations signal that some of the primary degenerative diseases of the CNS, like frontotemporal dementia, Parkinson's disease, Alzheimer's dementia, Huntington's dementia, primary cerebellar ataxias and amyotrophic lateral sclerosis, all of which affect the human species exclusively, may be due to astroglial dysfunction. 27581448: UNLABELLED: Microglial dysfunction is increasingly recognized as a key contributor to the pathogenesis of Alzheimer's disease (AD). 27599716: Mitochondrial dysfunction is known as one of causative factors in Alzheimer's disease (AD), inducing neuronal cell death. 27629410: These results further implicate endolysosome dysfunction in the pathogenesis of AD and HAND, and by virtue of its ability to prevent and/or block neuropathological features associated with AD and HAND caffeine might find use as an effective adjunctive therapeutic agent. 27634555: Mitochondrial dysfunction and ensuing oxidative damage is typically thought to be a primary cause of Huntington's disease, Alzheimer's disease, and Parkinson disease. 27634936: Cerebrovascular dysfunction is a critical component of Alzheimer's disease (AD) pathogenesis. 27653553: Mitochondrial dysfunction and impaired energy metabolism are important components of AD pathogenesis. 27834780: Therefore, to elucidate the causative mechanisms of mitochondrial dysfunction in aging brains is of paramount importance for our understanding of the pathogenesis of AD, in particular its sporadic form. 27987381: Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease. 28131207: BACKGROUND: Potential role of vascular dysfunction has been suggested in the pathogenesis of Alzheimer's disease (AD). 28237964: Microvascular dysfunction is considered an integral part of Alzheimer disease (AD) pathogenesis, but the possible relationship between amyloid pathology, microvascular dysfunction and cell death is still unclear. 28299814: They further support the concept of subtypes of Alzheimer's disease with distinct cognitive profiles due to prominent neocortical dysfunction early in the disease course. 28531191: Recent studies have shown that mitochondrial dysfunction is a causative factor of AD. 28934248: Dysfunction of retromer is a risk factor for the pathogenesis of Parkinson's disease (PD) and Alzheimer's disease (AD). 28956268: Alzheimer's disease (AD) is a progressive neurodegenerative disorder leading to dementia caused by advanced neuronal dysfunction and death. 28988799: Dysfunction of autophagy and endosomal-lysosomal pathways: Roles in pathogenesis of Down syndrome and Alzheimer's Disease. The same genetic factors that cause or increase AD risk are also direct causes of endosomal-lysosomal dysfunction, underscoring the essential partnership between this dysfunction and APP metabolites in AD pathogenesis. 29089996: Alzheimer's disease, a progressive neurodegenerative disease, affects learning and memory resulting from cholinergic dysfunction. Scopolamine has been employed to induce Alzheimer's disease-like pathology in vivo and in vitro through alteration of cholinergic system. These findings revealed the underlying mechanisms of scopolamine-induced Alzheimer's disease-like cellular dysfunctions, which provide evidence for developing drugs for the treatment of this debilitating disease. 29124106: (A?) accumulation and A?-related neural network dysfunction are considered central to the pathogenesis of Alzheimer's disease (AD) at the early stage. 29127191: Recent studies on Alzheimer's disease (AD) pathogenesis have suggested that accumulation of aggregated beta-amyloid (Abeta) peptides in the AD brain results from a dysfunction in these cellular clearance systems. 29255835: Mitochondrial dysfunction has been found to play an important role in the initiation of both aging and the pathogenesis of Alzheimer's disease. 29320772: This article examines the available evidence for a role of mTOR-driven cerebrovascular dysfunction in the pathogenesis of AD and of vascular cognitive impairment and dementia (VCID) and highlights the therapeutic potential of targeting mTOR and/or specific downstream effectors for vasculoprotection in AD, VCID, and other age-associated neurological diseases with cerebrovascular etiology. 29354787: We suggest that complex I dysfunction accelerate amyloid toxicity and mitochondrial complex I dysfunction in aging may contribute to the pathogenesis of sporadic AD. 29516292: Along with brain amyloid-beta (Abeta) deposits and neurofibrillary tangles, cerebrovascular dysfunction is increasingly recognized as fundamental to the pathogenesis of AD. 29551631: Although an accumulation of brain amyloid-beta (Abeta) peptide and hyperphosphorylated tau protein have been implicated in the pathogenesis of AD, the etiology of the disease remains unclear. Mitochondrial dysfunction has been identified as an early event in AD pathogenesis and is reflected by reduced metabolism, disruption of Ca2+ homeostasis, and increased levels of reactive oxygen species, lipid peroxidation, and apoptosis. 29777753: Recent studies suggest that neurovascular dysfunction may be an integral part of AD pathogenesis, contributing to the onset and development of AD pathologies such as neuronal death, inflammatory response, and breakdown of blood-brain barrier (BBB). 29863022: These findings indicate that the involvement of early demyelination at 3 months and the oligodendrocyte dysfunction at 6 months in APP/PS1 mice are in association with Alzheimer's disease pathogenesis. 29992725: While both Abeta plaques and tau aggregates could in turn enhance the dysfunction of these proteostatic pathways, eventually leading to apoptotic or necrotic neuronal death and pathogenesis of Alzheimer's disease. 30009706: Dysfunction of the cholinergic system plays an important role in pathogenesis of AD. 30144541: In summary, APOE epsilon4 may affect CSF SNAP levels in MCI patients, suggesting an important role of APOE epsilon4 in synaptic dysfunction leading to AD. 30292394: CONCLUSIONS: Our results reveal a role for RPS23RG1 in maintaining synaptic integrity and function and provide a new mechanism for synaptic dysfunction in AD pathogenesis. 30296191: CONCLUSION: Endogenous n-3 PUFAs delayed the onset of Alzheimer's disease caused by tau protein dysfunction, alleviating related symptoms and significantly prolonging survival in vivo. 30352630: Amyloid beta (Abeta)-mediated synapse dysfunction and spine loss are considered to be early events in Alzheimer's disease (AD) pathogenesis. 30362531: This review highlights the critical linkage of autophagy in the pathogenesis of AD, and avows a new insight to search for therapeutic target for blocking Alzheimer's pathogenesis. Autophagic dysfunction in Alzheimer's disease: Cellular and molecular mechanistic approaches to halt Alzheimer's pathogenesis. 30472149: Overtaken of High-fat, high-glucose or high-cholesterol diet may hasten the incidence of AD in later life, due to the metabolic dysfunction. 30478411: Moreover, our findings strongly suggest that mitochondrial dysfunction, NF-kappaB signalling and iNOS signalling are important dysregulated pathways in AD pathogenesis. 30481567: Importantly, dysfunction of such postsynaptic receptor trafficking can lead to severe brain diseases such as Alzheimer's Disease, autism spectrum disorder, and intellectual disability, yet underlying mechanisms remain elusive. 3539000: Two principal features of Alzheimer's disease (AD) are (1) the occurrence of neurofibrillary tangles (NFTs) and senile plaques, and (2) the loss of cortical cholinergic activity because of dysfunction of neurons in the basal forebrain cholinergic system. 7280699: The effects of diffuse cerebral dysfunction on oculomotor reaction time were assessed in patients with dementia of presumed Alzheimer's etiology and in normal age-matched control subjects. 8892355: Thus, the decrease we observe in overall PGSH-2 mRNA levels is likely to reflect both the known decline in numbers of neurons in AD as well as a lowered capacity for neuronal synthesis of PGHS-2, perhaps due to dysfunction or a loss of synaptic input. 9452785: Hypertension may also give rise to a blood-brain barrier dysfunction, which has been suggested to be involved in the aetiology and pathogenesis of Alzheimer's disease. 10037734: The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD. 10913280: Elevated levels of A beta(42) peptide formation have been linked to early-onset familial AD-causing gene mutations in the amyloid beta-protein precursor (A beta PP) and the presenilins. 12862394: Amyloid precursor protein gene mutations responsible for early-onset autosomal dominant Alzheimer's disease. The imbalance between A beta production and A beta clearance releases a cascade of subsequent cellular processes leading to AD. 16713961: To assess the potential of Drosophila to analyze clinically graded aspects of human disease, we developed a transgenic fly model to characterize Presenilin (PS) gene mutations that cause early-onset familial Alzheimer's disease (FAD). 18413473: Most of these mutations may also cause cognitive impairment, but the Arctic APP mutation is the only known intra-beta-amyloid mutation to date causing the more typical clinical picture of Alzheimer disease. Clinical and neuropathological features of the arctic APP gene mutation causing early-onset Alzheimer disease. 19276550: Presenilin 1 (PS1) gene mutations are the major causes of early-onset familial Alzheimer's disease. 19276551: Presenilin 1 (PS1) gene mutations are the major causes of early-onset familial Alzheimer's disease and are known to increase amyloid-beta42 (Abeta42) production as well as to promote apoptosis. 22491860: CONCLUSION: Our study shows that APP mutations and locus duplications are a very rare cause of EOFAD and that the contribution of common APP variants to AD susceptibility is insignificant. OBJECTIVES: More than 30 different rare mutations, including copy number variants (CNVs), in the amyloid precursor protein gene (APP) cause early-onset familial Alzheimer disease (EOFAD), whereas the contribution of common APP variants to disease risk remains controversial. 24114635: Gene mutations influence the outcome of age-related neuronal degeneration to cause early onset familial AD (EO-FAD). 25927677: Rare forms of early onset familial Alzheimer's disease are due to gene mutations. 26757189: Studies of presenilin (PSEN) gene mutations producing early onset Alzheimer's disease (AD) have helped elucidate the pathogenic mechanisms of dementia and guided clinical trials of potential therapeutic interventions. 29562513: In fact, while early-onset AD is a clear consequence of gene mutations, late-onset AD is more likely due to a gradual accumulation of age-related damages. 31296348: \Presenilin 1\ (PSEN1) gene mutations are the major known genetic cause of early-onset Alzheimer's disease. 34189411: One consistent observation for all PRESENILIN gene mutations causing EOfAD is that a transcript is produced with a reading frame terminated by the normal stop codon-the \reading frame preservation rule\. Background: Mutations in PRESENILIN 2 ( PSEN2 ) cause early onset familial Alzheimer's disease (EOfAD) but their mode of action remains elusive. 10069978: On the basis of the homology of genome maps, several other genes encoding these transporters, as well as the Na+/H+ exchanger and Na+-K+-2Cl- cotransporter, can be predicted in QTL related to the pathogenesis of hypertension. 10085242: Since the locus for a familial hypertension has been mapped to the overlapping region, LOX-1 might be the gene responsible for the hypertension. 10405784: Analyses of inbred rat models of hypertension have so far provided several candidate loci and genes that may be responsible for hypertension. 10406008: This study is designed to determine whether patients with aneurysmal subarachnoid hemorrhage have mutations in the phospholipase C-delta 1 (PLC-delta 1) gene, which was identified as a gene responsible for hypertension in spontaneously hypertensive rats. 10779121: To identify the genes responsible for hypertension, the construction of congenic rats is essential. 10904005: Our long-term objective is to identify genes whose expression results in hypertension and in phenotypic changes that may contribute to hypertension. 10976390: INTRODUCTION: This article attempts to summarise the genetic research that has taken place during the past decade to determine the identity of genes causing high blood pressure. 10981042: Genes play a very important role in the etiology of hypertension. 11304517: These findings provide direct evidence that a gene or genes on chromosome Y contribute to the pathogenesis of spontaneous hypertension in the SHR-BN model. 11411117: Disruption of endothelial NO synthase (eNOS) gene causes systemic hypertension and diminishes endothelium-dependent vasodilatation. 11459925: A genetic variant of the gene for the alpha(1)-isoform of Na(+)-K(+)-ATPase (Atp1a1) was suggested to be involved in the pathogenesis of salt hypertension in Dahl rats through altered Na(+):K(+) coupling ratio. 11532685: For the majority of hypertensive cases, no gene or combination of genes and environmental factors clearly leading to hypertension has been identified. 11641287: A putative 1079A-->T mutation in the alpha1 isoform of the Na(+), K(+)-ATPase (Atp1a1) gene of the Dahl salt-sensitive rat inbred by John Rapp (SS/Jr) strain was projected to cause a conformation change in the membrane hydrophobic region of the protein product, possibly resulting in hypertension. 12877070: Identification of genes responsible for both type 2 diabetes and hypertension will increase our understanding of molecular mechanisms of these conditions and facilitate the development of effective methods for prevention and intervention of diabetes and hypertension as well as metabolic syndrome. 12884521: The results obtained allowed us to localize the genes responsible for the stress-induced arterial hypertension in the ISIAH rats to the Atp1a1 locus (P < 0.05), chromosome 2 and to the Lngfr gene locus (P < 0.05), chromosome 10. 1361506: To address the issue whether the SA gene is one of the genes responsible for the hypertension of SHR, a genetic cosegregation analysis of the blood pressure values with the genotypes in an F2 rat population was undertaken in this study. Identification of a candidate gene responsible for the high blood pressure of spontaneously hypertensive rats. 14696769: The problem is that, in spite of such substantial contribution, the discovery of the \genes that cause hypertension\ has been quite discouraging. 14769432: We describe approaches others and we have undertaken to investigate gene expression profiles in hypertensive models in order to identify genes that contribute to the pathogenesis of hypertension. The combination of gene expression profiling and the phenotypic characterization of in vitro and in vivo loss or gain of function experiments for candidate genes have the potential to identify genes involved in the pathogenesis of hypertension and may present novel targets for therapy. 14987561: As more effort is made to identify genes responsible for hypertension in human populations and genetically hypertensive animal models, the need for experimental systems in which the functional significance of genes, gene variants, and quantitative trait loci (QTL) can be determined is becoming increasingly important. 15687840: How these genes fit into the complex pathophysiological network that induces hypertension remains unclear. 15710778: Genealogical relationships and SHR substrain intercrosses suggest that genes responsible for heritable hypertension in SHR are shared across SHR substrains. 16076282: It is a well-established fact that genes are involved in the etiology of hypertension. 16275913: Gain-of-function mutations in either of these genes cause an inherited syndrome featuring hypertension and hyperkalemia due to increased renal NaCl reabsorption and decreased K(+) secretion. 16473759: We applied this integrated genomic-transcriptomic approach to identify the genes that are involved in the pathogenesis of hypertension in the Sabra rat model of salt susceptibility. 1889856: Thus most familial aggregation of high blood pressure appears to be due to genes rather than shared family environment. 19143224: It is likely that studies of other genes polymorphisms, genegene interactions and the interaction between genes and--environmental factors lead to the identification of causes of so called spontaneous hypertension. 19943077: Consistent with these findings, targeted ablation of this gene causes severe arterial hypertension and ventricular hypertrophy in mice. 20422737: Although the genes causing hypertension or diabetes await elucidation, the environmental causes of these diseases are well known. 21191291: SUMMARY: The identification of Pdc as a gene for stress-induced hypertension offers new insights into the relationship between sympathetic nervous system activation, blood pressure regulation and genetic factors. 21487032: The present study has identified a diversity of genes and possible mechanisms involved in hypertension etiology and maintenance in the hypothalamus of BPH/2J mice, highlighting both common and divergent processes in each phase of the condition. 2181319: Here we describe the introduction of the mouse Ren-2 renin gene into the genome of the rat and demonstrate that expression of this gene causes severe hypertension. 22124177: The aim of the current study was to identify hypertension-causing genes for each QTL. 22476231: These multilateral approaches identified ATP2B1 as a gene responsible for hypertension in not only Japanese but also Caucasians. 22669047: RECENT FINDINGS: An era of cataloging epigenetic marks of the various diseased states has recently commenced, including those within the genes responsible for atherosclerosis, ischemia, hypertension and heart failure. 22977489: Since it was not always possible to completely demonstrate that these genes are responsible for hypertension in SHRs, further research into true candidate genes that participate in the genesis of hypertension in SHR substrains is warranted. 23346037: In this study, ROS-hypertension-related genes were collected by the biological literature-mining tools, such as SciMiner and gene2pubmed, in order to identify the genes that would cause hypertension through ROS. This study demonstrates that a text mining approach combined with association analysis may be useful to identify the candidate genes that cause hypertension through ROS or oxidative stress. 23525202: Genetic analysis of genes causing hypertension and stroke in spontaneously hypertensive rats. In this study, using these rats, we aimed to identify the genes causing hypertension and stroke, as well as the genes involved in ADHD. 24413707: Identification of these genes enriches the hypertension susceptibility gene list, thereby shedding light on the etiology of hypertension in Han Chinese. 24452243: Thus, in this study, we analyzed gene expression profiles in the brains of SHR in order to identify the genes responsible for causing hypertension and stroke, as well as those involved in ADHD. Analysis of genes causing hypertension and stroke in spontaneously hypertensive rats: gene expression profiles in the brain. The IPA of SHR-specific genes revealed that prostaglandin E receptor 4 (Ptger4) is one of the candidate genes responsible for causing hypertension in SHR, and that albumin (Alb) and chymase 1 (Cma1) are also responsible for causing hypertension in SHR in the presence of angiotensinogen (Agt). 24805951: BACKGROUND: In the 'Millennium Genome Project', we identified ATP2B1 as a gene responsible for hypertension through single-nucleotide polymorphism analysis. 25285356: The further studies of genes differentially expressed in ISIAH and WAG kidney will help to reveal new hypertensive genes and mechanisms specific for stress-induced arterial hypertension. 26165378: Genetic analysis of genes causing hypertension and stroke in spontaneously hypertensive rats: Gene expression profiles in the kidneys. In the present study, we aimed to identify the genes causing hypertension and stroke, as well as the genes involved in ADHD using these rats. 27322299: Hypertension is considered to be the result of genes, environment, and their interactions. 27572673: Less than 50% of those who agreed that genes cause hypertension lost their intention to lower their salt consumption when they found they did not possess the susceptibility gene. Genetic information regarding higher salt sensitivity increased motivation to reduce salt intake for both those who agreed that genes cause hypertension and those who did not. 27900368: Drawing upon clinical presentation, 27 genes were selected evidenced to cause monogenic hypertension and matched to the gene-based results. 28931564: Overall, the collective knowledge gained from rats and humans is disappointing in the sense that major hypertension-causing genes as targets for clinical management of essential hypertension may not be a clinical reality. 29222092: Mutations in the human inwardly rectifying K channel CNJ type (KCNJ) 5 (KCNJ5) gene encoding the G-coupled inwardly rectifying K channel 4 (GIRK4) cause abnormal aldosterone secretion and hypertension. 32630286: Genetic polymorphisms can influence drug responses through genes engaged in the pathogenesis of hypertension that are able to modify the effects of drugs, modifications in drug-gene mechanistic interactions, polymorphisms within drug-metabolizing enzymes, genes related to drug transporters, and genes participating in complex cascades and metabolic reactions. 36381851: The unique changes in the composition of the microbiota, functional changes in genes, and metabolome collectively help for a better understanding of the pathogenesis of HTN and also suggest the gut as a promising new therapeutic target for HTN. 7491928: Furthermore, these models can be used to test the significance of genes and gene variants identified via genome-wide searches as potential causes of hypertension. 8039837: We find neither completely successful, and we advance an alternative explanation of the adaptive importance of genes responsible for hypertension. 8387080: Finding genes that cause human hypertension. 8673114: Finding genes that cause human hypertension is not straightforward, since the determinants of blood pressure in primary hypertension are multifactorial. 8846256: [Research on genes causing hypertension]. 8846501: In search of genes causing spontaneous hypertension. 8997635: Recombinant inbred and congenic strains for mapping of genes that are responsible for spontaneous hypertension and other risk factors of cardiovascular disease. 9395555: Inheritance of high blood pressure is complex, with the gene(s) responsible for hypertension still remaining elusive. 9460275: In the last decade, two types of genes participating in the etiology of hypertension have been identified. 9544872: A genetic epidemiologic approach is useful to elucidate the genes responsible for hypertension. 9823786: The identification of genes responsible for high blood pressure is of major importance, because it provides a mechanistic classification of the common phenotype and guide therapy tailored to the underlying primary abnormality. 9832341: An I/D polymorphism in intron 16 of the gene coding for the angiotensin-converting enzyme (ACE) has been used to study the role of this gene in the aetiology of coronary atherosclerosis and hypertension. 9892728: The availability of such markers may be instrumental in the search for genes responsible for the hypertension. 10195399: Three genes responsible for early-onset autosomal dominant AD have been identified, and one gene, apolipoprotein E, has been confirmed as a susceptibility gene for late-onset forms of the disorder. 10349334: Although these data suggest that accumulation of A beta is an essential step in the pathogenesis of Alzheimer's disease, it still remains to be elucidated whether such process is causative for Alzheimer's disease. Recently another gene on chromosome 12 has been suggested to be involved in the development of late-onset Alzheimer's disease, and identification of the gene on chromosome 12 may bring a new insight into the pathogenesis of Alzheimer's disease. Amyloid precursor protein (APP), presenilin I (PS 1) and presenilin II (PS 2) genes have been identified as the causative genes for early-onset familial Alzheimer's disease. 10404731: The Asn141Ile mutation of the presenilin 2 gene is responsible for familial early-onset Alzheimer disease found in Volga-German kindreds. 10488446: Mutations in any one of three genes can cause autosomal dominant, early-onset Alzheimer's disease: these genes are the amyloid precursor protein (APP) gene on chromosome 21, the presenilin-1 (PS-1) gene on chromosome 14 and the presenilin-2 (PS-2) gene on chromosome 1. 10507458: At least 50 different mutations in the presenilin 1 gene have been shown to cause early onset familial Alzheimer's disease. 10768621: BACKGROUND: Pathogenic mutations in the presenilin 1 (PS1) gene leading to early-onset Alzheimer disease have been described in various populations. 11216203: Rare mutations in at least 3 genes are responsible for early-onset familial AD. 12604663: Discovery of mutations in three genes leading to severe early onset AD was critical in focusing attention on the role of amyloid peptides (Abeta) in neuronal cell death, and enhanced understanding of the biology of these peptides has led to an array of mechanism-based drug discovery strategies. 15010344: Three genes have been implicated in the etiology of early-onset autosomal-dominant Alzheimer disease (AD): the amyloid precursor protein, the presenilin-1, and presenilin-2 genes. 15119738: The beta-amyloid precursor protein (APP) gene (on chromosome 21), Presenilin 1 (PS1) gene (on chromosome 14) and Presenilin 2 (PS2) gene (on chromosome 1) are responsible for autosomal dominant early-onset Alzheimer's disease (EOAD). 15205973: Two siblings with the R269G mutation in the presenilin-1 gene causing early-onset Alzheimer's disease are presented, only the second family with this mutation to be reported. 15654674: With the identification of the genes responsible for autosomal dominant early-onset familial Alzheimer's disease (FAD genes), there is a considerable interest in the application of this genetic information in medical practice through genetic testing and counseling. 16628450: Founder effect for the Ala431Glu mutation of the presenilin 1 gene causing early-onset Alzheimer's disease in Mexican families. 17334805: Three genes have been identified causing earlier onset AD, and a fourth has been shown to be a risk factor for late onset AD (LOAD), while many more yet unrecognized genes are thought to contribute to susceptibility. 17645236: Over 100 mutations in the presenilin-1 gene (PSEN1) have been shown to result in familial early onset Alzheimer disease (EOAD), but only a relatively few give rise to plaques with an appearance like cotton wool (CWP) and/or spastic paraparesis (SP). A single point mutation, p.L420R (g.1508T > G) that gives rise to a missense mutation in the eighth transmembrane (TM8) domain of PS1 was identified in two affected members of the family. p.L420R (g.1508T > G) is the mutation responsible for EOAD, seizures and CWP without SP in this family. 19101658: AD occurs sporadically (SAD), or is caused by hereditary missense mutations in the amyloid precursor protein (APP) or presenilin-1 and -2 (PSEN1 and PSEN2) genes, leading to early-onset familial AD (FAD). 20097758: Four genes have been established to either cause familial early onset AD (APP, PSEN1, and PSEN2) or to increase susceptibility for late onset AD (APOE). 20594621: Three genes have been identified as the cause of early onset familial AD (EOAD). 21463452: Familial forms of CAA are because of mutations in the gene encoding the beta-amyloid precursor protein (APP) and duplications of this gene can cause early-onset Alzheimer's disease associated with CAA. 23575824: We have developed a Tg rat model (line TgF344-AD) expressing mutant human amyloid precursor protein (APPsw) and presenilin 1 (PS1DeltaE9) genes, each independent causes of early-onset familial AD. 25998699: This review summarizes CSF biomarker findings from studies on symptomatic and presymptomatic individuals carrying a mutation in one of the genes known to cause early-onset familial AD or FTD. 27540966: Mutations in the amyloid-beta protein precursor gene (AbetaPP), the presenilin 1 gene (PSEN1) or the presenilin 2 gene (PSEN2) that increase production of the AbetaPP-derived peptide Abeta42 cause early-onset Alzheimer's disease. 29945247: Triplication of APP, a gene on chromosome 21, is sufficient to cause early-onset Alzheimer's disease in the absence of Down syndrome. This indicates that triplication of chromosome 21 genes other than APP is likely to have an important role to play in Alzheimer's disease pathogenesis in individuals who have Down syndrome. 31862541: Genetic variants in presenilin (PSEN) 1 and 2 genes lead to autosomal dominant early-onset AD (ADAD); patients with PSEN gene variants also report seizures. 34193504: Pathogenic variants in the presenilin 1 (PSEN1) gene are the most frequent cause of early-onset AD. 37996068: Mutations in the Presenilin (PSEN) genes are the most common cause of early-onset familial Alzheimer's disease (FAD). 7550356: Genetic linkage studies place a gene causing early onset familial Alzheimer's disease (FAD) on chromosome 14q24.3 (refs 1-4). 8710164: The rat homologue of the presenilin-1 (PS-1) gene, which is responsible for early-onset familial Alzheimer's disease linked to chromosome 14, was cloned and sequenced. 8742474: A series of mutations has been reported in the presenilin-1 (PS-1) gene which cause early onset Alzheimer's disease (AD). 9044502: Genes responsible for the early-onset familial AD have been cloned and found to be membrane associated transport proteins. 9180219: To investigate whether presenilin 1 (PS1) gene, a major causative gene of familial early-onset Alzheimer's disease (AD), also contributes to the etiology of sporadic AD, we evaluated associations between Japanese AD and polymorphisms located at 14q24.3. 9197277: Immunohistochemical analysis of two A beta species (A beta 42/43 and A beta 40) deposition was undertaken using the carboxyl end-specific antibodies to determine the molecular alteration of these species in the brains of patients whose presenilin 1 (PS-1) gene, the major causative gene for the early-onset familial AD, bears the point mutation (H163R) and the deletion of exon 9. 9368568: BACKGROUND AND PURPOSE: An intronic polymorphism of presenilin-1 (PS-1), a gene responsible for early-onset familial Alzheimer's disease, has been reported to be associated with late-onset sporadic Alzheimer's disease. 9834545: The second part describes the three genes, amyloid precusor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) genes, which when mutated cause early-onset autosomal dominant AD. 9852298: Presenilin 2 (PS2) is a gene responsible for the early-onset familial Alzheimer's disease (AD). 9923762: CONCLUSION: These results demonstrate that a missense mutation in a region not conserved between PS1 and PS2 can cause Alzheimer disease. OBJECTIVE: To disclose a novel mutation of the presenilin 1 (PS1) gene responsible for early-onset Alzheimer disease and to clarify genotype-phenotype correlation that should help to establish the function of this protein. 10605685: CONCLUSIONS: The role of molecular diagnosis techniques is essential for the rapid diagnosis of cases of arterial hypertension secondary to familial glucocorticoid remediable aldosteronism. 10618671: Glucocorticoid-remediable aldosteronism (GRA) is a rarely recognised cause of arterial hypertension. This study indicates that GRA can cause severe hypertension even in children, associated with an abolished nocturnal BP fall. 11317201: INTRODUCTION: Glucocorticoid-remediable aldosteronism (GRA) is a rare inherited cause for hypertension associated with a significant morbidity and mortality at an early age. 12442092: Pheochromocytoma, hypercorticism, primary aldosteronism or glucocorticoid-remediable aldosteronism can be present or diagnosed at any term and may cause severe hypertension. Hypertension may be pregnancy-induced, essential or secondary to endocrine disorders. 15128476: Primary aldosteronism, congenital adrenal hyperplasia, Cushing's syndrome, glucocorticoid-remediable aldosteronism, and corticotropin-dependent forms of adrenal pathology can cause hypertension by excessive production of adrenocortical hormones. 16110193: These data suggest that GRA is unlikely to be a common cause of hypertension in Polish subjects. 16480676: Primary aldosteronism, congenital adrenal hyperplasia, Cushing's syndrome, glucocorticoid-remediable aldosteronism, and corticotropin-dependent forms of adrenal pathology can cause hypertension by excessive production of adrenocortical hormones. 18407135: Glucocorticoid-remediable aldosteronism (GRA) is a hereditary cause of human hypertension in which aldosterone secretion is regulated by ACTH. 21565670: Glucocorticoid-remediable aldosteronism (GRA) is a hereditary form of primary hyperaldosteronism and the most common monogenic cause of hypertension. 29445488: Glucocorticoid-remediable aldosteronism is a hereditary form of primary hyperaldosteronism and the most common monogenic cause of hypertension. 7792815: Glucocorticoid-remediable aldosteronism (GRA) is a hereditary cause of human hypertension in which aldosterone secretion is regulated by adrenocorticotropin (ACTH). 7988084: The rare \determinant\ gene for GRA by itself seems to produce severe hypertension and early strokes. 9203188: In particular among these disorders, glucocorticoid remediable aldosteronism (GRA) appears to be emerging as an important etiology of hypertension in the pediatric population. 9851772: Glucocorticoid remediable aldosteronism (GRA) is an autosomal dominant cause of primary aldosteronism and high blood pressure resulting from a chimeric 11beta-hydroxylase/aldosterone synthase gene. 10557325: The expressional down-regulation of endothelial NOS III may contribute to the hypertension caused by glucocorticoids. 10608467: This effect may be important for pharmacological side effects such as glucocorticoid-induced hypertension. 11078386: We therefore sought to determine the effects of glucocorticoids on renal PPET-1, ET(A)- and ET(B)-receptor expression in an animal model of glucocorticoid-induced hypertension. 1115068: It is suggested that glucocorticoid-induced hypertension may be initiated by alterations in vascular responsiveness to pressor agents and that elevated PRS levels may contribute to increase angiotensin formation. Steroid production, plasma renin activity (PRA) and plasma renin substrate (PRS) were measured in eight patients with hypertension due to Cushing's syndrome of benign origin. 11368234: We conclude that inhibition of BH4 synthesis by glucocorticoid regulation of GTP cyclohydrolase expression may contribute to reduced endothelium-dependent vasodilation characteristic of glucocorticoid-induced hypertension. 11379792: OBJECTIVE: The objective was to quantify and to describe microvascular endothelial cell death in glucocorticoid-induced hypertension. CONCLUSIONS: These results suggest capillary structural rarefaction by an increased rate of apoptotic endothelial cell death in glucocorticoid-induced hypertension. 11581014: Excessive exposure to glucocorticoids during late fetal development in the rat causes intrauterine growth retardation (IUGR), together with hypertension and hyperinsulinaemia in adulthood. 11738795: Here data are reviewed which show, in rodents and other model species, that antenatal exposure to glucocorticoids reduces offspring birth weight and produces permanent hypertension, hyperglycaemia, hyperinsulinaemia, altered behaviour and neuroendocrine responses throughout the lifespan. 11903301: Glucocorticoid-induced hypertension: from mouse to man. In both rat and humans, hypertension due to naturally occurring glucocorticoids is not prevented by drugs that block classical glucocorticoid or mineralocorticoid receptors. 11972433: Here data are reviewed which show, in rodents and other models, that antenatal exposure to endogenous or exogenous glucocorticoids reduces offspring birth weight and produces permanent hypertension, hyperglycaemia, hyperinsulinaemia, altered behaviour and neuroendocrine responses throughout the lifespan. 12023661: The nitric oxide system in glucocorticoid-induced hypertension. Recent evidence suggests that the nitric oxide system plays a key role in the hypertension produced by glucocorticoids. 12184988: Because such dysfunction is associated with several forms of adult hypertension, our results indicate the potential for consequences of antenatal glucocorticoid exposure on adult cardiovascular health. 12363278: In this review, the roles of nitric oxide and tetrahydrobiopterin in the pathogenesis of glucocorticoid hypertension will be discussed. Impaired vasodilation and nitric oxide synthase activity in glucocorticoid-induced hypertension. 12723895: The effect of Lisinopril (LS) 15 mg/kg per day and that of combination of LS and ASA; 100 and 25 mg/kg per day p.o. was studied on hypertension induced by glucocorticoid. 12826072: We hypothesize that xanthine oxidase (XO) may be a potential source of oxidants induced by glucocorticoid-induced hypertension. 1320077: OBJECTIVE: The aim of this study was to investigate the role of depressor systems in glucocorticoid-induced hypertension. 14618091: Administration of glucocorticoids results in hypertension, cardiac hypertrophy, and general myopathy. 14687590: The principal mechanism of GC-induced hypertension is overstimulation of the non-selective mineralocorticoid receptor (MR), resulting in renal Na(+) retention, volume expansion and finally to an increase in blood pressure. Cortisol and the renal handling of electrolytes: role in glucocorticoid-induced hypertension and bone disease. The prevention and treatment of GC-induced hypertension and osteoporosis include the use of the minimal effective dose of GC, some general measures, and the use of some specific drugs. 15026174: Excessive glucocorticoid exposure causes central obesity, hypertension, dyslipidaemia and insulin resistance, as seen with elevated plasma cortisol in Cushing's syndrome. 15050533: We conclude that the expressional downregulation of eNOS and the ensuing reduction in vascular NO production contributes to the hypertension caused by glucocorticoids. 15072571: Fetal exposure to excess glucocorticoids reduces birth weight and causes later hypertension. 15117602: Fetal exposure to maternally administered glucocorticoids in late gestation causes fetal hypertension. 15253942: The propensity of glucocorticoids to produce hyperglycaemia, hypertension, dyslipidaemia, and central obesity has long been a cause for concern among physicians regarding possible adverse cardiovascular events. 15379420: HYPOTHESIS: Long-term use of glucocorticoids at supra-physiological doses may result in high BP. 15850085: Increased levels of glucocorticoids (GC) can result in major complications such hypertension and vascular injury. 1625793: These changes suggest significant alterations in the aminergic activity of the brain circuitry known to regulate cardiovascular functions; the changes may play a basic role in the development and maintenance of glucocorticoid-induced hypertension. Brain amines in glucocorticoid-induced hypertension in the rat. 16522724: Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. 16891583: In animal models, prenatal stress, glucocorticoid exposure or inhibition/knockout of 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD-2), the feto-placental barrier to maternal glucocorticoids, reduces birth weight and causes permanent hypertension, hyperglycemia, increased hypothalamic-pituitary-adrenal (HPA) axis activity and behavior resembling of anxiety. 16980206: The various pathogenetic mechanisms that have been proposed for the development of glucocorticoid-induced hypertension in Cushing's syndrome and its management are discussed. 17276352: We conclude that a dynamic interaction between hepatic Ppara expression and a vagal afferent pathway is essential for glucocorticoid induction of diabetes and hypertension. An afferent vagal nerve pathway links hepatic PPARalpha activation to glucocorticoid-induced insulin resistance and hypertension. 1730435: These actions strongly support the mechanism by which the glucocorticoid induced hypertension through the increased sensitivity to vasoconstrictors. One of the mechanisms of glucocorticoid-induced hypertension has been thought to be the enhancement of vascular responsiveness to vasoconstrictors. 17375467: These results -showing ways through which the organism hinders the pathological occupation of mineralocorticoid receptors by glucocorticoids leading to sodium retention and hypertension- prompted the present study on the nature of the above-mentioned extra-adrenal factors. 17389675: Deficiencies in the conversion between active and inactive glucocorticoids in the kidney can lead to hypertension. 17439425: Glucocorticoid-induced hypertension (GC-HT) in the rat is associated with nitric oxide-redox imbalance. We studied the role of xanthine oxidase (XO), which is implicated in the production of reactive oxygen species, in dexamethasone-induced hypertension (dex-HT). 17715567: Humans and animals with GC-induced hypertension exhibit reduced nitric oxide levels; patients with excess GC levels also suffer from depression as a consequence of low levels of serotonin and melatonin. 1795208: The evidence for this view appears strongest for glucocorticoid-induced hypertension, but for most other forms the available data are conflicting and are mostly based on small numbers of patients without adequate control populations. 17954371: ACTH- but not Dex-induced hypertension was partially reversed by aspirin. The aim of the present study was to investigate the effects of aspirin, a potent antioxidant, on adrenocorticotropic hormone (ACTH) and dexamethasone (Dex)-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with increased oxidative stress. Aspirin prevented the development of hypertension caused by ACTH (P' < .01) and tended to prevent Dex-induced hypertension (P' = .07). 18067589: The vasoconstrictor 20-HETE may play a role in the genesis of ACTH-induced hypertension. Arachidonic acid metabolism in glucocorticoid-induced hypertension. 18307745: There is increasing evidence for a role of oxidative stress and nitric oxide deficiency in experimental glucocorticoid-induced hypertension, as evidenced by increased biomarkers of oxidative stress; the effectiveness of antioxidants or reduced NADPH oxidase antagonists in lowering blood pressure; and secondary upregulation of endogenous antioxidant enzymes in response to oxidative stress. Reactive oxygen species and glucocorticoid-induced hypertension. NADPH oxidase plays a significant role in the pathogenesis of glucocorticoid-induced hypertension in the rats, but xanthine oxidase and uncoupled eNOS pathways are not important sources of reactive oxygen species in these models. 18434569: A critical role for vascular smooth muscle in acute glucocorticoid-induced hypertension. Although glucocorticoid (GC)-induced hypertension has commonly been attributed to promiscuous activation of the mineralocorticoid receptor by cortisol, thereby promoting excess reabsorption of sodium and water, numerous lines of evidence indicate that this is not the only or perhaps even the primary mechanism. 18496130: Genetic predictors of glucocorticoid-induced hypertension in children with acute lymphoblastic leukemia. Our aim was to define the frequency of and clinical and genetic risk factors for steroid-induced hypertension. 1893930: Glucocorticoids appear to selectively induce endothelin release from vascular smooth muscle cells and this may be relevant to glucocorticoid-induced hypertension. 1934541: Characterization of alterations of hemodynamics and neuroendocrine hormones in dexamethasone induced hypertension in dogs. Glucocorticoid-induced hypertension mainly depends on the increases in total peripheral resistance but not volume factors. 19458537: The role of 20-hydroxyeicosatetraenoic acid in adrenocorticotrophic hormone and dexamethasone-induced hypertension. HET0016 also prevented the development of hypertension induced by ACTH (P < 0.01). In the present study, we investigated the effect of a specific enzyme inhibitor of 20-HETE production, N-hydroxy-N'-(4-butyl-2-methylphenyl) formamidine (HET0016), on glucocorticoid-induced hypertension in rats, a sodium-independent model. These results suggest that 20-HETE may play a role in the genesis of ACTH-induced hypertension but not in dexamethasone-induced hypertension. 19748967: Chronically elevated glucocorticoids can cause hypertension by acting in the periphery, but their effects within the brain on blood pressure regulation remain largely unexplored. 20186125: NOLA exacerbated dexamethasone-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with imbalance between nitric oxide (NO) and superoxide. Effects of sepiapterin supplementation and NOS inhibition on glucocorticoid-induced hypertension. In the present study, adrenocorticotrophic hormone (ACTH)- and dexamethasone-treated rats were further treated with sepiapterin, a precursor of tetrahydrobiopterin, or N-nitro-L-arginine (NOLA), an inhibitor of NOS, to investigate the role of eNOS uncoupling in glucocorticoid-induced hypertension. Sepiapterin did not prevent ACTH- (129 +/- 4 mm Hg, NS) or dexamethasone-induced hypertension (135 +/- 3 mm Hg, NS), although plasma total biopterin concentrations were increased. These data suggest that eNOS uncoupling does not play a major role in the genesis of glucocorticoid-induced hypertension in the rat. CONCLUSION: Sepiapterin did not prevent ACTH- or dexamethasone-induced hypertension. 20188070: To determine the site(s) of glucocorticoid receptor action relevant to the development of hypertension, we studied glucocorticoid-induced hypertension in a mouse with a tissue-specific knockout of the glucocorticoid receptor in the distal nephron. We conclude that the glucocorticoid receptor in the distal nephron is not necessary for the development or maintenance of dexamethasone-induced hypertension in our model. The glucocorticoid receptor in the distal nephron is not necessary for the development or maintenance of dexamethasone-induced hypertension. We have developed a mouse model of glucocorticoid-induced hypertension, which is dependent on the glucocorticoid receptor. The mechanism of glucocorticoid-induced hypertension is incompletely understood and has traditionally been attributed to promiscuous activation of the mineralocorticoid receptor by cortisol. 2040860: Glucocorticoid-induced hypertension in rats: role of the central muscarinic cholinergic system. These results suggest the presence of an enhanced muscarinic cholinergic activity in several brain nuclei in rats with glucocorticoid-induced hypertension. 20829617: Glucocorticoids cause hypertension through several mechanisms: their intrinsic mineralocorticoid activity; through activation of the renin-angiotensin system; by enhancement of vasoactive substances, and by causing suppression of the vasodilatory systems. 21125154: Long-term use of the glucocorticoids can cause to insulin resistance, hypertension, and obesity, increasing the risk of metabolic syndrome. 21565673: Several pathogenic mechanisms have been proposed for glucocorticoid-induced hypertension, including a functional mineralocorticoid excess state, upregulation of the renin angiotensin system, and deleterious effects of cortisol on the vasculature. 21565674: How do glucocorticoids cause hypertension: role of nitric oxide deficiency, oxidative stress, and eicosanoids. The exact mechanism by which glucocorticoid induces hypertension is unclear. 2172162: Suppression of the ANF-mediated response may play a role in glucocorticoid-induced hypertension. 21744056: Here we review recent developments in our understanding of the pathogenesis of glucocorticoid-induced hypertension. Glucocorticoid-induced hypertension. Glucocorticoid-induced hypertension is a common clinical problem that is poorly understood, thus rendering treatment strategies sub-optimal. In vitro studies in isolated kidney tissues as well as in vascular smooth muscle and vascular endothelial cells have attempted to elucidate the molecular physiology of glucocorticoid-induced hypertension, but have generally been limited by the inability to study signaling pathways in an intact organism. 21953707: These findings suggest that oleanolic acid (60 mg/kg i.p.) prevents dexamethasone-induced hypertension in rats, which may be attributed to its antioxidant and nitric oxide releasing action. (Loranthaceae) in glucocorticoid (dexamethasone)-induced hypertension in rats and to propose a probable mechanism of action for this effect. 23313327: The optimal pharmacological management of patients with glucocorticoid-induced diabetes or hypertension is uncertain. 23533693: The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. CONCLUSION: Glucocorticoid-induced hypertension in rats is prevented by alpha-lipoic acid via mechanisms other than mitochondrial superoxide reduction. AIMS: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition. 23544271: Neither RU486 nor spironolactone affected corticosterone-induced hypertension, whereas spironolactone, but not RU486, attenuated the effects of corticosterone on LV fibrosis and diastolic function. Glucocorticoid-induced hypertension and cardiac injury: effects of mineralocorticoid and glucocorticoid receptor antagonism. Corticosterone induced hypertension, left ventricular (LV) fibrosis, and LV diastolic dysfunction. 24383084: We further investigated whether glucagon-like peptide-2 (GLP-2) was effective for dexamethasone-induced hypertension. Peripheral administration of GLP-2 suppressed dexamethasone-induced hypertension in rats by enhancing inhibitory neuronal activity. In the present study, we investigated the sites associated with dexamethasone-induced hypertension in the central nervous system in rats. AIMS: Dexamethasone-induced hypertension models have been used to study the mechanisms of glucocorticoid induced hypertension, but the role of glucocorticoids in central cardiovascular regulation is not clearly understood. 2509553: Arachidonic acid exerted antihypertensive effects which were marginal initially but significant in the later phase of dexamethasone-induced hypertension (124 +/- 8 versus 139 +/- 8 mmHg in arachidonic acid-treated versus control rats after 7 days of dexamethasone). The goal of the present study was to determine whether dexamethasone-induced hypertension in Wistar rats is due to inhibition of the synthesis of the vasodilator prostaglandin I2 (PGI2) in vivo. The mechanism of glucocorticoid-induced hypertension is not known. 25129992: These results indicate that exogenous glucocorticoids induce hypertension, cardiac remodeling, and diastolic dysfunction in adrenalectomized DS rats fed a high-salt diet. 25204470: This article reviews the pathophysiology, incidence, risk factors, screening, and treatment of glucocorticoid-induced weight gain, lipodystrophy, diabetes, dyslipidemia, hypertension, and cardiovascular events. 25447448: AIMS: Elevated levels of glucocorticoid hormones cause glucose intolerance, visceral obesity, insulin resistance, hypertension, and dyslipidemia. 25461303: Glucocorticoid (GC)-induced hypertension is a common clinical problem still poorly understood. In conclusion, an impairment in EDHF/H2S signaling occurs in earlier state of GC-induced hypertension in rats suggesting that counteracting this dysfunction may be beneficial to manage DEX-associated increase in blood pressure. 2566614: Chronic cortisol treated rats had higher basal diastolic blood pressures after being pithed, suggesting that sympathetic outflow is not required to sustain elevated peripheral resistance in glucocorticoid-induced hypertension. 2580131: To test this hypothesis, we now administered sotalol (300 micrograms) intracerebroventricularly to unanesthetized adrenalectomized rats with glucocorticoid-induced hypertension (this hydrophilic beta-blocking agent does not cross the blood-brain barrier). Blood pressure and heart rate response to central beta-blockade in conscious rats with glucocorticoid-induced hypertension. 25810066: The role of sustained release isosorbide mononitrate on corticosteroid-induced hypertension in healthy human subjects. There is evidence implicating abnormalities in the nitric oxide (NO) pathway in the development of glucocorticoid-induced hypertension (GC-HT). 26139210: OBJECTIVE: Excess glucocorticoids are known to cause hypertension and cardiovascular disease (CVD). 26536898: Cushing's syndrome (CS) is a clinical state caused by chronic excess of glucocorticoid, and results in hypertension, impaired glucose tolerance, and dyslipidemia. 26578982: The increase in AQP2 activity promotes water reabsorption, which may contribute to glucocorticoid-induced water retention and hypertension. 26692754: BACKGROUND: Recently, we have reported antihypertensive activity of oleanolic acid (OA) in glucocorticoid-induced hypertension with restoration of nitric oxide (NO) level. 28228807: For induction of hypertension, Dex was injected subcutaneously for 14 days. These results suggest the antihypertensive and antioxidant effects of PCA against Dex-induced hypertension. The Effect of Protocatechuic Acid on Blood Pressure and Oxidative Stress in Glucocorticoid-induced Hypertension in Rat. 28624548: Bacterially derived glucocorticoid metabolites may cause hypertension in some patients by a similar mechanism. 2965178: Glucocorticoid-induced hypertension in rats has been studied using long-term, low-dose dexamethasone treatment. Glucocorticoid-induced decreases in ANP contrast with ANP increases in response to mineralocorticoid treatment in rats with deoxycorticosterone-induced hypertension. We conclude that low-dose infusions (less than 5 micrograms/day) of dexamethasone are suitable for studying glucocorticoid-induced hypertension without the complications of weight loss that have been reported by others or of the mineralocorticoid-like side effects which endogenous glucocorticoids may exhibit. 29726949: These results may also be relevant for hypertension induced by exogenous glucocorticoids. 2996769: The mechanism of glucocorticoid-induced hypertension is not clarified. 30372885: The aim of this study was to investigate the effect of celecoxib on blood pressure and plasma oxidant/antioxidant status in glucocorticoid-induced hypertension and in co-administration with captopril. 30385711: Salt loading increased BP in both types of offspring, suggesting that elevated hypothalamic Agtr1a expression is epigenetically modulated by excessive glucocorticoid and leads to adult-onset salt-sensitive hypertension. Maternal malnutrition, which causes prenatal exposure to excessive glucocorticoid, induces adverse metabolic programming, leading to hypertension in offspring. 30780842: Glucocorticoid hormones, both naturally occurring and synthetic, have long been recognized as a major cause of hypertension. Current evidence demonstrates the importance of the nitric oxide (NO) system and interactions between NO and reactive oxygen species in the development of glucocorticoid-induced hypertension. Glucocorticoid-induced hypertension and the nitric oxide system. There are well-described experimental models of glucocorticoid-induced hypertension, such as adrenocorticotropic hormone- and dexamethasone-induced hypertension in rats, although the exact mechanism of glucocorticoid-induced hypertension remains unclear. 3099705: [Normalization of renin secretion by neuropeptide Y in adrenalectomized rats with glucocorticoid-induced hypertension]. 31866814: However, chronic use of GCs can lead to hypertension. 32853260: Elevated blood pressure in high-fat diet-exposed low birthweight rat offspring is most likely caused by elevated glucocorticoid levels due to abnormal pituitary negative feedback. 3298796: Mechanisms of glucocorticoid-induced hypertension. 33305250: Primary endpoint is to evaluate whether very early introduction of ITs in GCA minimize the rate of GC-induced adverse events, in terms of infections, new onset systemic arterial hypertension, GC-induced diabetes and osteoporotic fractures. 3346065: Our previous finding that dexamethasone-induced hypertension in rats is associated with enhanced reactivity of mesenteric arteries to arginine vasopressin but not to angiotensin II (Ang II) or norepinephrine has led us to postulate that vasopressin contributes to the development or maintenance of glucocorticoid-induced hypertension. Contribution of vasopressin in dexamethasone-induced hypertension in rats. 3521516: The effect of adrenalectomy on renin secretion was investigated in conscious rats with glucocorticoid-induced hypertension. Regulation of renin secretion in conscious adrenalectomized rats with glucocorticoid-induced hypertension. These findings indicate that the activation of the renin-angiotensin system in adrenalectomized rats with glucocorticoid-induced hypertension is not directly mediated by the development of adrenal failure. 3776438: These studies show that Na+ depletion, but not KCl loading, reduced cortisol induced hypertension in sheep. The effect of sodium depletion and potassium loading on cortisol induced hypertension in sheep. These studies compare the effect of Na+ depletion and potassium (K+) loading on glucocorticoid hypertension induced by cortisol in conscious sheep. Glucocorticoid induced hypertension has been regarded as independent of sodium (Na), in contrast to mineralocorticoid induced hypertension, which is Na+-dependent. 3826386: The downregulation observed would be expected to diminish the ability of ANG II to influence glomerular hemodynamics in models such as mineralocorticoid and glucocorticoid-induced hypertension. 38481602: Objective: This study aimed to determine the predisposing factors for MLF during GC therapy; its association with GC-induced diabetes, hypertension, and dyslipidemia; and its effects on body image. 3864857: The purpose of the study was to clarify the mechanism(s) of glucocorticoid-induced hypertension. 3905217: Despite the diminished levels of vasodilator 2-series prostaglandins, the cod liver oil diet prevented the development of glucocorticoid induced hypertension. It therefore seems unlikely that glucocorticoid induced hypertension is a consequence of inhibition of vasodilator prostaglandin synthesis. Dietary fish oil prevents dexamethasone induced hypertension in the rat. 3910304: Enhanced renin secretion in adrenalectomized rats with glucocorticoid-induced hypertension. These data therefore indicate that in rats with glucocorticoid-induced hypertension the renin-angiotensin system is activated by adrenalectomy, despite the fact that adrenal insufficiency cannot develop. The role of circulating epinephrine in the regulation of renin release was studied in unanesthetized rats with glucocorticoid-induced hypertension. 4030047: Possible alterations in mesenteric vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin and its relationship to prostaglandins in dexamethasone-induced hypertension in rats were investigated. The increase in vascular reactivity to arginine vasopressin during long-term dexamethasone treatment may contribute to the development or maintenance, or both, of glucocorticoid-induced hypertension. 6256112: This helps to explain previous observations of a redistribution of sodium and water to the extracellular compartment in experimental glucocorticoid-induced hypertension. 6342118: Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism. 6441535: [Effect of an antiglucocorticoid steroid on the arterial hypertension induced by glucocorticoids in the rat]. It is suggested that glucocorticoid-induced hypertension may be related to vascular Na pump activation and to the subsequent ionic changes. In contrast administration of a steroid derivative with antiglucocorticoid properties, RU 38486, prevented glucocorticoid-induced hypertension in a large part. 7558228: Enhancement of vascular responsiveness is considered to be one of the major contributing factors observed in glucocorticoid-induced hypertension. 7576399: Glucocorticoid-induced hypertension was seen in 13 patients (37.1%); all patients with hypertension [steroid (glucocorticoid)-induced hypertension (SH(+)) group] received more than 20 mg of prednisolone daily, and BP rose rapidly within a week of commencing glucocorticoid administration. To explore the syndrome of glucocorticoid-induced hypertension in the elderly, we analyzed the clinical findings from 35 patients aged more than 65 years (12 men, 23 women) who received glucocorticoid therapy. Glucocorticoid-induced hypertension in the elderly. In conclusion, although the detailed mechanisms are as yet uncertain, glucocorticoid-induced hypertension occurs often in elderly patients, and is more common in patients with total serum calcium concentrations lower than the normal range, and/or in those with positive family history of essential hypertension. Glucocorticoid-induced hypertension is defined as systolic BP more than 160 mm Hg and/or diastolic BP more than 95 mm Hg after glucocorticoid administration. 7588382: Study on the mechanisms of glucocorticoid-induced hypertension: glucocorticoids increase transmembrane Ca2+ influx in vascular smooth muscle in vivo. We propose that this may be the main pathogenic mechanism of GC-induced hypertension. 7930550: To clarify whether this mechanism participates in glucocorticoid-induced hypertension, we investigated the effect of dexamethasone on the modulation of vascular AT1 receptor messenger RNA (mRNA) expression in rats. Increased expression of vascular angiotensin II type 1A receptor gene in glucocorticoid-induced hypertension. 8179849: Previous studies have indicated that ouabain-sensitive cation transport is increased in arteries obtained from rats with glucocorticoid-induced hypertension. 8199716: The mechanism of glucocorticoid induced hypertension in man remains undefined. 8586809: CONCLUSION: The present data strongly suggest that endogenous glucocorticoid in the central nervous system may not have a role in the regulation of systemic haemodynamics and hormones under resting conditions, but does play an important part during the glucocorticoid excess state, for example glucocorticoid hypertension caused by oral treatment with dexamethasone. OBJECTIVE: To determine whether the central nervous system has a pressor or a depressor role in glucocorticoid-induced hypertension. 8593833: Fetal exposure to excess glucocorticoids reduces birth weight and causes later hypertension. 8829818: Our studies indicate that the following multiple factors are involved in glucocorticoid-induced hypertension in humans and animals: 1) activation of the renin-angiotensin (R-A) system due to an increase in plasma renin substrate (PRS); 2) reduced activity of depressor systems, including the kallikrein-kinin (K-K) system, prostaglandins (PGs), and the endothelium-derived relaxing factor nitric oxide (NO); and 3) increased pressor responses to angiotensin II (Ang II) and norepinephrine. Despite many previous studies, the mechanism of glucocorticoid-induced hypertension remains unknown. It is concluded that the pathogenesis of glucocorticoid-induced hypertension is multi-factorial, involving the various mechanisms described above. Mechanism of glucocorticoid-induced hypertension. 9061651: To address possible mechanisms contributing to the glucocorticoid-induced fetal hypertension, fetal plasma catecholamine levels and changes in fetal femoral haemodynamics were assessed following fetal glucocorticoid treatment. Chronically instrumented, late-gestation fetal sheep were prepared to: (1) characterize cardiovascular, endocrine and behavioural effects of fetal treatment with clinical doses of betamethasone and dexamethasone; (2) define specific differences, if any, in the actions of betamethasone and dexamethasone of measured fetal responses; and (3) assess the contribution of changes in peripheral vascular resistance to the glucocorticoid-induced hypertension. 9858661: Recent studies have shown that exposing rats to excessive glucocorticoids in utero reduces birth weight and causes permanent hypertension and hyperglycaemia in the adult offspring. 12180271: As lithium is a relatively specific inhibitor of glycogen synthase kinase-3 (in comparison with other protein kinases), and other studies also point to a relevant role of this enzyme, we favor the view that glycogen synthase kinase-3 is a crucial element in the pathogenesis of Alzheimer's disease. 1336152: Glycogen synthase kinase-3 induces Alzheimer's disease-like phosphorylation of tau: generation of paired helical filament epitopes and neuronal localisation of the kinase. 14643380: Among the different kinases that are able to phosphorylate tau in these sites, GSK-3 has emerged as a key effector of AD pathogenesis in view of its interaction with many of the proteins involved in the ethiology of AD. 15959856: Activation of glycogen synthase kinase-3 induces Alzheimer-like tau hyperphosphorylation in rat hippocampus slices in culture. 16914869: GSK-3 is essential in the pathogenesis of Alzheimer's disease. 17456772: Glycogen synthase kinase 3 (GSK-3) is a major kinase implicated in the pathogenesis of Alzheimer's disease (AD), and reducing its activity may have therapeutic efficacy. 22966039: Thus the inflammation, insulin resistance, GSK-3, and mitochondrial dysfunction hypotheses are not opposing ideas but stages of the same fundamental, overarching, pathway of Alzheimer's disease pathogenesis. 23621307: In particular, the involvement of GSK-3 in several key pathophysiological pathways leading to AD and neurodegenerative diseases has placed this enzyme in a central position in this disorder. 24099155: In particular, the involvement of GSK-3 in several key pathophysiological pathways leading to AD and neurodegenerative diseases has placed this enzyme in a central position in this disorder. 26562543: In this review, we have enlightened Glycogen Synthase Kinase-3 which has been considered as a concrete cause for Alzheimer's disease. 26708942: This article also highlights Drp1 and its relationships to glycogen synthase kinase 3, cyclin-dependent kinase 5, p53, and microRNAs in AD pathogenesis. 28485573: Dysfunction of glycogen synthase kinase 3 (GSK-3) is implicated in the etiology of Alzheimer's disease, Parkinson's disease, diabetes, pain, and cancer. 31054862: Glycogen synthase kinase 3 (GSK-3) has become known for its multifactorial involvement in the pathogenesis of Alzheimer's disease. 34423266: Glycogen synthase kinase-3 (GSK-3) is a positron emission tomography (PET) imaging target with implications in the pathogenesis of Alzheimer's disease (AD). 37893156: Tau hyperphosphorylation is susceptible to GSK-3, which has led to an emerging hypothesis regarding the pathogenesis of AD. 18473848: Continuous hyperglycemia is a causative factor for diabetic vascular complications, and it enhances the generation of AGEs through the non-enzymatic glycation, thereby being involved in the pathogenesis of AD as well. 19275211: Many of the pathological components of diabetes, atherosclerosis, cancer, macular degeneration, Alzheimer's disease, and even the normal aging process are attributable to AGEs and their potential for aggregate formation in the vasculature. 21264887: Among these compounds, methylglyoxal (MG) can yield advanced glycation end products (AGEs), which are crucial in AD pathogenesis. 23799541: Recent studies have increasingly suggested that a high concentration of advanced glycation end products (AGEs) may be important in AD pathogenesis. 25556063: In conclusion, QFY could attenuate AGEs-induced, Alzheimer-like pathophysiological changes. Qifu-Yin attenuates AGEs-induced Alzheimer-like pathophysiological changes through the RAGE/NF-kappaB pathway. 26045684: RESULTS: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened the escape latency, remarkably increased the number of crossing times, significantly decreased the number of errors, and prolonged the latency in rats with AGE-induced AD. The present study evaluated the neuroprotective effects of PG and its possible neuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. 26587989: However, the role played by AGEs in the pathogenesis of AD remains unclear. 26738988: AGEs and receptor for AGEs (RAGE) play important roles in the pathogenesis of AD. 28210868: Impaired insulin signaling, inflammation, the accumulation of advanced glycation end-products and oxidative stress all play an essential role in the pathogenesis of both AD and diabetic complications. 29885514: Advanced glycation end products (AGEs) are known to play a leading part in the pathogenesis of human diseases, such as diabetes, Alzheimer's disease, lateral sclerosis, and atherosclerosis. 10474021: These results confirm that glycyrrhizin is able to induce hypertension, and provide evidence that it inhibits the transcriptions of both 11beta-HSD2 and CYP11B2 in the vasculature, leading to lower aldosterone and higher corticosterone production in vessels, and increased vasoconstrictor responses to norepinephrine. 11082698: GL and GA sometimes induce edema, hypertension, and hypokalemia in patients treated with higher doses and long-term administration. 11682659: CONCLUSIONS: In GA-induced hypertension, both aldosterone receptor antagonism and endothelin receptor antagonism normalize blood pressure and improve renovascular function and, thus, may represent a new therapeutic approach in cardiovascular disease associated with impaired 11beta-HSD2 activity. The present study investigated the effect of the aldosterone receptor antagonist spironolactone in comparison with the endothelin ET(A) receptor antagonist darusentan on renovascular endothelial function in liquorice-induced hypertension. Influence of aldosterone vs. endothelin receptor antagonism on renovascular function in liquorice-induced hypertension. 11798659: CONCLUSION: These results confirm that glycyrrhizin is able to induce hypertension. 16130766: But long-term excessive intake of GA may cause sodium retention and hypertension. 18693294: Increased renal expression of nitric oxide synthase and atrial natriuretic peptide in rats with glycyrrhizic-acid-induced hypertension. 20229524: However, its use as a cancer chemopreventive agent is rather limited, due to the fact that its principal component, glycyrrhizin, is known to induce hypertension. 20487583: However, chronic licorice consumption can lead to serious side effects due to the presence of considerable quantities of glycyrrhizin, which causes severe hypokalaemia and hypertension. 21429724: Although licorice is known to exert anticarcinogenic effects, it contains large quantities of glycyrrhizin (GL), which causes severe hypertension. 27314329: Because glycyrrhizin induces severe hypokalemia and hypertension, we prepared a hexane/ethanol extract of Glycyrrhiza uralensis (HEGU) that lacks glycyrrhizin, and showed that HEGU induces apoptosis and G1 cell cycle arrest and inhibits migration of DU145 human prostate cancer cells. 29538199: Licorice and glycyrrhizin induced hypertension has been widely reported, yet licorice and glycyrrhizin induced hypertensive crisis has been rarely known. LESSONS: Licorice and glycyrrhizin induced hypertension due to pseudo-hyperaldosteronism has been widely reported, yet only 3 cases reported that excessive consumption of licorice could lead to hypertensive emergencies. 6239715: In unilaterally adreno-nephrectomized rats, GR induced hypertension and hypokalemia as seen in DOC treated rats. 7858558: Role of glucocorticoid in the development of glycyrrhizin-induced hypertension. 11016804: Endothelin-1 (ET-1), one of the endogenous pathological humoral factors of cardiovascular diseases such as hypertension and heart failure, has a strong vasoconstrictive action and could induce hypertension and cardiac hypertrophy. Benidipine could thus be a useful tool for preventing cardiac hypertrophy due to hypertension. 11792993: Mild PPHT is reversible with LiTx, but more severe PPHT is a contraindication to LiTx given the high intraoperative mortality due to heart failure. 18689134: 44.3% presented in Heart failure and causes included Hypertension (14.9%), Cardiomyopathies particularly the dilated type (15.1%), Rheumatic heart disease (6.6%) and Anaemia (7.7%). 21067596: CASE PRESENTATION: We report four patients (a 36-year-old Caucasian female, a 59-year-old White-Asian male, a 64-year-old Caucasian female and a 61-year-old Caucasian female) that developed an intra-abdominal hypertension due to heparin-induced retroperitoneal hematomas after implantation of ventricular assist devices because of heart failure. 21712170: We evaluated all comorbidities such as history of ischemic stroke, coronary artery disease, peripheral arterial disease, chronic obstructive lung disease, hypertension, diabetes mellitus and chronic kidney disease in CHF patients who were hospitalized due to decompensated heart failure in Kocaeli University, Faculty of Medicine's Hospital between January 2003 and July 2009. 21977826: Patients with normal LVEF tended to be older and female and were more likely to have a history of hypertension whereas patients with reduced LVEF had a longer history of heart failure due to dilated cardiomyopathy or valvular heart disease. 22763603: After starting hemodialysis, manifestations of hypertension and renal failure improved, but he died at 6.8 years of age as a result of respiratory failure and heart failure. 23591024: Existing epidemiologic and clinical trial data suggest that the blood pressure in patients with hypertension at high risk for cardiovascular events because of coronary artery disease, diabetes mellitus, chronic kidney disease, stroke, or heart failure should be reduced to <140/90 mm Hg in patients younger than 80 years and the systolic blood pressure be reduced to 140-145 mm Hg if tolerated in patients aged 80 years and older. 24794785: CASE REPORT: A 88-years-old female (body-mass-index = 19.95) with AF, hypertension and diabetes mellitus, hospitalized because of heart failure and a non-convulsive epileptic state, was treated by valproate, mirtazepin, nebivolol, digitoxin, lisinopril, gliclazide and amlodipine. 26771977: Currently, research connected with the CB is focused on establishing the significance of chronically increased activity of the CB in the progression of heart failure and in the genesis of hypertension. 28790111: Here, we report for the first time the potent antimyeloma activity of amiloride, an old potassium-sparing diuretic approved for the treatment of hypertension and edema due to heart failure. 33654248: Thus, natriuresis due to hypertension and hydrodiuresis due to heart failure may cause nocturia, which can effectively be treated by the administration of thiazide diuretics and loop diuretics in the morning, respectively. 34229732: Amiloride, a diuretic drug, is clinically used for treatments of hypertension and edema due to heart failure. 37843942: Treatment of hypertension reduces morbidity and mortality due to coronary artery disease, myocardial infarction, heart failure, stroke, and chronic kidney disease. 6464439: Those changes are associated with the post-capillary alveolar hypertension and the interstitial lund changes, preconditioned by it as a result of latent cardiac insufficiency of left ventricle and the following disorder of intrapulmonary circulation. 11258753: The peripheral and central nervous system are harbouring herpes simplex virus type 1 (HSV-1) and this virus has been proposed to be implicated in the aetiology of Alzheimer's disease (AD). 15607565: To further examine the role of HSV-1 in the etiology of AD, we have formulated a Neuroinvasive Score that quantifies the presence and viral load of HSV-1 in eight brain regions. 17725689: There is growing evidence that herpes simplex virus type 1 (HSV-1), together with the apolipoprotein E 4 (APOE4) allele, contribute to the pathogenesis of Alzheimer's disease (AD), although the mechanism of their interaction remains uncertain. 18300070: Following the authors' previous studies implicating herpes simplex virus type 1 (HSV1) in brain of APOE-epsilon 4 carriers as a major cause of AD, the authors propose here, on the basis of their and others' recent studies, that not only does HSV1 generate the main components of amyloid plaques and neurofibrillary tangles (NFTs) - beta-amyloid (A beta) and abnormally phosphorylated tau but also, by disrupting autophagy, it prevents degradation of these aberrant proteins, leading to their accumulation and deposition, and eventually to AD. 19542624: There is growing body of evidence for the involvement of herpes simplex virus type 1 (HSV1) in the etiology of Alzheimer's disease (AD). 20450378: Herpes simplex virus type 1 persists in the brain of most aged individuals and may contribute to the pathogenesis of Alzheimer's disease. 20674092: These findings indicate that HSV-1 causes functional changes in cortical neurons that promote APP processing and Abeta production, and they are compatible with the co-factorial role for HSV-1 in the pathogenesis of AD suggested by previous findings. 21085580: Epidemiological and experimental findings suggest that HSV-1 might contribute to the pathogenesis of Alzheimer's disease (AD). 22252837: Given that HSV-1 is considered a risk factor for AD, our results suggest a new way in which to understand the relationships between HSV-1 infection and the pathogenic mechanisms leading to AD. 22475795: Moreover, HSV-1 has been related to the pathogenesis of Alzheimer's disease. 25963683: Herpes simplex virus-1 has been proposed as potential cause of AD because of its ability to form beta amyloid(Abeta) and neurofibrillary tangles due to tau hyperphosphorylation and action of beta & gamma secretase on amyloid precursor protein(APP) together with genetic association with apolipoprotein-E4(ApoE-E4), which points out to latent Herpes Simplex virus-1 as an agent causing AD. 26401998: Herpes Simplex Virus Type 1 and Other Pathogens are Key Causative Factors in Sporadic Alzheimer's Disease. 27470229: These results reinforce the hypothesis for a role for HSV-1 in the pathogenesis of AD. 27664135: Herpes simplex virus (HSV) type 1 affects a majority of the population and recent evidence suggests involvement in Alzheimer's disease aetiology. 28765170: Recent studies that provide further support for the occurrence of repeated reactivation of latent HSV1 in the brain in AD pathogenesis are also discussed.-Itzhaki, R. 29559905: Studies are reviewed supporting subclinical chronic reactivation of latent HSV-1 in the brain as significant in the pathogenesis of AD. This review focuses on research in the areas of epidemiology, neuropathology, molecular biology and genetics that implicates herpes simplex virus type 1 (HSV-1) as a causative agent in the pathogenesis of sporadic Alzheimer's disease (AD). 30250480: Itzhaki presented her work on the role of viruses, specifically HSV-1, in the pathogenesis of AD. 31455413: Several evidences suggest that, together with inflammation, an immunological response incapable to counteract HSV-1 reactivation plays a role in the pathogenesis of Alzheimer's (AD) and Parkinson's (PD) diseases. 9219743: CONCLUSION: The presence of one neurotropic virus--HSV1--and the absence of another--VZV--in aged human brains is consistent with a role for HSV1 in the aetiology of Alzheimer's disease. 9789723: In this review, we consider the arguments implicating HSV1 in the pathogenesis of AD. 1328375: DESIGN: Recent studies suggest that Ca-regulating hormones may contribute to the genesis of hypertension. 2846456: Moreover, increased pressure conditions during diving caused significantly higher secretion rates of all of these hormones, resulting in a higher systolic blood pressure. 28971835: Here I describe how those ideas led to the discovery that the CTS-like hormone is endogenous ouabain (EO), a key factor in the pathogenesis of hypertension and heart failure. 29087170: If the tumor is functional, it may produce?hormones causing symptoms such as high blood pressure, low potassium level, heart palpitations, nervousness, feelings?of anxiety or panic attacks, excessive perspiration, diabetes, Cushing syndrome, unexplained weight gain or weight loss,?weakness, abdominal stretch marks, excessive hair growth, changes in genitalia, change in libido, etc. 3514449: The studies were performed in dogs to determine the extent to which moderately inappropriate elevations of these hormones could enhance each other's ability to produce chronic hypertension and influence Na and water homeostasis. 3945215: The major cardiovascular problems are those of hormone-induced hypertension, deep vein thrombosis, coronary artery disease, and stroke. 4025541: Because neural actions of ANG II are thought to contribute importantly to the ability of this hormone to cause chronic hypertension, the purpose of the present experiments was to explore the cardiovascular effects of chronic administration of ANG III either into the bloodstream or directly into the brain via the cerebral ventricles. 6954833: The PGF2 alpha-metabolite as hormone and partly PGE in the kidneys seem to be involved in the pathogenesis of arterial hypertension as compensatory factors. 7862590: [Role of opioid receptors and hormones participating in volemic regulation in pathogenesis of arterial hypertension in patients with glomerulonephritis and pyelonephritis]. 8196287: The pathogenesis of hypertension induced by recombinant human erythropoietin (rHuEPO) remains a subject of intense interest. Antiplatelet therapy and development of hypertension induced by recombinant human erythropoietin in uremic patients. Since the antiplatelet drugs used in this study did not have a significant hemodynamic effect, we infer that changes in platelet aggregability induced by rHuEPO may be involved in the pathogenesis of hypertension induced by this hormone. 8911713: Despite strong evidence that the renal medulla releases a vasodepressor hormone in response to increased renal perfusion pressure, much is still to be determined regarding the physiology of this hormone and its involvement in the aetiology of hypertension. 10694834: The mechanism of cortisol-induced hypertension remains unknown. 10760070: In AME, compromised 11betaHSD2 enzyme activity results in overstimulation of the MR by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. 10824333: Congenital deficiency of 11 beta-HDS2 results in inappropriate activation of the renal mineralocorticoid receptor by cortisol, leading to hypertension, hypokalaemia and metabolic alkalosis. 11082157: 11beta-Dehydrogenation, converting cortisol to its inactive metabolite, cortisone, mediated by vascular 11beta-hydroxysteroid dehydrogenase type 2 is essential for the control of vascular tone, and the reduced activity may be relevant to the pathogenesis of hypertension. Therefore, the present study provides important information for understanding the mechanism of ACTH-induced hypertension. 11212969: CONCLUSION: Cortisol-induced hypertension is accompanied by a fall in plasma nitrate/nitrite concentrations. OBJECTIVE: The aim of this study was to determine whether cortisol-induced hypertension can be reversed by co-administration of oral L-arginine. 11751713: Loss-of-function mutations or inhibition of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD-2) results in overstimulation of the mineralocorticoid receptor by cortisol and causes salt-sensitive hypertension. 12707296: L-arginine transport in humans with cortisol-induced hypertension. 12911547: The decreased activity of 11beta-HSD2 increases the intracellular availability of cortisol, which might be relevant for the pathogenesis of hypertension and preeclampsia. 15004413: Glycyrrhizic acid (GA) inhibits the activity of 11beta-hydroxysteroid dehydrogenase type 2 in the kidney, with the resulting increase in intrarenal cortisol concentration leading to hypertension and suppression of the renin-aldosterone system. 15134813: Mutations in the gene encoding 11beta-HSD2 (HSD11B2) account for an inherited form of hypertension, the syndrome of \Apparent Mineralocorticoid Excess\ (AME) where cortisol induces hypertension and hypokalaemia. 15199296: Overexpression of 11beta-HSD1 specifically in adipose tissue in mice caused central obesity, a metabolic syndrome and hypertension due to increased intracellular cortisol concentrations. 15543761: These data suggest a potential influence of cortisol in the genesis of hypertension. 15743397: If cortisol-induced hypertension is mediated by suppression of NO activity in humans, it seems likely that these changes take more than 3 h to become detectable. 15810994: Taken together with our previous observations that sympathetic activity is unaltered or reduced by cortisol, these results suggest that cortisol induced hypertension in humans is not a result of overactivity of the autonomic nervous system. Ganglion blockade does not prevent cortisol-induced hypertension in man. 16778331: In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. 16893715: Although initial studies in transgenic mice and humans are encouraging, more data are required to conclusively prove the hypothesis that the adipose-tissue-specific overexpression of HSD1 and the resultant increase in tissue-specific cortisol concentrations result in human obesity, insulin resistance, high blood pressure, and metabolic syndrome. 17558491: CONTEXT: Changes in cortisol metabolism due to altered activity of the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD) have been implicated in the pathogenesis of hypertension, obesity and the metabolic syndrome. 17973874: Decreased threshold for the nitric oxide donor glyceryl trinitrate in cortisol-induced hypertension in humans. Decreased nitric oxide (NO) availability is thought to be a feature of cortisol-induced hypertension in humans. 19909806: In AME, compromised 11betaHSD2 enzyme activity results in activation of the MR by cortisol, causing sodium retention, hypokalaemia, and salt-dependent hypertension. 2172062: Patients with apparent mineralocorticoid excess (AME) have low or absent activity of the enzyme 11 beta OH steroid dehydrogenase (11SD), and inappropriately high intrarenal levels of cortisol resulting in Na+ retention and hypertension. 2558818: Neurocirculatory regulation in cortisol-induced hypertension. 2722224: Hydrocortisone-induced hypertension in humans: pressor responsiveness and sympathetic function. 3776438: These studies show that Na+ depletion, but not KCl loading, reduced cortisol induced hypertension in sheep. The effect of sodium depletion and potassium loading on cortisol induced hypertension in sheep. These studies compare the effect of Na+ depletion and potassium (K+) loading on glucocorticoid hypertension induced by cortisol in conscious sheep. Glucocorticoid induced hypertension has been regarded as independent of sodium (Na), in contrast to mineralocorticoid induced hypertension, which is Na+-dependent. 533676: Cortisol at 20 mg/hr produced hypertension (MAP + 25 mm Hg on day 5, p less than 0.01) but also produced the 'mineralocorticoid' effect of severe hypokalaemia. These results supported the contention that ACTH induced hypertension in sheep represents a mechanism different from a simple 'mineralocorticoid' or 'glucocorticoid' action. 6237583: We measured dehydroisoandrosterone sulfate, cortisol, and lipoprotein-cholesterol in umbilical cord plasma of newborn infants delivered (30 to 41 weeks' gestation) of 120 women whose pregnancies were uncomplicated and of 98 women with pregnancy-induced or long-term hypertension. 7145656: Excessive cortisol production is probably the main cause of hypertension, but the precise pathophysiological mechanism is controverted. 7473517: We have clear evidence from a number of studies that cortisol-induced hypertension is modulated by, but not dependent on, exogenous sodium. Experimental studies on cortisol-induced hypertension in humans. 7792821: Although cortisol-induced hypertension is characterized by sodium retention and volume expansion, studies with synthetic glucocorticoids or sodium restriction suggest that the hypertension is, to a substantial degree, independent of sodium and volume. Mechanisms of cortisol-induced hypertension in humans. 7917157: The hypothesis that cortisol-induced hypertension might be secondary to steroid-induced hyperinsulinemia was examined by determining whether reversal of hyperinsulinemia by octreotide would reverse cortisol-induced hypertension. Thus, octreotide was effective in lowering plasma insulin concentrations but di not lower blood pressure in normal subjects with cortisol-induced hypertension. These data do not support the notion that steroid-induced hyperinsulinemia is responsible for steroid-induced hypertension. 7955553: Neuropeptide Y in cortisol-induced hypertension in male volunteers. These data do not support a role for sympathetic activation in the genesis of cortisol-induced hypertension. 8252105: [The Ca2(+)-binding capacity of the thrombocytes in rats with hydrocortisone-induced steroid hypertension]. 8507448: Hydrocortisone-induced hypertension in men. 9034789: This deficiency allows mineralocorticoid receptors to be occupied by cortisol, leading to hypertension, because plasma concentrations of cortisol are much higher than those of aldosterone. 9043802: We investigated the role of the autonomic nervous system (ANS) in cortisol induced hypertension using the technique of total autonomic blockade (AB). Autonomic blockade amplifies cortisol-induced hypertension in man. 9120683: Dose-response relationships and mineralocorticoid activity in cortisol-induced hypertension in humans. Spironolactone blocked the mineralocorticoid effects of cortisol but not the blood pressure rise, suggesting that these mineralocorticoid effects are not responsible for cortisol-induced hypertension. OBJECTIVE: This study was designed to define the dose-response relationships for cortisol-induced hypertension in humans and to test the hypothesis that cortisol-induced hypertension is a consequence of classical mineralocorticoid actions using the mineralocorticoid antagonist spironolactone. 9140709: Reflex sympathetic function in cortisol-induced hypertension in humans. 9247761: Cortisol induced hypertension cannot be explained by increases in vasopressor or decreases in vasodepressor hormone concentrations, or by any increase in sympathetic nervous activity. Our working hypothesis is that cortisol induced hypertension is a consequence of increases in renal vascular resistance. 9807669: These data support a role for the NO system in cortisol-induced hypertension in humans. The nitric oxide system and cortisol-induced hypertension in humans. 9809193: Co-administration of the type I (mineralocorticoid) receptor antagonist spironolactone does not prevent the onset of cortisol-induced hypertension. Cortisol-induced hypertension is accompanied by a significant sodium retention and volume expansion. Direct and indirect measures of sympathetic activity are unchanged or suppressed during cortisol administration, suggesting that cortisol-induced hypertension is not mediated by increased sympathetic tone. 9858113: We conclude that cortisol-induced hypertension is not due to increased muscle sympathetic vasomotor drive. AIM: This study was undertaken to test the hypothesis that increased sympathetic vasomotor drive is responsible for cortisol-induced hypertension. Muscle sympathetic vasoconstrictor activity in hydrocortisone-induced hypertension in humans. 1172830: Hypertension resulting from hydronephrosis. 13116007: [Angor and hypertension secondary to hydronephrosis, with recovery after nephrectomy; drop in beta globulins after operation]. 13356040: Hypertension due to hydronephrosis: relief after nephrectomy. 13697970: [Arterial hypertension caused by hydronephrosis (pvelo-ureteral stenosis treated by pveloplasty)]. 14947547: [Surgical treatment of a case of permanent hypertension caused by unilateral hydronephrosis and hypertensive paroxystic crisis due to homolateral adrenal hematoma]. 16646311: In this particular case hypertension develops as the result of renal hypoperfusion and subsequent activation of the renin-angiotensin-aldosterone system, caused by hydronephrosis and compression of renal vessels by pathologic tissue. 16794495: BACKGROUND: Hypertension is a common disease in the Western world and approximately 5% of all cases are secondary to kidney malfunction. Hydronephrosis causes salt-sensitive hypertension in rats. 17280558: CONCLUSION: Hydronephrosis in rats causes salt-sensitive hypertension that can be markedly reduced by removing the hydronephrotic kidney or relieving the obstruction by ureterovesicostomy. 17305709: Hydronephrosis causes salt-sensitive hypertension and impaired renal concentrating ability in mice. AIM: Hypertension is a common disease in the industrialized world and approximately 5% of all cases are secondary to kidney malfunction. We have recently shown that hydronephrosis due to partial unilateral ureteral obstruction (PUUO) causes salt-sensitive hypertension in rats. 19403858: Hydronephrosis causes renal dysfunction and salt-sensitive hypertension, which is associated with nitric oxide deficiency and abnormal tubuloglomerular feedback (TGF) response. 22878855: The speed of resolution of hypertension following relief of obstruction suggests that humorally mediated vasoconstriction can play an important role in the mechanism by which hydronephrosis causes hypertension. Hypertension secondary to hydronephrosis is not commonly reported in the medical literature. 25852907: A consistent percentage of patients affected by ECD develop renal failure and hypertension as a consequence of renal artery stenosis and hydronephrosis. 2699010: Thus we conclude that in young people, asymptomatic unilateral hydronephrosis can lead to hypertension and renal failure like renal artery stenosis. 30293474: We have previously demonstrated in animals and in pediatric patients that hydronephrosis causes hypertension, which was attenuated by surgical relief of the ureteropelvic junction (UPJ) obstruction. 30381529: Long-standing untreated VUR results in renal scarring and hydronephrotic changes ultimately leading to chronic renal failure and arterial hypertension. 32318499: Hypertension secondary to hydronephrosis is rarely described in clinical studies. Initial evaluation for a secondary cause of hypertension was negative. 34400099: In addition, some urological disorders such as hydronephrosis can cause hypertension due to an increase in intraglomerular pressure that activates the renin angiotensin system. 3780805: A case of hypertension secondary to unilateral hydronephrosis due to congenital obstruction of ureteropelvic junction in a 6-year-old boy is reported. A case of hypertension due to unilateral hydronephrosis in a child. 4728410: [Successful surgical treatment of unilateral hydronephrosis associated with polyglobulia, causing hypertension]. 6854804: We review the literature regarding ureteral valves and discuss the mechanism by which unilateral hydronephrosis probably produces hypertension. 7003901: Hypertension with elevated renal vein renin secondary to unilateral hydronephrosis. A case of hypertension secondary to unilateral hydronephrosis is reported. 7005461: This unique case is discussed and the literature regarding hypertension secondary to hydronephrosis is reviewed. Hypertension secondary to massive upper pole hydronephrosis. Hypertension secondary to hydronephrosis is uncommon, and when a duplex system is involved it is rare. 11896504: Primary aldosterone excess or hyperaldosteronism is an important cause of hypertension which, when associated with an aldosterone secreting adenoma, is amenable to surgical cure. 12468575: These data provide strong evidence that hyperaldosteronism is a common cause of resistant hypertension in black and white subjects. 12589175: PURPOSE OF REVIEW: Hyperaldosteronism in its various forms is a recognized secondary cause of hypertension, yet the frequency of these disorders and the appropriate evaluation of suspected patients remain controversial. 13485616: [Adrenalectomy in a case of severe arterial hypertension caused by probable aldosteronism]. 14503982: Hyperaldosteronism represents one of the few treatable causes of hypertension and a systematic approach is therefore needed to ensure that the few patients with an aldosterone-secreting adrenal adenoma are identified. Primary hyperaldosteronism is an important cause of hypertension. 15218335: A 26-year-old woman presented with hypokalemia and hypertension due to hyperaldosteronism. 16814132: BACKGROUND: Uncontrolled hypertension (UH) may be caused by hyperaldosteronism, and some experts recommend the routine use of aldosterone antagonists in this condition. 18326968: Hyperaldosteronism is now recognized as the most common cause of resistant hypertension, and all patients with resistant hypertension should be screened with a plasma aldosterone/renin ratio even if the serum potassium level is normal. 18437332: Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats. 18689909: We describe a case of hypokalaemic hypertension due to hyperaldosteronism caused by a unilateral adrenocortical tumour with unfavourable histopathology suggestive of malignancy. 19253285: Despite equivalent systemic HTN produced by chronic hyperaldosteronism, 114 unique proteins were altered in Kir6.2-KO compared to WT hearts. KCNJ11 null mutants, lacking Kir6.2 ATP-sensitive K(+) (K(ATP)) channels, exhibit a marked susceptibility towards hypertension (HTN)-induced heart failure. 19496385: Truly drug-resistant hypertension is commonly caused by chronic kidney disease, obstructive sleep apnea, or hyperaldosteronism, all of which can lead to fluid retention. 19556540: We conclude that the majority of the hypertension of Kcnmb1(-/-) is due to aldosteronism, resulting from renal potassium retention and hyperkalemia. 22447138: Familial hyperaldosteronism (FH) encompasses 3 types of autosomal dominant hyperaldosteronisms leading to inheritable hypertension. FH type II (FH-II), undistinguishable from sporadic hyperaldosteronism, represents the most frequent cause of inheritable hypertension and is believed to only manifest in adults. 23092384: Hyperaldosteronism as a common cause of resistant hypertension. 2388399: The association is not clear in this case, but there is a possibility that myocardial hypertrophy was deteriorated with hypertension caused by aldosteronism. 25108298: BACKGROUND: Spironolactone is often used to treat hypertension caused by hyperaldosteronism, and as a result, can form concentrically laminated electron dense spironolactone body inclusions within the adrenal gland. 27222295: Aldosterone plays an important role in regulating ion and fluid homeostasis and thus blood pressure, and hyperaldosteronism results in hypertension. 29352074: Hyperaldosteronism, a common cause of hypertension, is strongly connected to Na+, K+, and Mg2+ dysregulation. 29538199: Licorice and glycyrrhizin induced hypertension has been widely reported, yet licorice and glycyrrhizin induced hypertensive crisis has been rarely known. LESSONS: Licorice and glycyrrhizin induced hypertension due to pseudo-hyperaldosteronism has been widely reported, yet only 3 cases reported that excessive consumption of licorice could lead to hypertensive emergencies. 31911970: Hypertension was caused by primary hyperaldosteronism due to an adenoma of the adrenal gland. Hyperaldosteronism causes arterial hypertension and might predispose to stroke, atrial fibrillation, and heart failure. 3476050: The hypertension was found to be secondary to hyperaldosteronism from a well differentiated adrenocortical carcinoma. 35384577: RfHTN is largely attributable to increased sympathetic activity, unlike RHTN, which is mainly due to increased intravascular fluid volume frequently caused by hyperaldosteronism and chronic excessive sodium ingestion. 37198444: Mineralocorticoid receptor-associated hypertension is a broad concept of hypertension that includes not only PA, but also hypertension caused by borderline aldosteronism, obesity, diabetes, and sleep apnea syndrome. 37906287: Mineralocorticoid excess commonly leads to hypertension and kidney disease. 3895890: Herein, we describe two infants (ages 4 and 5 months, respectively) with sustained hypertension and low PRA secondary to dexamethasone-suppressible hyperaldosteronism. 4720573: [Significance of hyperaldosteronism in the pathogenesis of arterial hypertension in pheochromocytoma]. 6101532: Diffuse renal vasculitis with secondary hyperreninemia and hyperaldosteronism appears to be an important cause of hypertension in patients with systemic necrotizing vasculitis. 7033569: Hyperaldosteronism was established as the cause of the hypertension by observing suppressed plasma renin activity and nonsuppressible plasma aldosterone concentration. 15217180: Acute hypercalcemia-induced hypertension: the roles of calcium channel and alpha-1 adrenergic receptor. OBJECTIVE: To study the mechanism(s) of acute hypercalcemia-induced hypertension in dogs. 16538974: Hypercalcemia may also provoke acute renal failure (ARF) or hypertension, or aggravate the tubular necrosis that is frequently found in cases of ARF. 1848266: We conclude that hypercalcaemia-induced hypertension is caused by direct effects of calcium on arterial smooth muscle. 19715927: Hypercalcemia per se causes hypertension. 2645906: In apparent contrast with the notion that hypercalcemia can cause hypertension, more recently it has been proposed that calcium deficiency may be important in the genesis of hypertension both in humans and in spontaneously hypertensive animals. 29658374: Hypercalcemia-induced hypertension and polyhydramnios ameliorated before C-section was performed two weeks later and unrelated to the intervention. 31588082: A 77-year-old man with a history of hypertension, prostate hyperplasia, and urolithiasis was admitted for acute kidney injury caused by hypercalcemia. 3706544: However, in chronic renal failure (CRF) and secondary hyperparathyroidism, the hypercalcemia-induced hypertension is more severe. 6859080: The mean serum calcium levels in the normotensive and hypertensive patients were very similar (11.6 +/- 0.1 [SEM] mg/dl, and 11.8 +/- 0.1), ruling against the hypothesis that hypercalcemia per se is the dominant cause of the hypertension of hyperparathyroidism. 8475626: Thus, hypercalcemia seems to be mainly responsible for hypertension in primary hyperparathyroidism. 10082486: Hyperglycemia causes capillary vasodilation and high glomerular capillary hydraulic pressure, which lead to glomerulosclerosis and hypertension in type 1 diabetic subjects. 11906471: Hyperglycaemia can lead to hypertension in long- standing diabetes through cumulative effects to cause progressive glomerular injury. We have reported recently that onset of hyperglycaemia causes severe hypertension in rats that are treated chronically with N(G)-nitro-L-arginine methyl ester and the hypertension is accompanied by a progressive increase in AngII and absence of hyperfiltration. 15185899: Diabetic patients have an increased risk of coronary disease partly due to a higher frequency of associated risk factors including hypertension and hyperlipidemia but also from specific risks largely resulting from insulin resistance, hyperinsulinemia and hyperglycemia. 15287987: These conditions such as hypertriglyceridemia, hypercholesterolemia, obesity, and hyperglycemia might induce hypertension through various mechanisms. 17217745: CONCLUSION: Except for age and hypertension, risk factors were all induced by hyperglycemia. 18607151: Associated hyperinsulinemia, hyperglycemia, and elevated adipokine levels (adipose cytokines) lead to vascular endothelial dysfunction, an abnormal lipid profile, hypertension, and vascular inflammation, all of which promote the development of atherosclerotic cardiovascular disease. 2075280: This paper synthesizes the pathogenic steps of arterial hypertension in diabetes mellitus: hyperosmolarity due to the hyperglycemia and increased sodic tubular reabsorption accounting for the expansion of the extracellular volume with hypervolemia; abnormalities of the ionic membrane pumps leading to abnormal intracellular calcium distribution, thereby inducing an increased vascular tone; atypical vasomotor reactivity to cathecolamines; modifications of the renin-angiotension-aldosterone system. The pathophysiological derangements by which hypertension could induce nephropathy are examined: the vasodilatation which can be detected from the onset of diabetes, may be a determinant in the transmission of systemic hypertension to the glomerular microcirculation with resulting enhancement of the hydrostatic transglomerular pressure gradient (i.c. the major factor producing glomerular injury), glomerular plasmatic flow and filtration rate. 22617754: PURPOSE OF REVIEW: Type 2 diabetes mellitus (T2DM) and related syndromes exhibit a deadly triad of dyslipoproteinemia, which leads to atherosclerosis, hyperglycemia, which causes microvascular disease, and hypertension. 24812425: These data identify a novel mechanism, Nrf2-mediated stimulation of intrarenal Agt gene expression and activation of the renin-angiotensin system, by which hyperglycemia induces hypertension and renal injury in diabetic mice. 28476968: Hyperglycaemia leads to cataracts, oedema, hypertension, polyuria, and polydipsia. 28556994: Hyperglycaemia during pregnancy induces vascular dysfunction and hypertension in male offspring. Exposure to maternal hyperglycaemia induces hypertension and vascular dysfunction in adult male offspring. We demonstrated that hyperglycaemia in pregnant rats induced vascular dysfunction and hypertension only in male offspring. 29114945: Hyperglycaemia induced by chronic i.p. and oral glucose loading leads to hypertension through increased Na+ retention in proximal tubule. 8720605: Furthermore, these data do not indicate a major role for hyperglycaemia and hyperinsulinaemia per se in the aetiology of hypertension and suggest that IGT and hypertension share one or more pathogenetic factor(s) (i.e., insulin resistance, hyperactivity of the sympathetic nervous system, etc.), which induce deterioration of blood pressure control first, and hyperglycaemia later. 10354294: BACKGROUND: Insulin resistance and hyperinsulinemia induce glomerular hypertension and hyperfiltration, which may result in glomerulosclerosis. 10466472: BACKGROUND: It has been suggested that hyperinsulinemia and insulin resistance participate in the pathogenesis of hypertension, in part by activating sympathetic activity. 10691995: It appears unlikely, however, that hypertension is a direct consequence of hyperinsulinaemia. CONCLUSION: The data are consistent with the concept that hypertension and insulin resistance are a characteristic consequence of the genetic constellation leading to obesity in the NZO strain, and that these traits reflect related mechanisms. 11057433: OBJECTIVE: To clarify the role of insulin resistance and hyperinsulinaemia in the pathogenesis of obesity-related hypertension. 11352784: Chronic exogenous hyperinsulinaemia-induced hypertension in pregnant rats: effect of chronic treatment with l-arginine. 11368463: These data suggest that, in vivo, the mechanisms of hyperinsulinemia-induced hypertension are not operative in the face of pre-existing insulin resistance in obese Zucker rats. 11475857: Obesity, insulin resistance and hyperinsulinaemia are responsible for hypertension in diabetes mellitus type 2. 12877091: Some mechanisms are reported in the conditions of hyperinsulinemia to induce hypertension and atherosclerosis. 1332021: This common association has prompted the hypothesis that hyperinsulinemia may be a causative factor rather than the consequence of obesity, diabetes, hypertension, and hyperlipidemia. 1509713: The authors analyze mechanism by which hyperinsulinism causes NIDDM, hypertension, hyperlipoproteinaemia and hirsutism (5H syndrome). 15185899: Diabetic patients have an increased risk of coronary disease partly due to a higher frequency of associated risk factors including hypertension and hyperlipidemia but also from specific risks largely resulting from insulin resistance, hyperinsulinemia and hyperglycemia. 1541035: This insulin resistance and the resulting hyperinsulinaemia are now recognised as common background factors that may be responsible for hypertension, hyperlipidaemia, decreased thrombolysis and also impaired glucose tolerance and diabetes. 15668356: Hyperinsulinemia has been suggested to be involved in the etiology of obesity-associated hypertension. 16502970: We therefore suggest that hyperinsulinemia leads to hypertension through increased renal sodium reabsorption in the distal nephron. 1730459: Moreover, insulin-induced hypertension was associated with a shift of renal pressure natriuresis, since sodium balance was maintained at elevated arterial pressures. These observations indicate that chronic hyperinsulinemia in rats produced hypertension that was not salt-sensitive and not dependent on sodium retention or increased renin secretion. 1930926: In those with type 2 diabetes insulin resistance and hyperinsulinaemia may play a part in the pathogenesis of hypertension independent of obesity. 1946784: Hypertension may be either accentuated or caused by hyperinsulinemia secondary to insulin resistance. 2043218: Whether hyperinsulinaemia is the cause of hypertension is currently unknown. 2045166: Although controversy exists as to the role insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension, data are presented from both obese and nonobese subjects that strongly suggests that selective insulin resistance and hypertension are directly related. 2076856: It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. 21796124: We previously reported that chronic hyperinsulinemia and insulin resistance induced by fructose-drinking loading elicited hypertension associated with abnormal neuronal regulation of vascular tone in an in vivo study using pithed rats. Hyperinsulinemia induces hypertension associated with neurogenic vascular dysfunction resulting from abnormal perivascular innervations in rat mesenteric resistance arteries. 2180321: These findings suggest that additional factors besides hyperinsulinemia per se are responsible for obesity-associated hypertension. 24225770: The present findings suggest that the abnormal innervation of perivascular nerves in mesenteric resistance arteries induced by chronic hyperinsulinemia disturbs the neuronal regulation of vascular tone and may cause hypertension in OLETF rats. 2569446: The role of insulin resistance and hyperinsulinemia in the etiology of fructose-induced hypertension was studied in male Sprague-Dawley rats. 2697985: Hypertension is thus the unfortunate consequence of hyperinsulinemia, which increases renal sodium reabsorption, and sympathetic stimulation of the heart, kidney, and vasculature. 28971990: Hyperinsulinemia has been hypothesized to cause hypertension in obesity, type 2 diabetes, and metabolic syndrome through a renal mechanism. Thus, by developing a novel approach for chronic, continuous renal artery insulin infusion, we provided new evidence that insulin causes hypertension in rats through actions initiated within the kidney. 2920097: These findings suggest that additional factors besides hyperinsulinemia per se are responsible for obesity-associated hypertension. 32349626: Objective : To investigate if insulin resistance per se or the accompanying hyperinsulinemia induced hypertension and its underlying mechanisms. 3293359: Obesity has been associated with numerous metabolic complications, such as changes in the concentration and/or composition of plasma lipoproteins, glucose intolerance and hyperinsulinemia leading to diabetes and hypertension. 33076803: Patients with T2D often have hyperinsulinemia, dyslipidemia, inflammation, and oxidative stress, which then lead to hypertension, chronic kidney disease, cardiovascular disease, and increased risk of morbidity and mortality (9th leading cause globally). 34996843: We found that the shift in Insr promoter usage was significantly associated with insulin levels and blood pressure within a panel of HXB/BXH recombinant inbred rat strains, suggesting that hyperinsulinemia due to insulin resistance might lead to hypertension in SHR. 38102585: Additionally, high truncal and leg BF% and high HOMA-IR accounted for the hypertension risk in women, but not in men. 7657073: It has been proposed that the resulting hyperinsulinemia may induce hypertension through four possible mechanisms: Its trophic effect on vascular smooth muscle cells, increasing cytosolic calcium, increasing tubular sodium reabsorption or by stimulating adrenergic activity. 7700881: The few long-term studies that have been conducted in dogs and humans do not support the hypothesis that hyperinsulinemia causes hypertension or potentiates the hypertensive effects of other pressor agents such as angiotensin II or increased adrenergic tone. Although resistance to insulin's metabolic effects has been suggested to be essential for hyperinsulinemia to cause hypertension, chronic increases in plasma insulin concentrations do not cause hypertension in dogs or humans even in the presence of insulin resistance. 7700882: We have briefly reviewed the controversy regarding the role of insulin resistance and hyperinsulinemia in the pathogenesis of hypertension in an attempt to emphasize the evidence in support of this concept. 7782934: Although controversy exists as to the role that insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension, data are presented that strongly suggest that selective insulin resistance and hypertension are directly related. 7898093: Therefore, it is still unclear whether hyperinsulinemia induces hypertension or is only casually associated with it. 7986471: Correlations between insulin resistance, hyperinsulinemia, and hypertension do not appear to be explainable by the concept that insulin resistance occurs secondary to hypertension. Although hyperinsulinemia and insulin resistance have been speculated to cause hypertension, most of the evidence supporting this hypothesis has come either from correlation studies or from short-term studies of the cardiovascular, renal, and sympathetic effects of insulin. 8206593: Hyperinsulinemia and insulin resistance are implicated in the etiology of hypertension, but the mechanisms involved have not been established. 8231616: According to the current hypothesis, hyperinsulinemia which is probably a physiologic adaptation to obesity, plays a key role in the pathogenesis of arterial hypertension. 8299479: There is still a paucity of epidemiological data to support a role for hyperinsulinemia in the etiology of hypertension. 8417411: Although controversy exists as to the role that insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension there are ample data from both obese and nonobese subjects strongly suggesting that selective insulin resistance, hyperlipidemia, and essential hypertension are directly related. 8568012: Hyperinsulinemia and insulin resistance may cause systemic hypertension through multiple mechanisms. 8720605: Furthermore, these data do not indicate a major role for hyperglycaemia and hyperinsulinaemia per se in the aetiology of hypertension and suggest that IGT and hypertension share one or more pathogenetic factor(s) (i.e., insulin resistance, hyperactivity of the sympathetic nervous system, etc.), which induce deterioration of blood pressure control first, and hyperglycaemia later. 8760230: Hyperinsulinemia has been reported to cause hypertension in rats; however, the renal and hemodynamic mechanisms are not known. 8914428: Hyperinsulinemia is one of the important candidates to cause hypertension in the patients with diabetes mellitus. 8972890: Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats. This study tested whether combined alpha1- and beta-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. 9162436: Patients with non-insulin dependent diabetes mellitus and obesity show an elevated risk for development of arterial hypertension, while many non-obese, non-diabetic patients with essential hypertension display resistance to insulin-induced glucose disposal, accompanied by hyperinsulinaemia. 9162438: Hyperinsulinaemia induces hypertension through increased renal tubular reabsorption of sodium and water, increased sympathetic nervous system activity, proliferation of vascular smooth muscle cells, and alterations of transmembrane cation transport. 9719048: Angiotensin receptor blockade blunts hyperinsulinemia-induced hypertension in rats. These results indicate that angiotensin type 1 receptors play a determinant role in the pathogenesis of insulin-induced hypertension in rats. The study was conducted to examine the effects of the angiotensin subtype 1 and 2 receptor antagonists (losartan and PD123319, respectively) on blood pressure (BP) and renal excretory function in chronic hyperinsulinemia-induced hypertension in rats. 9719050: These results indicate that chronic hyperinsulinemia-induced hypertension requires the presence of intact renal nerves in rats. After hyperinsulinemia-induced hypertension had been fully established (from 134+/-2 to 157+/-2 mm Hg), bilateral renal denervation reversed the elevated systolic blood pressure to normotensive levels within 2 weeks. Experiments were performed to evaluate the role of the renal nerves in hyperinsulinemia-induced hypertension. 9737194: Hyperinsulinism and coagulation disorders were considered as more important etiopathological factors leading to heart failure or hypertension rather than obesity alone. 9854458: Hyperinsulinaemia and insulin resistance are thought to be intimately involved in the development of hypertension, but controversy remains as to whether hyperinsulinaemia is a consequence or a cause of hypertension per se, and whether it plays a role in the short-term regulation of blood pressure. 9869010: OBJECTIVE: To investigate the role of angiotensin II in the pathogenesis of hyperinsulinemia-induced hypertension in rats. CONCLUSIONS: Angiotensin converting enzyme inhibition or angiotensin II type 1 receptor antagonism can prevent and reverse insulin-induced hypertension in rats, suggesting that angiotensin II itself or an angiotensin II-dependent mechanism has an etiological influence in the pathogenesis of this hypertension model. When the insulin-induced hypertension had become established (systolic blood pressure increased from 132+/-3 to 155+/-2 mmHg 4 weeks after the infusion, P< 0.05 ), subsequent fosinopril or losartan treatment for 2 weeks reversed the elevated systolic blood pressure and heart rate to the control levels. 10070030: Hereditary salt-losing syndromes have been ascribed to loss of function mutations in the alpha-, beta-, or gamma-ENaC subunit genes, whereas gain of function mutations (located in the COOH terminus of the beta- or gamma-subunit) result in hypertension due to Na+ retention (Liddle's syndrome). 10505492: Selection of antihypertensive agents in the overweight patient should take into account the mechanisms leading to hypertension and the metabolic abnormalities that characterize the obese patient. Hyperinsulinemia, which is characteristic of obesity, can contribute to the probability of developing hypertension by activating the sympathetic nervous system (SNS) and by causing sodium retention. 11752037: Licorice-associated hypertension is thought to be due to increased renal sodium retention. 1190320: The data support the concept that sodium retention causes hypertension almost entirely because of sodium-induced expansion of the extracellular fluid volume. The goal of these studies was to determine whether the hypertension caused by excessive salt loading results from sodium-induced expansion of the extracellular fluid volume or whether the salt increases the pressure in some other way, such as by causing vascular constriction. 1379154: Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. 13896894: The influence of intermittent bretylium tosylate (darenthin) on the development of vascular disease in rats with hypertension caused by sodium retention. 14603734: In the past, it had been presumed that hypertension in chronic renal failure is due to enhanced sodium retention, chronic hypervolemia and increased activity of the renin-angiotensin-aldosterone-system. 15372097: As COX inhibition is often associated with sodium retention leading to edema and hypertension, prostanoids appear to have a role in preventing the development of high blood pressure. 16787194: PGE2 inhibition results in sodium retention, which leads to hypertension, peripheral edema and potentially exacerbation of heart failure. 18268143: Deoxycorticosterone acetate (DOCA)-salt hypertension is characterized by a suppressed plasma renin level due to sodium retention but manifests in eNOS uncoupling; however, how endogenous BH4 regulates blood pressure is unknown. 19018744: Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. 19679708: BACKGROUND: Previous research has suggested that dehydration in infancy may lead to high blood pressure in later life because of sodium retention. 2009143: Although such hypertension may be partly sodium-mediated as a consequence of inappropriate sodium retention by the normal and ischemic nephrons, the source of the problem lies in the renin production from ischemic nephrons. 21966935: Sodium retention has been proposed as the cause of hypertension in the LP rat (offspring exposed to a maternal low-protein diet in utero) model of developmental programming because of increased renal NKCC2 (Na+/K+/2Cl- co-transporter 2) expression. 2309737: CONCLUSION: Hypertension in patients with NIDDM is frequently salt-sensitive, which may be due to sodium retention and enhanced vascular reactivity to angiotensin II. 24095127: In pathophysiological states, such as hypertension, heart failure and chronic renal disease, there may be an inappropriate sympathoexcitation causing sodium retention which exacerbates the disease process. 25163793: This includes sodium retention, resulting in arterial hypertension, heart failure, and atherosclerotic events. 2547710: We interpret these data as suggesting that increased renal nerve activity in this model contributes to hypertension by causing excess sodium retention. 26253568: A popular hypothesis is that resistant hypertension is due to excessive Na(+)-retention, and that 'further diuretic therapy' will be superior to alternative add-on drugs. 26414968: We aimed to test the hypotheses that resistant hypertension is most often caused by excessive sodium retention, and that spironolactone would therefore be superior to non-diuretic add-on drugs at lowering blood pressure. 2687519: On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE. 27072827: One hypothesis is that resistant hypertension is due to abnormal sodium retention, mediated by aldosterone breakthrough occurring despite blockade of the renin-angiotensin-aldosterone system with angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB). 27571851: BACKGROUND: Sodium retention causes posttransplant hypertension, and sodium restriction is recommended in kidney allograft recipients. 27689106: Extra cellular volume expansion and Na retention remain the main cause of hypertension. 28445205: Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1?-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. 29031360: The pathologic consequences of sodium retention in the CKD population can lead to hypertension, edema, and progressive disease. 29144530: In South Africa, novel variants in the epithelial sodium channel (ENaC) have been described to be associated with varying degrees of hypokalaemia and hypertension due to primary sodium retention. 30969802: Increased Na+ retention through ENaC with subsequent volume expansion causes hypertension. 31402728: INTRODUCTION: Achieving sodium balance is important for peritoneal dialysis patients, as sodium excess may lead to hypertension and extracellular water expansion. 33167351: Characterized by increased blood pressure due to excessive sodium retention and plasma volume, it is caused by a mutation in the HSD11B2 gene encoding the oxydoreductase enzyme 11beta-hydroxysteroide dehydrogenase type 2. 34779863: The mechanism may be involved that paternal PM2.5 exposure-associated oxidative stress induces the elevated renal GRK4 level, leading to the enhanced AT1R expression and its-mediated sodium retention, consequently causes hypertension in male offspring. 37169600: BACKGROUND: Sodium retention causes post-transplant hypertension, and sodium restriction is recommended in kidney transplantation recipients. 6360883: Increasing evidence indicates that sodium retention due to increased sodium intake or decreased sodium excretion causes hypertension by releasing a humoral pressor substance from brain. 7321015: Sodium excess or potassium lack as a cause of hypertension: a discussion paper. 7954538: Hypertension and oedema resulting from sodium retention are the main indications for diuretic treatment in patients with chronic renal failure. Pathophysiology and treatment of hypertension and oedema due to renal failure. 11452332: Increased elastance (or stiffness, inverse of compliance) of the central elastic arteries is the primary cause of increased systolic and pulse pressure with advancing age and in patients with cardiovascular disease, including hypertension, and is due to degeneration and hyperplasia of the arterial wall; diastolic pressure decreases as arterial elastance increases. 11668363: Hypertension in the SHR rats was associated with an increased lumenal stenosis due to increased intimal hyperplasia. 12795664: INTRODUCTION: Intimal hyperplasia of renal allograft arteries is a cause of hypertension and graft loss and the predisposing factors are poorly understood. 1318127: Structural changes within the blood vessel wall such as hyperplasia and hypertrophy of vascular smooth muscle cells are important factors in the pathogenesis of hypertension. 1708014: Hypertension may result from vascular hypertrophy or hyperplasia due to enhanced growth of vascular smooth muscle cells (VSMCs), which has been demonstrated in VSMCs from spontaneously hypertensive rats (SHRs) compared to Wistar-Kyoto (WKY) rats. 1839822: Newborn rats of four different strains with spontaneous hypertension show heart enlargement mainly due to cardiac hyperplasia. 22672087: Over time, uric acid uptake into vascular smooth muscle cells causes cellular proliferation and secondary arteriolosclerosis that impairs pressure natriuresis, causing sodium-sensitive hypertension. While more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early-onset hypertension. 29771623: Moreover, the effects of mulberry on vascular remodeling events such as hyperplasia, an important etiology in the pathogenesis of hypertension and arteriosclerosis, are also ambiguous. 5891868: Segmental intimal hyperplasia of the abdominal aorta and renal arteries producing hypertension in an infant. 6170579: These results would indicate that, in this type of hypertension, the increase in artery mass is mainly the result of cellular hyperplasia, which is active during the early phase of the process; afterward the vascular wall reaches a new steady state characterized by a greater number of cells and no further cell proliferation. 733062: A case of arterial hypertension due to suprarenal medulla hyperplasia is reported. 8153365: A 55-year-old woman was admitted to our hospital with complaints of obesity, hypertension, and back pain caused by left adrenal hyperplasia after surgical resection of the right adrenal gland. 10981166: It is uncertain, however, whether this adrenergic overactivity is specific for renovascular hypertension per se, or the cause of severe hypertension with target organ damage. 1098252: Renovascular hypertension, comprising a small percentage of the total hypertensive population, stands out as remarkably important, being the most common cause of surgically correctable hypertension. 11273151: Renovascular hypertension is an important but not so common cause of hypertension. Rarely the extrinsic compression of renal arteries by retroperitoneal structures may be responsible for hypertension. 167: There are different types of renal hypertension: hypertension due to parenchymal renal disease, renovascular hypertension, hypertension due to urological disease, hypertension of endstage renal disease. 17377375: Renovascular hypertension is a recognized secondary potentially curable cause of hypertension since the work of Harry Goldblatt. 18288504: Segmental renal infarction (SRI) is a rare condition that causes renovascular hypertension (RVH), which accounts for 8-10% of all causes of pediatric hypertension. 21279728: Renovascular hypertension (RVH) is an unusual cause of hypertension in children that is important to diagnose as it is potentially curable with angioplasty or surgery. 23152163: Although renovascular hypertension is one of the commonest causes for severe hypertension in children, HHS is rarely reported in childhood. 24615925: Renovascular hypertension (RVH) is an important cause of hypertension in children. 25318796: We herein report two cases of pregnant women who had chronic hypertension caused by renovascular hypertension due to multiple intrarenal microaneurysms from unknown causes, who had similar clinical courses. These cases suggest that an uneventful term delivery may be achieved with adequate blood pressure control in pregnant women with chronic hypertension caused by renovascular hypertension, and a prior eventful clinical course of delivery does not affect the subsequent clinical course. 25546991: [Difficulty in diagnosis of primary hyperaldosteronism as the cause of resistant hypertension and severe hypokalemia--case report]. Renovascular hypertension, Cushing syndrome and pheochromocytoma were excluded as potential causes of drug-resistant hypertension in the presented case. 26724918: BACKGROUND: Renovascular hypertension accounts for 51-52% of all cases of hypertension in the general population, but plays a major role in treatable causes for hypertension in the young. 27122924: UNLABELLED: Renovascular hypertension due to fibromuscular dysplasia is an uncommon but important cause of pediatric hypertension. 27369816: Renovascular hypertension is a common cause of pediatric hypertension. 28370243: Renovascular hypertension accounts for 5-10% of the secondary causes of hypertension in children and is mainly related to fibromuscular dysplasia and neurofibromatosis type 1. 28505045: Renovascular HTN remains an underlying cause for resistant HTN, and revascularization may prove to be an effective treatment for many of these patients. 28779201: Renovascular hypertension is an uncommon but important secondary cause of hypertension in the pediatric population that can be associated with substantial morbidity. 28950261: BACKGROUND/AIMS: Renovascular hypertension (RVHT) is an important cause of childhood hypertension. 30787570: Patients <45 years of age with uncontrolled hypertension secondary to renovascular hypertension (RVH) and refractory to medical management and renal arterial disease unfavorable for percutaneous intervention were included in the study. 30792585: Aims: Renovascular hypertension is a rare cause of paediatric hypertension. 32276020: Surgical Management of Pediatric renin-mediated Hypertension seCONDARY TO RENAL ARTERY OCCLUSIVE DISEASE AND ABDOMINAL AORTIC COARCTATION.INTRODUCTION: Renovascular hypertension (RVH) associated with renal artery and abdominal aortic narrowings is the third most common cause of pediatric hypertension. 35860166: Introduction: and importance: Renovascular hypertension accounts for 1-2% of all cases of hypertension in the general population, but plays a major role in treatable causes of hypertension in the young. 36090342: Renovascular hypertension (RVH) is considered to be one of the important causes of hypertension in patients with moyamoya disease. 3668590: Renovascular hypertension appeared to be the primary cause of this hypertension, judging from the significant decrease in blood pressure induced by an angiotensin II analog and a renal vein renin ratio of 7.3. 37658875: BACKGROUND: Renovascular hypertension (RenoVH) is a cause of hypertension in children. 37746936: Renovascular hypertension (RHV) is the cause of high blood pressure due to left renal ischemia, and obesity and hypertension cause an inflammatory response. 7667614: Renovascular hypertension (RVH) remains a leading cause of potentially curable hypertension. Advances in percutaneous transluminal renal angioplasty (PTRA) have renewed interest in developing better noninvasive screening tests for identifying patients with potentially correctable hypertension or renal impairment due to renovascular disease caused by either fibromuscular dysplasia (FMD) or arteriosclerosis. 8760657: Renovascular hypertension represents 1 to 2% of all causes of hypertension. 1318127: Structural changes within the blood vessel wall such as hyperplasia and hypertrophy of vascular smooth muscle cells are important factors in the pathogenesis of hypertension. 1708014: Hypertension may result from vascular hypertrophy or hyperplasia due to enhanced growth of vascular smooth muscle cells (VSMCs), which has been demonstrated in VSMCs from spontaneously hypertensive rats (SHRs) compared to Wistar-Kyoto (WKY) rats. 17461020: Treatment with different types of antihypertensive drugs during second month age has not prevented development of arterial hypertension and myocardial hypertrophy in the adult rats with inherited stress-induced arterial hypertension. 23849622: Pseudohypertension has been described as a cause of resistant hypertension, due to medial hypertrophy of the artery from atherosclerosis. 24736482: Early hypertension and progressive renal failure due to massive enlargement of cysts and fibrosis are hallmarks of the disease. 2527201: We suggest that the initial (primary) component of vascular hypertrophy precedes the rise in blood pressure and may be critical in the pathogenesis of hypertension. 2694754: Early rise in blood pressure, sympathetic overresponsiveness, early development of cardiovascular hypertrophy, increased salt-sensitivity and membrane abnormalities detected in vascular smooth muscle cells (VSMC) from SHR and SHRSP, which are related to the pathogenesis of hypertension, have been examined for their applicability to the prediction of hypertension in man. The development of genetic models for research on hypertension and stroke, spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP), have contributed not only to the elucidation of the pathogenesis of hypertension-related cardiovascular diseases (CVD) but also to their prediction and prevention. 28012599: Second, one or more signaling molecules are stimulated to produce vascular hypertrophy resulting in hypertension. 29174227: Systemic hypertension, proteinuria and kidney injury - such as enlargement and glomerular fibrin deposit, capillary occlusion due to edema, and hypertrophy of endocapillary cells - are some of these changes. 30755792: Early hypertension and progressive renal failure due to massive enlargement of cysts and fibrosis are hallmarks of the disease. 31360915: Renal artery dissections (RADs) are lesions that disrupt vessels that primarily occur in patients with a known history of hypertension and caused by stenosis or enlargement of the renal artery typically due to underlying connective tissue disorders. 35556970: During this process, pulmonary artery smooth muscle cell (PASMC) proliferation and hypertrophy contribute to the thickening of the pulmonary artery wall, leading to heightened blood pressures. 7277951: The pressure in the pulmonary circulation is determined only by the level of the left ventricular end-diastolic pressure, which is moderately elevated in the patients with arterial hypertension due to manifest myocardial hypertrophy. 7449279: These results indicate that hypertrophy of the media is a consequence of high blood pressure rather than a genetically determined pathogenetic factor for the development of hypertension in spontaneously hypertensive rats. The increased peripheral resistance observed in established hypertension has been attributed to structural changes in the resistance vessels, which are considered to be due mainly to medial hypertrophy. 7508023: These data allow us to conclude that HHIF could play a role in the vascular hypertrophy that is associated with the pathogenesis of hypertension. 7889202: Is hypertrophy of the walls of pre-glomerular vessels responsible for hypertension in spontaneously hypertensive rats? 8777475: In conclusion, hypertension resulted in an enhanced pressor effect, possibly caused by vascular hypertrophy, whereas the diabetic state counteracted this effect. Opposite influences of hypertension and diabetes mellitus on pressor responses induced by different alpha-adrenoceptor agonists and angiotensin II in pithed rats. 8833076: Histological observation showed that the wall thickening caused by hypertension is mainly due to the hypertrophy of the lamellar units of the media, especially in the subintimal layer where the stress increase developed by hypertension is larger than in the other layers. 897862: Vena caval pressure measurements and inferior vena cavography are helpful in the diagnosis of surprahepatic causes of portal hypertension, such as constrictive pericarditis and inferior vena caval diaphragm, and are also useful in the diagnosis of vena caval hypertension due to caudate lobe enlargement. 9862388: There are clinical and experimental evidences that the cardiopulmonary reflex function is impaired in chronic hypertension, but it could be due to myocardial hypertrophy rather than to hypertension itself. 11711505: In conclusion, mild hyperuricemia causes hypertension and renal injury in the rat via a crystal-independent mechanism, with stimulation of the renin-angiotensin system and inhibition of neuronal NO synthase. 12372787: Mild hyperuricemia induces glomerular hypertension in normal rats. 15610247: CONCLUSION: Hyperuricemia induces arteriolopathy of preglomerular vessels, which impairs the autoregulatory response of afferent arterioles, resulting in glomerular hypertension. 15660330: In conclusion, hyperuricemia impairs the autoregulatory response of preglomerular vessels, resulting in glomerular hypertension. 15840020: Thus, hyperuricemia induces endothelial dysfunction; this may provide insight into a pathogenic mechanism by which uric acid may induce hypertension and vascular disease. Furthermore, rat studies have shown that hyperuricemia-induced hypertension and vascular disease is at least partially reversed by the supplementation of the nitric oxide synthase (NOS) substrate, L-arginine. 15991921: It is entirely possible that hyperuricaemia is part of a pathologic process that underlies fundamental alterations in renal function, as well as other metabolic pathophysiologies that ultimately lead to hypertension and cardiovascular disease. 16361844: Hyperuricemia induced systemic hypertension, glomerular hypertrophy/hypertension, afferent arteriolar sclerosis, and macrophage infiltration in normal rat kidney. 16672144: Supporting arguments for this theory maintain that experimental hyperuricemia induces hypertension and renal damage. 18048425: We therefore tested the hypothesis that Fx might be useful in treating hyperuricemia-induced hypertension and renal damage. 19008712: BACKGROUND AND OBJECTIVES: It has been demonstrated that hyperuricemia induces reno-cardiovascular damage resulting in hypertension and renal injury because of vascular endothelial dysfunction. CONCLUSION: These findings suggest that the activation of ATP-sensitive potassium channels by iptakalim can protect endothelial function against hypertension and renal injury induced by hyperuricemia. Activation of ATP-sensitive potassium channels protects vascular endothelial cells from hypertension and renal injury induced by hyperuricemia. 20138901: Additional metabolic effects from the fructose fraction of these beverages may also promote accumulation of visceral adiposity, and increased hepatic de novo lipogenesis, and hypertension due to hyperuricemia. 20484295: Hyperuricemia is associated with renal disease, and recent studies have reported that mild hyperuricemia results in hypertension, intrarenal vascular disease, and renal injury. 23370375: There are data to suggest that hyperuricaemia itself causes hypertension and renovascular disease, and that lowering of serum urate may assist in control of hypertension. 23538309: An overview of the potential roles that hyperuricemia plays in the pathogenesis of hypertension and CKD and current blood pressure treatment guidelines in populations with CKD are discussed. 23662072: Hyperuricemia might trigger the development of hypertension, chronic renal failure, and insulin resistance. 24025986: Gout, a common disease, is a consequence of hyperuricemia, and increases the risks of hypertension, cardiovascular diseases, cerebrovascular diseases and renal failure. 24072559: Over the last decade, the biologic interference of uric acid with the cardiovascular (CV) system and the kidney has been intensively investigated, and several experimental studies in animal models and in vitro documented that hyperuricemia may trigger hypertension and incite endothelial dysfunction, vascular damage and renal disease. 24122470: Recent studies have reported that hyperuricemia (HU) results in hypertension, intrarenal vascular disease, and renal injury. 24404368: This is the report of a child presented with proteinuira, hypertension, and glomerular scelrosis secondary to hypouricosuric hyperuricemia, who was treated by uric acid lowering management. 24745926: Several experimental and clinical studies reported that hyperuricemia may trigger hypertension, metabolic syndrome, vascular damage and renal disease. 25371715: Endothelial dysfunction plays a key role in the development of cardiovascular diseases, renal injuries and hypertension induced by hyperuricemia. 25918583: Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels. Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction. We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia. 26318389: These observations have stimulated several epidemiological researches suggesting that hyperuricemia is linked or even provokes hypertension and coronary artery disease. 26455995: Hyperuricemia may induce glomerular hypertension, whereas the increased urinary uric acid may directly injure renal tubules. 26892518: Hyperuricemia induces hypertension through activation of renal epithelial sodium channel (ENaC). 28986198: HUA plays a role in the development and pathogenesis of metabolic syndrome, hypertension, stroke, and atherosclerosis. 29393088: SUMMARY: Mild hyperuricemia in rodents induces hypertension associated to renal microvascular disease, tubulointerstitial inflammation, vasoconstriction, and glomerular hypertension. 29934052: Taken together, these data suggested that mangiferin has played an important part in alleviating hypertension induced by hyperuricemia via increasing NO secretion and improving endothelial function. In this study, we aimed to evaluate the effect of mangiferin on alleviating hypertension induced by hyperuricemia. 30142173: The hypouricemic effect conferred by probiotic supplementation also prevented the renal changes and hypertension caused by hyperuricemia. We confirmed that oxonic acid-induced hyperuricemia produced hypertension and renal functional and structural changes, along with modest changes in the overall composition of fecal microbiota. 30245716: Conclusion: Mild hyperuricemia produces hypertension together with changes in the cardiac hypertrophy, fibrosis, and increased thickness of the intima media in hypogonadic rats fed high-fructose diet. 33346219: We aimed to calculate the attribute risk of hypertension due to hyperuricemia by Levin's formulas compare to direct PAR calculation method. 34340595: Meanwhile, untreated hyperuricemia was also suggested to lead to hypertension. 11834024: A 16-year-old adolescent presented with systemic hypertension due to a hypoplasia of the aortic arch resulting in a significant stenosis. 13284642: Diminutive kidney, hypoplasia or atrophic pyelonephritis, may be the cause of hypertension, lumbar or abdominal pain, obscure gastrointestinal symptoms or chronic urinary infection accompanied by chills and fever. 14262491: HYPOPLASIA OF THE ABDOMINAL AORTA AS THE CAUSE OF JUVENILE ARTERIAL HYPERTENSION. 16195649: The patient was admitted to our hospital after presenting with severe hypertension secondary to abdominal aortic hypoplasia and renal artery stenosis. 23494884: BACKGROUND: Hypoplasia of the transverse arch may result in residual systemic hypertension and may be amenable to stenting. 31703697: Vertebral artery hypoplasia (VAH) with an incomplete posterior circle of Willis (ipCoW; VAH + ipCoW) is associated with increased cerebrovascular resistance before the onset of increased sympathetic nerve activity in borderline hypertensive humans, suggesting brainstem hypoperfusion may evoke hypertension to maintain cerebral blood flow: the \selfish brain\ hypothesis. 5118997: [Arterial hypertension caused by segmental unilateral renal hypoplasia with vascular abnormality and abdominal aorta hypoplasia]. 5475595: [Arterial hypertension in adults due to segmental aglomerular hypoplasia]. 7181171: Five cases of hypoplasia of the descending thoracic and/or abdominal aorta as a rare cause of hypertension are presented. Hypoplasia of descending aorta as a rare cause of hypertension. 7369807: In most cases the mechanism of hypertension is elevated blood renin levels secondary to associated renal artery stenosis. Coarctation or hypoplasia of the abdominal aorta is a rare cause of life-threatening hypertension. 10589822: Hypoxia produced hypertension, transient bradycardia followed by tachycardia, and respiratory facilitation, which characterize the chemoreflexes. 10773238: Each gene appeared to have its own timetable of expression and responded differently to hypoxia-induced hypertension. 10963773: This review focuses upon the development of a small animal model that incorporates exposure to chronic-intermittent hypoxia to produce systemic hypertension similar to that experienced by humans with the obstructive sleep apnea syndrome. 11247965: The long-term consequences of chronic intermittent hypoxia may have detrimental effects, including hypertension, cerebral and coronary vascular problems, developmental and neurocognitive deficits, and neurodegeneration due to the cumulative effects of persistent bouts of hypoxia. 11447290: HO-1 transgenic mice were protected from the development of both pulmonary inflammation as well as hypertension and vessel wall hypertrophy induced by hypoxia. 12121987: Proteomic analysis reveals alterations in the renal kallikrein pathway during hypoxia-induced hypertension. We used proteomic analysis to examine differences in rat kidney protein expression during EH, and their potential relationship to EH-induced hypertension. We conclude that EH-induced hypertension may result, at least in part, from altered regulation of the renal kallikrein system. Transgenic hKLK1 animals were protected from EH-induced hypertension. 12753295: RESULTS: Chronic hypoxia induced hypertension and erythrocytosis at 24 days. 14597643: We therefore analyzed the biosynthetic pathways of catecholamines in peripheral nervous system structures involved in the pathogenesis of intermittent hypoxia-induced hypertension, namely, carotid bodies, superior cervical ganglia, and adrenal glands. Chronic intermittent hypoxia, a characteristic feature of sleep-disordered breathing, induces hypertension through augmented sympathetic nerve activity and requires the presence of functional carotid body arterial chemoreceptors. 14643579: CONCLUSIONS: Chronic hypoxia-induced hypertension in rats is associated with marked downregulation of NOS isotypes, which can, in part, account for the previously reported L-arginine-responsive hypertension in this model. In view of the latter observations, we hypothesized that hypoxia-induced hypertension may be associated with downregulation of NO synthase (NOS). 15498265: [Changes of angiotensin II and its receptor during the development of chronic intermittent hypoxia-induced hypertension in rats]. CONCLUSION: CIHO can cause the levels of circulating RA and ATII to increase, but has no effects on AT1R mRNA expression in tissue, which suggests that activated renin-angiotensin system may contribute to the pathogenesis of CIHO-induced hypertension. OBJECTIVE: To observe the changes of angiotensin II (ATII) and ATII type-1 receptor (AT1R) during the development of chronic intermittent hypoxia (CIHO)-induced hypertension in rats, and the effect in the mechanism of CIHO-induced hypertension. 15528223: Linked mechanical and biological aspects of remodeling in mouse pulmonary arteries with hypoxia-induced hypertension. 15669002: The new hypothesis can then be addressed rapidly by conventional molecular biology methods, as demonstrated by identification of an altered renal elastin-elastase system in diabetic nephropathy and alterations in the renal kallikrein-kallistatin pathway in hypoxia-induced hypertension. 15738350: We reported previously that simulating sleep apnea in rats by exposing them 7 hours per day to intermittent hypoxia/hypercapnia (IH) elevates plasma endothelin-1 and causes hypertension, which is reversed by an endothelin-1 antagonist. Augmented endothelin vasoconstriction in intermittent hypoxia-induced hypertension. We hypothesized that in this model of sleep apnea-induced hypertension, vascular sensitivity to endothelin-1 is increased in combination with the elevated plasma endothelin-1 to cause the endothelin-1-dependent hypertension. 16125867: This ischemic hypoxia is a causative, or at least a permissive factor for hypertension and/or non-insulin dependent diabetes mellitus. 16215633: Differential expression of three hypoxia-inducible factor-alpha subunits in pulmonary arteries of rat with hypoxia-induced hypertension. 16484362: Long-term exposure to intermittent hypoxia (IH), such as that occurring in association with sleep apnea, may result in systemic hypertension; however, the time course changes in arterial pressure, autonomic functions, and baroreflex sensitivity are still unclear. Enhanced sympathetic outflow and decreased baroreflex sensitivity are associated with intermittent hypoxia-induced systemic hypertension in conscious rats. The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats. We investigated the changes in cardiovascular neural regulations during the development of chronic IH-induced hypertension in rats. 16521269: OBJECTIVES: Long-term hypoxia results in hemodynamic breakdown in patients in the intensive care unit; however, intermittent hypoxia causes hypertension in individuals with sleep apnea. 16607489: Finally, animal models of OSA have delineated that daytime arterial hypertension is the consequence of the OSA-associated chronic intermittent hypoxia. 16761101: Differential and reciprocal regulation between hypoxia-inducible factor-alpha subunits and their prolyl hydroxylases in pulmonary arteries of rat with hypoxia-induced hypertension. 17627473: Exposure of rodents to CIH is sufficient to induce hypertension by activation of the carotid body and sympathetic nervous system, leading to increased levels of circulating catecholamines. 17669692: OBJECTIVES: We report in the present study the role of endothelin (ET-1) and ET-1 receptors in the sustained hypoxia-induced systemic hypertension. Despite of this hypoxia-induced hypertension, ET-1 plasmatic concentration was not different between N and CH rats. Aortic vasoconstriction related to smooth muscle cells ET-A and ET-B receptors is not involved in hypoxia-induced sustained systemic arterial hypertension in rats. 18083893: We reported previously that simulating sleep apnea by exposing rats to eucapnic intermittent hypoxia (E-IH) causes endothelin-dependent hypertension and increases constrictor sensitivity to endothelin-1 (ET-1). 18091352: Perinatal exposure to chronic hypoxia induces sustained hypertension and structural and functional changes in the pulmonary vascular bed. 1818778: The data suggested that CSE can strengthen pulmonary vasoconstriction and hypertension induced by acute alveolar hypoxia. 18359899: Consistent with this hypothesis, we found that H-IH (20 brief exposures per hour to 5% O(2)-5% CO(2) for 7 h/day) induces systemic hypertension in mice [mean arterial pressure (MAP) = 97 +/- 2 vs. 124 +/- 2 mmHg, P < 0.05, n = 5] and increases NFATc3 transcriptional activity in aorta and mesenteric arteries. Therefore, we hypothesized that NFATc3 is activated by H-IH and is required for H-IH-induced hypertension. NFATc3 is required for intermittent hypoxia-induced hypertension. More importantly, H-IH-induced hypertension was attenuated in cyclosporin A-treated mice and prevented in NFATc3 KO mice. 18388204: This suggests that sleep fragmentation and its effects may be more important than hypoxia in the pathogenesis of the hypertension associated with human sleep apnoea. 18408145: OSA imposes a series of brief, intense episodes of hypoxia and hypercapnia, leading to persistent, maladaptive chemoreflex-mediated activation of the sympathetic nervous system which culminates in hypertension. 18463194: Nevertheless, it has been proposed that one of the possible contributing mechanisms to CIH-induced hypertension is a potentiation of carotid body (CB) hypoxic chemoreflexes. However, the early cardiovascular changes that precede CIH-induced hypertension are not completely understood. 18515645: We hypothesized that E-IH causes systemic hypertension through the increased ET-1 activation of vascular ET type A (ET(A)) receptors. We have reported that eucapnic intermittent hypoxia (E-IH) causes systemic hypertension, elevates plasma endothelin 1 (ET-1) levels, and augments vascular reactivity to ET-1 and that a nonspecific ET-1 receptor antagonist acutely lowers blood pressure in E-IH-exposed rats. 18850054: Expression and role of factor inhibiting hypoxia-inducible factor-1 in pulmonary arteries of rat with hypoxia-induced hypertension. 18952568: These findings demonstrate that NADPH oxidase-derived ROS contribute to the development of pulmonary vascular remodeling and hypertension caused by CIH. 19345616: Our data show that NO is not altered in the NTS of juvenile CIH rats, suggesting that nitrergic mechanisms, at least in the NTS, are unlikely to be involved in the sympathetic excitation that generates the hypertension observed after 10 days of CIH. Changes in central regulation of sympathetic activity may underlie CIH-induced hypertension. 19358946: CONCLUSIONS: In SHR, activation of the ET system, mediated by HIF-1 activity, is responsible for the enhanced susceptibility to chronic IH and for its associated cardiovascular consequences leading to hypertension and ischemic injury. 19386793: In conclusion, the PDE4 inhibitor roflumilast significantly attenuates pulmonary vascular remodeling and hypertension induced by chronic hypoxia or MCT and reverses established PH after MCT administration. 19435263: Obstructive apnea during sleep is accompanied by intermittent hypoxia (IH) leading to hypertension and other cardiovascular disturbances. 19506314: These animal studies have demonstrated that IH exposure in the absence of any other comorbidity causes hypertension, endothelial dysfunction, and augmented constrictor sensitivity, all due at least in part to increased vascular oxidative stress. 19536496: It has been proposed that chronic intermittent hypoxia (CIH) contributes to generate hypertension in patients with obstructive sleep apnea syndrome and animal models, due to an enhanced sympathetic outflow. Thus, our results support the idea that hypertension induced by long-term CIH was preceded by alterations in the autonomic balance of HRV, associated with an enhance CB chemoreflex sensitivity to hypoxia. A possible contributing mechanism to the CIH-induced hypertension is a potentiation of carotid body (CB) chemosensory responses to hypoxia, but early changes that precede the CIH-induced hypertension are not completely known. 19801450: Thus the disruption of PPARgamma signaling in EC is sufficient to cause mild PAH and to impair recovery from CH-induced PAH. 19818095: Mechanisms of intermittent hypoxia induced hypertension. 20217364: Thus, our results support the idea that the hypertension induced by CIH was preceded by alterations in the autonomic balance of HRV, associated with an enhance chemoreflex ventilatory reactivity in normotensive animals. One potential contributing mechanism to the OSA-induced hypertension is the potentiation of the carotid body chemosensory responses to hypoxia, which is responsible for the augmented sympathetic modulation of heart rate variability (HRV) and the enhanced ventilatory response to hypoxia found in OSA patients and animal exposed to chronic intermittent hypoxia (CIH). 20863915: This study was carried out to investigate the role of reactive oxygen species (ROS) in the elevation of cardiorespiratory responses during the development of intermittent hypoxia (IH)-induced hypertension. 21242253: Although elevated SNA may contribute to CIH-induced hypertension, reduced adrenergic vascular reactivity buffers the cardiovascular impact of exaggerated acute rises in SNA. 21445804: A co-morbidity of sleep-disordered breathing is hypertension associated with elevated sympathetic nerve activity, which may result from chronic intermittent hypoxia (CIH). 22085999: CONCLUSION: Intermittent hypoxia can induce high blood pressure, which may be related to the sympathetic over-activity and the oxidative stress. 22455939: The results suggested that CIH-induced higher blood pressure was associated with increased sympathetic activity. OBJECTIVE: To observe the changes of blood pressure and sympathetic nerve activity under different degrees of chronic intermittent hypoxia (CIH) in rats, and therefore to explore the effects of CIH on blood pressure and sympathetic nerve activity and the correlation between blood pressure and sympathetic nerve activity in the pathogenesis of CIH-induced hypertension. 22883993: OBJECTIVE: To study the role of sympathetic nerve activity during the development of hypertension resulting from chronic intermittent hypoxia, and whether or not elevated sympathetic nerve activity is related to oxidative stress, and to investigate the preventive effect and possible mechanism of Tempol. 23080163: A critical process involved in the CIH-induced hypertension is the potentiation of the carotid body (CB) chemosensory responses to acute hypoxia. Exposure to chronic intermittent hypoxia (CIH) produces hypertension. 23167993: These results indicate that resetting of the sympathetic baroreflex control, rather than an impairment of its sensitivity, is associated with an onset of hypertension induced by CIH. 23281754: Supplementing NaHS or H(2)S could be a strategy for reducing hypoxia-induced hypertension in broilers. 23860120: Hypoxia produces hypertension, tachycardia followed by bradycardia, and hypothermia. 24026072: These data indicate that the central and peripheral RAS contribute to CIH-induced hypertension and transcriptional activation of autonomic nuclei and that the contribution of the central RAS is greater during the normoxic dark phase of CIH hypertension. 24027362: Endothelial dysfunction and hypertension in obstructive sleep apnea - Is it due to intermittent hypoxia? 24270180: CONCLUSION: We suggest that the CIH-induced arterial hypertension is mediated by ROS derived from an activation of NOX2 within cells located outside the cardiovascular system. 24448370: We developed a model of hypertension in rabbits via exposure to severe CHH and we believe that ADMA is an important parameter in the development and permanence of CHH-induced hypertension. The main finding of this sudy was the depressor effect of AIH on blood pressure and heart rate in CHH- induced hypertension model. 24467360: BACKGROUND AND PURPOSE: Dysfunction and injury of endothelial cells in the pulmonary artery play critical roles in the hypertension induced by chronic hypoxia. 25063839: Chronic intermittent hypoxia (CIH) in animal models has been shown to result in hypertension and elevation of sympathetic nervous system activity. We conclude that increased CO is sufficient to explain the development of CIH-induced hypertension, which may be an early adaptive response to raise O2 flow. We sought to determine the contribution of cardiac output (CO) and lumbar sympathetic control of the hindlimb circulation to CIH-induced hypertension. 25295010: Second, we review what is known about drug efficacy to reverse HT induced by CIH in animals. 25429271: It has been proposed that a crucial step in the development of the hypertension is the potentiation of the carotid body (CB) chemosensory responses to hypoxia, but the temporal progression of the CB chemosensory, autonomic and hypertensive changes induced by CIH are not known. Present results show that CIH-induced persistent hypertension was preceded by early changes in CB chemosensory control of cardiorespiratory and autonomic function. 25523440: We discuss a possible role for pro-inflammatory cytokines in development of the hypertension produced by CIH, acting on cardiorespiratory centres located in the CNS. This article describes the contribution of oxidative stress and pro-inflammatory cytokines to the enhanced carotid body chemosensory responsiveness to the hypoxia and systemic hypertension induced by chronic intermittent hypoxia. 25583660: Available evidence from studies on experimental animals suggests that catecholamines secreted from adrenal medulla (AM), an end-organ of the sympathetic nervous system is a major contributor to CIH-induced hypertension. Studies on rodents established that exposure to chronic intermittent hypoxia (CIH) alone is sufficient to induce hypertension similar to that seen in patients with SDB. 25629363: CONCLUSION: The current results suggest that endothelial dysfunction in CIH-induced hypertension may result from imbalanced arginase-1 to eNOS expression, vascular remodelling and increased contractile capacity, rather than decreased vascular response to nitric oxide. 25631702: Chronic intermittent hypoxia (CIH) induces hypertension in male rats. 25772710: Physiological studies have identified that augmented carotid body chemosensory reflex and the resulting increase in sympathetic nerve activity are major contributors to CIH-induced hypertension. This article reviews the physiological and molecular basis of CIH-induced hypertension. Rodent models patterned after the O2 profiles seen with SDB patients showed that CIH is the major stimulus for causing systemic hypertension. 25880505: Available evidence suggests that carotid body chemoreflex contributes to hypertension caused by IH in both adults and neonates. 26248515: Roles of Canonical Transient Receptor Potential 6 in Basal [Ca(2+)]i Regulation in Pulmonary Venous Smooth Muscle Cells Under Chronic Hypoxia-Induced Hypertension. 26291659: We aimed to investigate the efficacy of carvedilol (CVDL), an unselective beta-blocker that exhibits intrinsic anti-alpha1-adrenergic and antioxidant activities in a rat model of CIH-induced hypertension. Efficacy of carvedilol in reversing hypertension induced by chronic intermittent hypoxia in rats. 26303489: Exposure to chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, produces autonomic and cardiorespirartory alterations, and leads to systemic hypertension. Exposure to CIH produces hypertension, increased the chemoreflex ventilatory hypoxic responses, and decreased BRS. 26752660: In young animals, CIH caused hypertension and in aged animals, whose baseline blood pressure was augmented, CIH did not augment it further. 26798430: Oxidative stress is involved in the development of carotid body (CB) chemosensory potentiation and systemic hypertension induced by chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea. 27381902: Carotid Body Ablation Abrogates Hypertension and Autonomic Alterations Induced by Intermittent Hypoxia in Rats. CIH induced hypertension, enhanced ventilatory response to hypoxia, induced autonomic imbalance toward sympathetic preponderance, reduced baroreflex gain, and increased arrhythmias and atrial fibrosis. Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to hypoxia and produces autonomic dysfunction, cardiac arrhythmias, and hypertension. Present results show that autonomic alterations induced by CIH are critically dependent on the CB and support a main role for the CB in the CIH-induced hypertension. We tested whether autonomic alterations, arrhythmogenesis, and the progression of hypertension induced by CIH depend on the enhanced CB chemosensory drive, by ablation of the CB chemoreceptors. 27402667: Intermittent hypoxia (IH) occurs in association with obstructive sleep apnea and likely contributes to the pathogenesis of hypertension. 27531649: In rodents, blockade of H2S synthesis by CSE, by either pharmacologic or genetic approaches, inhibited carotid body activation and hypertension induced by intermittent hypoxia. A rodent model of intermittent hypoxia that mimics blood O2 saturation profiles of patients with sleep apnea has shown that increased generation of reactive oxygen species (ROS) in the carotid body enhances the chemosensory reflex and triggers hypertension. H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea. 28076452: We aimed to study the renal injury and hypertension induced by chronic intermittent hypoxia (CIH) and the protective effects mediated by angiotensin 1-7 [Ang(1-7)]. 28078487: OBJECTIVE: This study aimed to investigate the role of the NADPH oxidase 4 (Nox4)-induced ROS/RhoA/ROCK pathway in CIH-induced hypertension in rats. The role of the Nox4-derived ROS-mediated RhoA/Rho kinase pathway in rat hypertension induced by chronic intermittent hypoxia. CIH elicits systemic oxidative stress and sympathetic hyperactivity, which lead to hypertension. 28189710: Since estradiol has two main receptors (ERalpha and ERbeta) we will discuss their relative implications, and present new data showing a key role for ERalpha to prevent the hypertension induced by intermittent hypoxia. 28451849: Although it is well known that CIH produces hypertension, the underlying mechanisms are not totally elucidated. In this review, we will discuss the supporting evidence for a critical role of the CB in the generation and maintenance of the hypertension induced by CIH, also, the contribution of oxidative stress to enhance CB chemosensory drive and the activation of sympathetic-related centers in the brain. 28811528: Prenatal hypoxia leads to hypertension, renal renin-angiotensin system activation and exacerbates salt-induced pathology in a sex-specific manner. 28835062: Conclusions: Repeated intermittent hypoxia can induce hypertension and myocardial contractibility damage in OSA model rabbit simulating upper airway obstruction. 28901415: However, the association between chronic inflammation and high blood pressure caused by hypoxia remains to be fully elucidated. 29386711: Background: Chronic intermittent hypoxia is known to induce systemic arterial hypertension whereas chronic hypoxia causes pulmonary arterial hypertension. 29604069: Severe hypoxia causes hypertension with cardiovascular sequelae; however, the rare studies using moderate severities of hypoxia indicate that it can be beneficial, suggesting that hypoxia may not always be detrimental. 29897299: Advances in our understanding of brain mechanisms for the hypoxic ventilatory response, coordinated changes in blood pressure, and the long-term consequences of chronic intermittent hypoxia as in sleep apnea, such as hypertension and heart failure, are giving impetus to the search for therapies to \erase\ dysfunctional memories distributed in the carotid bodies and central nervous system. 29988603: We suggest that the sex-based difference in neuroplasticity of this structure contributes to the reported sex-based difference in CIH-induced hypertension. This structure contains neurons that generate the sympathetic tone and which are involved in CIH-induced sustained hypertension during waking hours. 30022321: Paroxysmal sympathetic hyperactivity occurs after brain injury, hypoxia and cerebrovascular and other events, causes paroxysmal tachycardia, hypertension, tachypnoea and hyperthermia and is associated with a poorer prognosis and prolonged intensive care treatment. 30050461: Oxidative stress and pro-inflammatory molecules contribute to the activation of the CB chemoreflex pathway in CIH-induced hypertension. Oxidative stress, inflammation, and sympathetic overflow have been proposed as possible mechanisms underlying the CIH-induced hypertension. In this brief review, we will discuss new evidence for a critical role of oxidative stress and neuro-inflammation in development of the CIH-induced hypertension through activation of the CB chemoreflex pathway. 30087615: CIH-induced hypertension (~8 mmHg) was reverted by ABH, NAC, and ABH/NAC administration. 30112560: The purpose of this study is to investigate the effect of the oral endothelin antagonist Bosentan on blood pressure and renal sympathetic nerve activity (RSNA) in rats exposed to chronic intermittent hypoxia (CIH), and to explore the sympathoexcitation mechanism of endothelin-1 (ET-1) in CIH-induced hypertension. 30246291: Also, microRNA-223 (miR-223) plays a role in the regulation of CIH-induced PH process. 30259991: This study aimed to investigate the effect of hydrogen (H2 ) gas on hypertension induced by intermittent hypoxia in rats. 30279800: The oxygen-triggered nocturnal BP monitoring that was conducted at home around the same time indicated remarkable hypoxia-induced hypertension (Day 1: hypoxia-peak nocturnal BP 181/117 mmHg, Day 2: hypoxia-peak nocturnal BP 204/137 mmHg). Remarkable hypoxia-induced nocturnal hypertension was identified by oxygen-triggered blood pressure (BP) monitoring. A daytime normotensive patient with nocturnal hypoxia-induced hypertension and severe obstructive sleep apnea. 30354709: Further in vivo studies showed that intra-fourth ventricle infusion of K41498 did not affect the basal blood pressure but significantly attenuated the IH-induced hypertension; intra-fourth ventricle infusion of Urocortin II significantly increased basal blood pressure and exacerbated the IH-induced hypertension. CRHR2 (Corticotropin-Releasing Hormone Receptor 2) in the Nucleus of the Solitary Tract Contributes to Intermittent Hypoxia-Induced Hypertension. This study tested the hypothesis that CRHRs (corticotropin-releasing hormone receptors) in the nucleus of the solitary tract (NTS) contribute to the hypertension induced by intermittent hypoxia (IH) exposure in rats. Collectively, these results suggest that CRHR2 in the NTS contributes to the IH-induced hypertension; downregulation of CRHR2 and CRHR2-mediated calcium influx in the NTS may serve as an adaptive response to protect against the IH-induced hypertension. 30357735: Sympathetic overflow, oxidative stress and inflammation have been associated with the CIH-induced hypertension. 30357737: Previous data showed the lack of efficacy of an adrenoceptor antagonist to revert hypertension induced by chronic intermittent hypoxia (CIH). Cysteine Oxidative Dynamics Underlies Hypertension and Kidney Dysfunction Induced by Chronic Intermittent Hypoxia. 30446434: INTERPRETATION: Increased carotid body chemo-afferent signalling appears obligatory for the development of CIH-induced hypertension and elevated chemoreflex control of breathing commonly reported in mammals, with hypoxia-sensitive carotid bodies. BACKGROUND: Carotid body (peripheral oxygen sensor) sensitisation is pivotal in the development of chronic intermittent hypoxia (CIH)-induced hypertension. 30466186: In this study, we examined whether activation of CNS MC4R contributes to chronic intermittent hypoxia (CIH)-induced hypertension and ventilatory responses to hypercapnia. Role of melanocortin 4 receptor in hypertension induced by chronic intermittent hypoxia. However, when MC4R-deficient rats were food restricted to prevent obesity, CIH-induced hypertension was attenuated by 32%. CIH-induced hypertension was not attenuated by MC4R antagonism (average increase of 10 +/- 1 vs 9 +/- 1 mm Hg for untreated and SHU-9119 treated rats). 30609027: We hypothesized that sensory plasticity of the carotid body (CB) and oxidative stress in the paraventricular nucleus (PVN) are involved in CIH-induced hypertension. Chronic intermittent hypoxia (CIH) is known to induce hypertension, but the mechanism is not well understood. 30635990: We hypothesized that agonists of oestradiol receptors (ER) alpha and beta prevent CIH-induced hypertension and brain mitochondrial dysfunction. CONCLUSIONS: We conclude that in OVX female rats, the ERalpha agonist prevents from CIH-induced hypertension while both ERalpha and ERbeta agonists prevent the brain mitochondrial dysfunction and metabolic switch induced by CIH. 30810064: In rodents, endothelin (ET)-1 contributes to IH-induced hypertension, and ET-1 levels inversely correlate with glomerular filtration rate in patients with end-stage chronic kidney disease (CKD). 30889910: Taken together, in organisms with hypoxia induced oxidative stress 5-HT levels were found to be abnormally elevated, indicating that 5-HT could regulate oxidative stress, and the decrease in the 5-HT levels, behavioral abnormalities after treatment with cinnabar and Zuotai, we may conclude that the therapeutic and pharmacologic effect of cinnabar and Zuotai may be based on the regulation of 5-HT metabolism and relief of oxidative stress. 30892911: Angiotensin type 1a receptors in the median preoptic nucleus support intermittent hypoxia-induced hypertension. 30930131: Obstructive sleep apnea patients face episodes of chronic intermittent hypoxia (CIH), which has been suggested as a causative factor for increased sympathetic activity (SNA) and hypertension. 31105584: Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension? We draw focus to the potential contribution of aberrant renal afferent signaling in the development, maintenance and progression of high blood pressure, which may have relevance to CIH-induced hypertension. 31163095: Chronic intermittent hypoxia-induced hypertension: An expired hypothesis laid to rest? 31482626: Brainstem adrenomedullin facilitates intermittent hypoxia-induced hypertension: A sympathetic story of a selfish brain. 31675258: We hypothesized that pathway-specific lesions of the projection from the MnPO to the PVN would attenuate the sustained component of chronic intermittent hypoxia -induced hypertension. 31820496: Active expiration and chronic intermittent hypoxia-induced hypertension: A hypothesis that still breathes! 32416216: First evidence of aryl hydrocarbon receptor as a druggable target in hypertension induced by chronic intermittent hypoxia. 32664461: DOM, acute or chronically administered during the last 15 days of CIH, reversed the hypertension produced by CIH, an analogous effect to that obtained with CB denervation. 32779153: Sprague Dawley rats were exposed to chronic intermittent hypoxia (CIH) for 8 weeks to induce OSAS-hypertension. miR-126a-3p targets HIF-1alpha and alleviates obstructive sleep apnea syndrome with hypertension.The obstructive sleep apnea syndrome (OSAS) is a common sleep-related breathing disorder and an important cause of refractory hypertension. 33002479: Renal denervation improves chronic intermittent hypoxia induced hypertension and cardiac fibrosis and balances gut microbiota. Renal denervation improves chronic intermittent hypoxia induced hypertension and cardiac fibrosis and balances gut microbiota.AIMS: Investigate the effect of renal denervation (RDN) on chronic intermittent hypoxia (CIH) induced high blood pressure (BP) and cardiac injury, and explore whether the effect is associated with gut microbiota alteration and its product, trimethylamine N-oxide (TMAO). 33210151: This study evaluated whether beta-blocker treatment with propranolol (Prop) prevented the development of CB hyperactivity, vascular sympathetic nerve growth and hypertension caused by CIH. 33253916: Therefore, targeting mtROS may serve as an effective therapeutic strategy to prevent hypoxia-induced hypertension. 33595364: Chronic intermittent hypoxia is a model of the hypoxemia associated with sleep apnea and results in a sustained hypertension that is maintained during normoxia. 3381706: Morphometry of right ventricular papillary muscle in rat during development and regression of hypoxia-induced hypertension. 33928137: PE is initiated by inadequate spiral artery remodeling and subsequent placental ischemia/hypoxia, which stimulates release of bioactive factors into maternal circulation, leading to hypertension and renal damage. 34257425: In summary, we have identified that physiological testosterone protects against hypoxia-induced hypertension through inhibition of NRF1, which transcriptionally regulates ACE and ET-1 expression. Hypertension induced by hypoxia at high altitude is one of the typical symptoms of high-altitude reactions (HARs). Testosterone attenuates hypoxia-induced hypertension by affecting NRF1-mediated transcriptional regulation of ET-1 and ACE. 34297635: Collectively, these findings indicate that KDM6B functions as a coactivator of HIF-1-mediated Nox4 transactivation and demonstrate a hitherto uncharacterized role for KDM's in IH-induced hypertension by HIF-1. Hypoxia-inducible factor (HIF)-1-dependent transcriptional activation of NADPH oxidases (Nox) and the resulting increase in reactive oxygen species (ROS) levels is a major molecular mechanism underlying IH/OSA-induced hypertension. 34580424: Reply to a letter to the Editor regarding the article \Testosterone attenuates hypoxia-induced hypertension by affecting NRF1-mediated transcriptional regulation of ET-1 and ACE\. 34845629: Gestational chronic intermittent hypoxia induces hypertension, proteinuria, and fetal growth restriction in mice. 35150411: Correction to: Gestational chronic intermittent hypoxia induces hypertension, proteinuria, and fetal growth restriction in mice. 35270026: Prenatal hypoxia during the prenatal period can interfere with the developmental trajectory and lead to developing hypertension in adulthood. 35319374: The available evidence supports the theory that oxidative stress and hypoxic inducible factors upregulate and activate STIM-activated TRPC-ORAI Ca2+ channels, contributing to the pulmonary remodeling and hypertension induced by sustained hypoxia. 35554421: Chronic intermittent hypoxia (CIH) in rodents mimics the hypoxia-induced hypertension seen in these individuals. 35560693: Blockade of Trpm7 in the Carotid Body area attenuated intermittent hypoxia-induced Hypertension. We hypothesize that IH causes hypertension acting on CB TRPM7. CONCLUSION: Our study has shown that inhibition of TRPM7in the carotid bodies abolished IH-induced hypertension. We discovered that obesity-induced hypertension is mediated via the transient receptor potential melastatin 7 (TRPM7) channel in the glomus cells of CB. FTY720 hydrogel abolished IH-induced hypertension by decreasing blood pressure to 106.6+/-1.6 mmHg (p<0.005) on Day 1 of IH and to 101.5+/-1.6 mmHg (p<0.001) on Day 5 of IH. In contrast, control hydrogel had no effect on IH-induced hypertension. Intermittent hypoxia (IH), a hallmark manifestation of OSA, is an established cause of hypertension. 35677200: On the contrary, intermittent hypoxia in OSA causes hypertension, metabolic syndrome, vascular function impairment, quality of life and cognitive scores reduction, advanced brain aging, increase in insulin resistance, plasma hydrogen peroxide, GSH, IL-6, hsCRP, leptin, and leukocyte telomere shortening. 35682548: However, the reason why hypertension is induced by IH is elusive. 36721994: Mice with global and VSMC-specific knockout of Atic were utilized to investigate the role of ATIC in both hypoxia- and lung interleukin-6/hypoxia-induced murine PH. 36794581: This study aimed to determine if chemogenetic activation of hypothalamic OXT neurons in animals with existing obstructive sleep apnea-induced hypertension would reverse or blunt the progression of autonomic and cardiovascular dysfunction. Hypothalamic OXT (Oxytocin) Neuron Activation Attenuates Intermittent Hypoxia-Induced Hypertension and Cardiac Dysfunction in an Animal Model of Sleep Apnea. BACKGROUND: Obstructive sleep apnea is a prevalent and poorly treated cardiovascular disease that leads to hypertension and autonomic imbalance. METHODS: Two groups of rats were exposed to chronic intermittent hypoxia (CIH), a model of obstructive sleep apnea, for 4 weeks to induce hypertension. 36963360: We found that butyrate intervention further inhibited systemic inflammatory response and vascular wall remodeling by improving the intestinal microenvironment in IH rats, thereby attenuating IH-induced hypertension. BACKGROUND: We aimed to investigate whether Taraxacum officinale (T. officinale)-derived exosome-like nanovesicles (ELNs) exerted hypotensive effects in intermittent hypoxia (IH)-induced hypertensive disorders and their potential mechanisms. CONCLUSIONS: T. officinale-derived ELNs were effective in the treatment of IH-induced hypertensive disease, whereas butyrate played a major role in mediating the effects of ELNs in anti-IH-induced hypertensive disease. Taraxacum officinale-derived exosome-like nanovesicles modulate gut metabolites to prevent intermittent hypoxia-induced hypertension. Therefore, we further evaluated whether butyrate was a key target for ELNs to exert their effects in IH-induced hypertensive disease. We found that ELNs effectively reduced IH-induced hypertension, exhibited local anti-inflammatory effects on intestinal tissues in a rat model of IH-induced hypertension, and reduced intestinal tissue damage, including loss of goblet cells and barrier integrity damage, and ultimately inhibited the systemic inflammatory response. 3739598: Scanning electron microscopy of pulmonary vascular endothelium in rats with hypoxia-induced hypertension. 37823770: Gestational intermittent hypoxia induces endothelial dysfunction and hypertension in pregnant rats: role of endothelin type B receptor?. Treatment with IRL-1620 during IH exposure significantly attenuated IH-induced hypertension in pregnant rats. 37882783: CIH causes hypertension, centred on sympathetic nervous overactivity, which persists following removal of the CIH stimulus. 37932867: RESULTS: Twenty-one days of CIH induced autonomic imbalance and hypertension in rats. 38276286: Possible Molecular Mechanisms of Hypertension Induced by Sleep Apnea Syndrome/Intermittent Hypoxia. Since SAS is linked to various serious cardiovascular complications, especially hypertension, many studies have been conducted to elucidate the mechanism of hypertension induced by SAS/IH. This review outlines the molecular mechanisms of hypertension in IH, which include the regulation systems of reactive oxygen species (ROS) that activate the renin-angiotensin system (RAS) and catecholamine biosynthesis in the sympathetic nervous system, resulting in hypertension. As hypertension is the most common complication of SAS, cell and animal models to study SAS/IH have developed and provided lots of hints for elucidating the molecular mechanisms of hypertension induced by IH. 38310188: In conclusion, ZFX knockdown protected mice from hypoxia-induced PAH injury. 38406843: The effect of sex on the pathophysiology of sleep apnea and associated intermittent hypoxia-induced hypertension is of important consideration in the screening, diagnosis, and treatment of the disease and its cardiovascular complications. The lack of protection in men and postmenopausal women implicates estrogen and progesterone as protective agents but testosterone as a permissive agent in sleep apnea-induced hypertension. A better understanding of how sex hormones contribute to the pathophysiology of sleep apnea-induced hypertension is important for future research and possible hormone-based interventions. 4357176: Fine structural alterations of bovine peripheral pulmonary arteries in hypoxia-induced hypertension. 6342920: It is paradoxical that hypoxia, whose lesions are more reversible, produces a more severe hypertension and faster than the others. 687468: Hypertension resulting from hypoxia, hypercapnia, shivering, or arousal from anaesthesia was excluded from consideration. 7484175: We have therefore evaluated the effects of ET-infusion in the porcine pulmonary circulation after hypoxia-induced hypertension. 8576865: It is concluded that adenosine mediates the fetal bradycardia and hypertension produced by hypoxia, indicating that adenosine modulates fetal autonomic responses to acute oxygen deficiency. 8594026: Exposure to hypoxia (2-5 wk) results in systemic hypertension in rats and in humans. 8731114: Given the transient nature of the rise in its plasma concentration, endogenous EPO does not appear to play a role in the genesis of the observed systemic HTN. Sustained systemic arterial hypertension induced by extended hypobaric hypoxia. Thus, prolonged hypobaric hypoxia leads to a severe hematocrit-independent systemic hypertension (HTN) that persists long after the restoration of normoxia. 9284071: Moderate hypoxia resulted in a modest hypertension of approximately 15 mmHg, and in the expression of Fos (a marker of neuronal activation) in many neurons in the nucleus tractus solitarius, the rostral, intermediate and caudal parts of the ventrolateral medulla, the Kolliker-Fuse nucleus, locus coeruleus, subcoeruleus and A5 area in the pons as well as in several midbrain and forebrain regions, including the periaqueductal grey in the midbrain and the paraventricular, supraoptic and arcuate nuclei in the hypothalamus. 9488210: Hypertension caused by chronic intermittent hypoxia--influence of chemoreceptors and sympathetic nervous system. 9612293: The purpose of the present study was to determine the effect of hypoxia-induced hypertension on the structure and function of PASM. 9648078: CONCLUSIONS: We conclude that hypoxia-induced HTN is associated with depressed NO production and can be mitigated by L-arginine supplementation. This study was designed to test the hypothesis that hypoxia-induced HTN may be mediated by increased endothelin and/or decreased NO production. BACKGROUND: We have recently demonstrated that prolonged hypobaric hypoxia can lead to a hematocrit-independent sustained arterial hypertension (HTN) in genetically normotensive Sprague-Dawley rats. Role of endothelin and nitric oxide imbalance in the pathogenesis of hypoxia-induced arterial hypertension. 9878890: Chronic intermittent hypoxia (CIH) may cause sustained systemic hypertension by increasing sympathetic neural discharge (SND). 15681798: One of the logical approaches to this problem is to study the effects of ischemia and hypoxia on the metabolism of amyloid precursor protein, which plays one of the key roles in the pathogenesis of AD. 17121991: Taken together, our results clearly demonstrate that hypoxia can facilitate AD pathogenesis, and they provide a molecular mechanism linking vascular factors to AD. 17999180: Hypoxia is one of the major common components of vascular risk factors for pathogenesis of Alzheimer's disease. 18063223: The greatly increased incidence of AD following stroke and cerebral ischemia suggests that hypoxia is a risk factor which may accelerate AD pathogenesis by altering amyloid precursor protein (APP) processing. 21909359: Cerebrovascular integrity was characterized in Tg2576 AD model mice that overexpress the human amyloid precursor protein (APP) containing the double missense mutations, APPsw, found in a Swedish family, that causes early-onset AD. 22886562: This article systematically delineates the steps in the complex cascade leading to AD, focusing on pathology caused by chronic intermittent hypoxia, hypertension, brain hypoperfusion, glucose dysmetabolism, and endothelial dysfunction. Owing to the pathological impact of hypoxia, hypertension, hypoperfusion and impaired glucose metabolism, the adverse cardiovascular, neurocirculatory and metabolic consequences upregulate amyloid beta generation and tau phosphorylation, and lead to memory/cognitive impairment-culminating in AD. 23345083: However, the mechanism of hypoxia in the pathogenesis of AD remains unclear. 23400634: Strong evidence underscores that cerebral amyloidogenesis and tau phosphorylation--two cardinal features of Alzheimer's disease (AD), are triggered by hypoxia. 24650677: Our previous studies have documented that chronic hypoxia is one of the environmental factors that may trigger the AD development and aggravate the disease progression. 26351108: This study suggests that there is an association between chronic intermittent hypoxia and increased Abeta levels, implying that hypoxia may contribute to the pathogenesis of Alzheimer's disease. 26617286: Hypoxia and GABA shunt activation in the pathogenesis of Alzheimer's disease. 28562318: Intermittent hypoxia produces Alzheimer disease? 29423001: Hypoxia promotes the accumulation of amyloid-beta (Abeta), which is related to the pathogenesis of Alzheimer's disease (AD). 29867325: In summary, all these findings suggest that acute hypoxia could induce the AD-like pathological damages in the brain of APPswe/PS1dE9 mice and Wt mice to some extent. 29931858: OBJECTIVE: To further study the regulation of hypoxia on Alzheimer's disease (AD) pathogenesis, we investigate the effect of hypoxia on the effect of cell survival and expression of related proteins in HEK293 cells stably expressing APP695 Swedish mutantK595N/M596L (HEK293-APP695 cells). 31934303: In the present study, a cellular model of hypoxia-induced AD was established by exposing HT-22 mouse hippocampal neurons to the chemical hypoxia-mimicking agent cobalt chloride (CoCl 2 ). 32548235: Introduction: It has been reported that environmental factors such as hypoxia could contribute to the pathogenesis of Alzheimer's disease (AD). 34130857: CONCLUSIONS: CIH-induced increase in pathologic human tau seeding and spread and exacerbation of other AD-related impairments provide new insights into the role of CIH and obstructive sleep apnea in AD pathogenesis. 35799509: Hypoxia is one of the important factors that contribute to the pathogenesis of AD. 37490963: This review summarizes the effects of normoxia and hypoxia on AD pathogenesis and discusses the underlying mechanisms. 32034489: These changes could have an impact on the pathogenesis of HT and progression of CAD. 32999396: The C variant of a new component of the RAS, C9orf3 (rs4385527) might have a considerable impact on the pathogenesis of hypertension in diabetes. 33025414: This peptide also exerts significant impact at the level of vasculature leading to lowering high blood pressure and reversal of endothelial dysfunction and atherosclerosis. 33640277: BACKGROUND: High-fat diet (HFD) had a complex impact on the myocardium and resulted in diastolic dysfunction and hypertension on left ventricular (LV) hypertrophy, which can cause cardiac remodeling. 33793336: These conditions activate the immune system either directly or through their impact on the gut microbiome, which ultimately produces chronic inflammation and hypertension. 34327456: The extraordinary expansion of cardiometabolic risk factors, the impact they generate in the development of hypertension and its specific phenotypes, and its implications in cardiovascular risk and therapeutic decision-making deserve an extensive and careful reflection. 35333120: These findings have important implications for the role of mechanosensitive proteins in CFs and their impact on cardiomyocyte function in the pathogenesis of hypertension and cardiac hypertrophy. 36315414: Therefore, long-term treatment has a negative impact on different metabolic systems and can lead to hypertension, dyslipidemia and insulin resistance. 37909881: SUMMARY: NCC and ENaC are integral components, and their malfunctions lead to disorders like LS and PHAII, hereditary causes of hypertension. Although lifestyle choices and environmental factors are known to have a significant impact on its development, there is growing recognition of the influence of genetic factors in the pathogenesis of hypertension. 38383871: These insights allow characterization of the impact of regionally varying vascular remodeling on hemodynamics and mouse-to-mouse variations due to induced hypertension. 32479244: CONCLUSION: Examining the impact, as well as the consequences of protein misfolding, could help to uncover the molecular etiologies behind the complicated AD pathogenesis. 33679375: In this review, we focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of AD, emphasizing a framework of existing and potential therapeutic approaches. Over the last few years, remarkable efforts have been made to investigate the impact on the pathogenesis of Alzheimer's disease (AD) of various forms of mitochondrial dysfunction, such as excessive reactive oxygen species (ROS) production, mitochondrial Ca 2+ dyshomeostasis, loss of ATP, and defects in mitochondrial dynamics and transport, and mitophagy. 34052817: New theories on the link between sleep and beta-amyloid and tau secretion, accumulation and clearance, and its interaction with hypocretins/orexins (key neuropeptides regulating wakefulness) suggest mechanistic ways to better understand the impact of sleep alterations in the pathogenesis of AD. 34292312: Finally, we outline future directions for delineating the microglial impact in AD pathogenesis. 34685649: Here, we investigated the impact of NF-kappaB-initiated neuroinflammation on AD pathogenesis using the APP23 mouse model of AD in combination with conditional activation of IKK2/NF-kappaB signaling in astrocytes. 35034901: The combination of biochemical/biophysical and 'omics-based studies of these variants needed to elucidate their downstream impact and molecular contributions to AD pathogenesis is highlighted. 35109353: CONCLUSION: There are some evidences of common molecular pathways involved in AD and ischemic stroke, which require further investigations to evaluate cerebral vascular impacts on the pathogenesis of AD. 35289012: We consider how abnormalities of the constituent cells of the neurovascular unit - particularly of endothelial cells and pericytes - and impairment of the blood-brain barrier (BBB) impact on the pathogenesis of AD. 35572126: The following review will explore the impact of p53 PTMs on its function and consequential involvement in AD pathogenesis. 35624892: The provocative question arising is the following: is it possible that the beneficial effects of regular exercise on AD are due to the systemic impact of training, rather than just the effects of exercise on the brain? 36395955: Here, we generated a novel AD mouse model deficient for Neil3 to study the impact of impaired oxidative base lesion repair on the pathogenesis of AD. 37176104: Many preclinical and clinical trials have explored the impact of adjusting the whole-body and intracellular metabolism on the pathogenesis of AD. 37556014: This study aims to determine if two distinct doses of myco-fabricated ZnO-NPs have a positive impact on behavioral impairment and several biochemical markers associated with inflammation and oxidative stress in mice that have been treated by aluminum chloride (AlCl 3 ) to induce AD. 37801071: To assess the impact of vitamin D3 (Vit.D) on neurogenesis, we investigated its role in mitigating cognitive impairment and mitochondrial dysfunction through calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2)-mediated phosphorylation of Sirtuin1 (SIRT1) in an aluminum-chloride-D-galactose (AlCl3-D-gal)-induced AD rat model. 37878335: We investigated the impact of BHB on Abeta oligomer (AbetaO)-stimulated human iPS-derived microglia (hiMG), a model relevant to the pathogenesis of Alzheimer's disease (AD). 38617186: Future studies exploring this impact on the pathogenesis of AD and related biomarkers are needed. 12398296: Combinations using an alpha2-adrenoceptor agonist and ketamine have been shown to be effective for immobilization but are not reversible and can produce severe hypertension and prolonged or rough recoveries. 32039692: We developed a combined mechano-electrical acupuncture device (MEA) and examined the effects of acupuncture at Neuro-Sps on systolic blood pressure (BP) in a rat model of immobilization-induced hypertension (IMH) and the mediation of endogenous opioid systems in its effect. 32956833: Stimulatory effects of the Neuro-Sps were examined in a rat model of immobilization-induced hypertension (IMH). 3682581: These experiments demonstrate different hemodynamic mechanisms of immobilization-induced hypertension in rabbits and rats. 3735586: Immobilization resulted in an initial hypertension which was normalized after tolazoline HCl administration. 37358315: All three drug combinations provided smooth inductions and effective immobilisations but resulted in hypertension. 3801131: The radioactive microsphere technique was used to study hemodynamic mechanisms of action of 2 calcium antagonists--foridon and nifedipine in conscious rabbits with acute hypertension evoked by immobilization. 4701493: Serum dopamine-beta-hydroxylase during development of immobilization-induced hypertension. 5059316: Hypercalcemia associated with hypertension due to prolonged immobilization. 6995969: Acute immobilization stress induced in rats with normal blood pressure caused activation of the adrenal cortex glucocorticoid function without increase of aldosterone biosynthesis or of its blood content, whereas in rats with hypertension the same stress led to adrenal cortex mineralocorticoid function activation and to the sharp blood plasma aldosterone elevation. 10477041: Nitric oxide in cyclosporine A-induced hypertension: endothelin receptors gene expression. Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. 11993718: Nitric oxide in CsA-induced hypertension: role of beta-adrenoceptor antagonist and thromboxane A2. This suggests that PKC mediate, in part, CsA-induced hypertension. Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. 18249224: Transplant recipients have an unfavorable cardiovascular risk profile and experience more cardiovascular morbidity and mortality compared with the general population, primarily because of immunosuppressant-induced diabetes, hypertension, and hyperlipidemia. 23809336: Cyclosporin A (CsA) is a widely used immunosuppressive agent that also causes hypertension. However, the molecular basis for CsA-induced hypertension remains elusive. Furthermore, this organ culture system would be an ideal in vitro tool to study the molecular mechanisms of CsA-induced hypertension. 25216697: It is strongly related to hypertension induced by steroids and other immunosuppressive agents. 35227873: Immunosuppressive agents can cause hyperlipidemia, hypertension, post-transplant diabetes, and glomerulopathy. 37708245: alpha2delta-1 as a New Target for Immunosuppressant-Induced Hypertension. 9072458: Cyclosporine A-induced hypertension in SHR and WKY: role of the sympatho-adrenal system. It is concluded that immunosuppressive agents like cyclosporine or FK506 activate the sympatho-adrenal system in normotensive and genetically hypertensive rats, thereby inducing hypertension. Depletion of catecholamine stores by reserpine also diminished significantly the cyclosporine induced hypertension. Selective alpha1-adrenergic receptor blockade by prazosin blunted acute hypertension induced by cyclosporine. 9551405: Cyclosporine A (CsA), a widely used immunosuppressive agent, causes renal vasoconstriction and systemic hypertension. 9822443: Cyclosporine A (CsA) is an immunosuppressive agent that also causes hypertension. 21504127: Mild cognitive impairment (MCI) is recognized as a prodromal phase of dementing disorders, and it has been suggested that oxidative stress may play a role in the pathogenesis of Alzheimer's disease (AD), and in predicting progression of MCI to AD. 32804131: The Contribution of Vascular Pathology Toward Cognitive Impairment in Older Individuals with Intermediate Braak Stage Tau Pathology.BACKGROUND: The pathological features of Alzheimer's disease (AD) are well described but little is known as to how both neurodegeneration and vascular changes might interact in causing cognitive impairment. 32847949: 1 This represents an important advance because it allows us to investigate the relationship of risk factors with cognitive impairment at the level of the etiology of AD. 33206363: Many evidence confirms that amyloid beta 1-42 fragment (Abeta 1-42 ) causes neuroinflammation, oxidative stress, and cell death, which are related to progressive memory loss, cognitive impairments and mental disorders that will lead to Alzheimer's disease (AD) progression. 33670778: The Role of Butyrylcholinesterase and Iron in the Regulation of Cholinergic Network and Cognitive Dysfunction in Alzheimer's Disease Pathogenesis. 33941272: Meanwhile, COVID-19 has also been reported to cause various neurologic symptoms including cognitive impairment that may ultimately result in AD, probably through the invasion of SARS-CoV-2 into the central nervous system, COVID-19-induced inflammation, long-term hospitalization and delirium, and post-COVID-19 syndrome. 36270437: In conclusion, this study demonstrates the importance of early-stage prevention of microgliosis on the development of cognitive impairment in APP/PS1 mice, which might be clinically relevant in preventing memory loss and delaying AD pathogenesis. 36949264: Emerging evidence recommended that resistance in insulin production develops cognitive dysfunction, which generally leads to AD. 37481287: Alzheimer's disease (AD) brings with it the need to think about the loss of autonomy caused by cognitive impairment, and how to manage it. 37864249: Impaired autophagy in plaque-associated microglia (PAM) has been reported to accelerate amyloid plaque deposition and cognitive impairment in AD pathogenesis. 38158451: Altered empathic mechanisms observed in AD may be a consequence of cognitive impairment, more specifically of reduced mental flexibility and self-regulation. 38159199: Downregulation of ATF-4 Attenuates the Endoplasmic Reticulum Stress-Mediated Neuroinflammation and Cognitive Impairment in Experimentally Induced Alzheimer's Disease Model. 38212861: APOE modifies microstructural patterns associated with aging and cognitive impairment, which may advance the development of biomarkers to distinguish microstructural changes characteristic of normal brain aging, APOE-dependent pathways, and non-AD etiologies. 32564756: Alzheimer's disease: new concepts on the role of autoimmunity and of NLRP3 inflammasome in the pathogenesis of the disease.Alzheimer's disease (AD), recognized as the most common neurodegenerative disorder, is clinically characterized by the presence of extracellular beta amyloid (Abeta) plaques and by intracellular neurofibrillary tau tangles, accompanied by glial activation and neuroinflammation. 33181351: The NLRP3 inflammasome triggers sterile neuroinflammation and Alzheimer's disease. 34209586: This review summarizes the current literature on the role of the NLRP3 inflammasome in the pathogenesis of AD, and its involvement in infections, particularly SARS-CoV-2. 34219728: Among the known inflammasomes, the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome plays a critical role in the pathogenesis of AD. 34381452: By researching the activation or inactivation of NLRP3 inflammasome, it is possible to reveal the pathogenesis of AD from a new perspective and provide a new idea for the prevention and treatment of AD. Activation of the NLRP3 inflammasome play a key role in the pathogenesis of Alzheimer's disease (AD). 35250595: In this review, we summarize current literatures on the activation of NLRP3 inflammasome and activation-related regulation mechanisms, and discuss its possible roles in the pathogenesis of AD. 35382471: Amyloid beta-peptide (Abeta) aggregation and nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome play crucial roles in the pathogenesis of AD. 35966798: Here, we studied the expressional change of HECT-E3 ligase using M01 on autophagy and inflammasome pathways in the context of AD pathogenesis. 36802053: Mechanistic and therapeutic role of NLRP3 inflammasome in the pathogenesis of Alzheimer's Disease. 37055801: However, the specific mechanism of NLRP1 inflammasome in the pathogenesis of AD is still unclear. 12646422: In this study, we tested the hypothesis that inflammation leads to altered mucosal 5-HT signaling. 17003837: For instance, oxidative stress in the kidney and vascular tissue is the primary mediator in the pathogenesis of angiotensin-induced, and perhaps lead-induced, hypertension. Mechanisms of disease: oxidative stress and inflammation in the pathogenesis of hypertension. Animal studies have shown that oxidative stress and renal tubulointerstitial inflammation are associated with, and have major roles in, the pathogenesis of hypertension. 17023572: Since earlier studies have provided compelling evidence for the role of oxidative stress and tubulointerstitial inflammation in the pathogenesis of hypertension, we tested the hypothesis that partial SOD2 deficiency may result in hypertension. High-salt diet induced hypertension in 6-mo-old SOD2-deficient mice but not in wild-type mice. 17567935: Since oxidative stress, renal inflammation, and angiotensin activity are closely linked characteristics in experimental models of hypertension, we decided to investigate whether lead-induced hypertension would be ameliorated by suppressing renal inflammation with the immunosuppressive drug mycophenolate mofetil (MMF). 17698879: Inflammation in the genesis of hypertension and its complications--the role of angiotensin II. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 19770776: These data suggest that inflammation and endothelial dysfunction may play a role in the cause of hypertension. 20686485: The present investigations are directed to gain insight in the role of the intrarenal T-cell reactivity and autoimmunity in driving the tubulointerstitial inflammation and its participation in the pathogenesis of salt-sensitive hypertension. 20944659: It has been suggested that inflammation is important in the aetiology of hypertension and that this may be most relevant among obese persons. 21196131: In recent years a major research effort has focused on the role of inflammation, and in particular adaptive immunity, in the genesis of hypertension. 21642978: This form of hypothalamic inflammation-induced hypertension involved the sympathetic upregulation of hemodynamics and was reversed by sympathetic suppression. 21723497: A recent paper in Nature Medicine (Purkayastha et al., 2011) suggests that obesity and hypertension are caused by inflammation in distinct hypothalamic neuronal populations. 21833043: BACKGROUND: Inflammation and oxidative stress have been identified as integral parts in the pathogenesis of hypertension. 22381923: OBJECTIVE: Inflammation plays a role both in the mechanisms leading to hypertension alone and in the mechanisms leading to atherosclerosis with hypertension. 22713149: Inflammation and activation of immunity are central features in the pathogenesis of atherosclerosis, ischemic myocardial injury, and hypertension-induced target-organ damage. 23036901: Reducing the renal infiltration of T cells prevents or ameliorates hypertension and the induction of tubulointerstitial inflammation results in salt-sensitive hypertension. 23165109: Renal tubulointerstitial inflammation results in salt-sensitive hypertension and, until recently, the changes in pressure natriuresis induced by renal inflammation received little attention. 23325143: Based on the recent studies that highlight the involvement of inflammation in the development of hypertension, we hypothesize that changes in DNA methylation of leukocytes are involved in the pathogenesis of hypertension. 23472597: The cooperative roles of inflammation and oxidative stress in the pathogenesis of hypertension. CRITICAL ISSUES: Inflammation and oxidative stress thereby act as cooperative and synergistic partners in the pathogenesis of hypertension. 24078347: Severe psoriasis has been associated with increase cardiovascular mortality, due to a higher prevalence of traditional cardiovascular risk factors such as diabetes, hypertension, dyslipidemia and obesity, and premature atherosclerosis, as a consequence of its systemic inflammation. 25107929: These approaches and the outcomes of genome-wide-association studies broaden our view of blood pressure control, suggesting that renal sympathetic nerve activity and local inflammation can impair pressure natriuresis to cause hypertension. 25221387: RATIONALE: Accumulated evidence implicates sympathetic activation as inducing oxidative stress and systemic inflammation, which in turn lead to hypertension, endothelial dysfunction, and atherosclerosis in obstructive sleep apnea (OSA). 25244096: Here, we have described a pathway in which hypertensive stimuli promote dendritic cell (DC) activation of T cells, ultimately leading to hypertension. Oxidative damage and inflammation are both implicated in the genesis of hypertension; however, the mechanisms by which these stimuli promote hypertension are not fully understood. 25411054: This finding may have important implications for understanding the effects of DPP4 in promoting inflammation and oxidative stress in the pathogenesis of hypertension. 25498375: We also propose a hypothesis for why mechanisms underlying inflammation-induced hypertension are sex-specific. 25623850: SIGNIFICANCE: These findings indicate that NO induced-hypertension is associated with up-regulation of NADPH oxidase, oxidative stress production and overexpression of key inflammatory mediators. Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension. Nitric oxide (NO) inhibition with N(w)-nitro-L-arginine methyl ester (L-NAME) has previously been reported to produce hypertension, increased expression of Angiotensin II (Ang II) and renal dysfunction. The current study was designed to test the hypothesis that AT1R activation promotes renal NAD(P)H oxidase up-regulation, oxidative stress and cytokine production during L-NAME induced-hypertension. KEY FINDINGS: After two weeks, L-NAME induced high blood pressure, renal overexpression of AT1R, NAD(P)H oxidase sub-units gp91, p22 and p47, increased levels of oxidative stress, interleukin-6 (IL-6) and interleukin-17 (IL-17). 25761698: Given the role of oxidative stress and inflammation in the pathogenesis of hypertension, we conducted this study to test the hypothesis that long-term administration of resveratrol will attenuate renal inflammation and oxidative stress and, hence, progression of hypertension in the young spontaneously hypertensive rats (SHR). Compelling evidence supports the role of oxidative stress and renal interstitial inflammation in the pathogenesis of hypertension. 26082362: CONCLUSION: Elevated leukocyte count is associated with increased blood pressure value and hypertension among Chinese community-based population, suggesting that inflammation may participate in the pathogenesis of hypertension. 26295295: Obesity, insulin resistance (IR), inflammation, and hyperandrogenism may lead to polycystic ovary syndrome (PCOS) and hypertension. 27223823: Impaired Nrf2 regulation of mitochondrial biogenesis in rostral ventrolateral medulla on hypertension induced by systemic inflammation. 28103274: Prenatal exposure to inflammation results in hypertension during adulthood but the mechanisms are not well understood. 28629772: This further aggravates cardiovascular inflammation and leads to hypertension, induction of the pathological tissue remodeling and cardiac fibrosis. 28844481: These data suggest that the protective effects of tBHQ in salt induced hypertension are partly due to inhibiting oxidative stress and inflammation in PVN. Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension. Excessive oxidative stress and inflammation in hypothalamic paraventricular nucleus (PVN) are implicated in the pathogenesis of hypertension. The objective of this study was to investigate the effects of tBHQ in high salt induced hypertension and to identify whether the beneficial effects were induced by inhibiting PVN oxidative stress and inflammation. 28932306: In RA, increased levels of mediators of inflammation may cause arterial stiffness consequently leading to arterial hypertension. 29084442: Inflammation and endothelial dysfunction may play an important role in the multifactorial pathogenesis of hypertension. 29391930: Gut modulation via prebiotics may ameliorate hypertension caused by inflammation. 29651914: We hypothesised that hypertension is caused by remodelling of the cerebral arteries, which is triggered by inflammation. 29714061: Excessive proliferation, inflammation, oxidative stress, and migration induced by angiotensin II (Ang II), occurring in vascular smooth muscle cells (VSMCs) during vascular remodelling, are major pathogenesis of hypertension. 30022276: As clinicians, we understand the development of atherosclerosis as a consequence of cholesterol deposition and inflammation in the arterial wall, both being triggered by traditional risk factors such as hypertension, hyperlipidaemia or diabetes mellitus. 30332305: Recent evidence suggests hypertension may be secondary to chronic inflammation that results from hypoactive neuro-immune regulatory mechanisms. To further understand this association, we used systemic lupus erythematosus (SLE) as a model of inflammation-induced hypertension. 30354446: Fibrosis is a common consequence of inflammation- and oxidative stress-related endothelial dysfunction in aging, hypertension, diabetes mellitus, obesity, ischemia, and organ injury. 30715101: BACKGROUND: Although numerous recent studies have shown a strong link between inflammation and hypertension, the underlying mechanisms by which inflammatory cytokines induce hypertension remain to be fully elucidated. Here we sought to investigate the TG2-mediated AT1R stabilization in inflammation-induced hypertension and its functional consequences with a focus on receptor abundance and Ang II responsiveness. METHODS AND RESULTS: Using an experimental model of inflammation-induced hypertension established by introducing the pro-inflammatory tumor necrosis factor cytokine LIGHT, we provide pharmacologic and genetic evidence that TG2 is required for LIGHT-induced hypertension (systolic pressure on day 6: LIGHT = 152.3 +/- 7.4 vs. 30968773: Evidence also suggests that inflammation may lead to atherosclerosis, Alzheimer's, hypertension, stroke, cysts and cancers. 31655529: Role of aortic stiffness and inflammation in the etiology of young-onset hypertension. CONCLUSION: In this study, increased PWVs and the levels of inflammation markers were associated with aortic stiffness and inflammation in patients with young-onset hypertension, suggesting their role in the etiology of hypertension. We aimed to explore the relationship between inflammation and aortic stiffness and investigate their role in the etiology of young-onset hypertension. 31930845: CONCLUSION: The results concluded that inflammation as a major cause of hypertension was significantly decreased in patients using OLE tablets. 32044963: SR-A1 Prevents Obesity-Associated Blood Pressure Elevation through Suppressing Overproduction of VEGF-B in Macrophages.AIMS: Dysfunctional innate immune function and inflammation contributes to the pathogenesis of obesity-associated hypertension, in which macrophage infiltration in the perivascular adipose tissue (PVAT) plays a key role. TRANSLATIONAL PERSPECTIVE: An accumulating body of evidence indicates that obesity is a major cause of hypertension. 32389337: Inflammation in Hypertension.For more than 50 years, evidence has accumulated that inflammation contributes to the pathogenesis of hypertension. 32530318: Inflammation is associated with the pathogenesis of hypertension. 32968066: These findings confirm macrophage miR-106b-5p secretion from impaired vitamin D receptor signaling causes inflammation-induced hypertension. 33017187: Evolving evidence shows that immune cell-derived EVs can modulate the IS in a paracrine fashion and therefore may mediate the effects of inflammation in the pathogenesis of HTN. Therefore, we aimed to understand if specific subtypes of leukocyte/immune-cell-derived EVs are altered in essential HTN using an in-vivo model of Angiotensin-II induced HTN. 33076803: Patients with T2D often have hyperinsulinemia, dyslipidemia, inflammation, and oxidative stress, which then lead to hypertension, chronic kidney disease, cardiovascular disease, and increased risk of morbidity and mortality (9th leading cause globally). 33128414: Also, the cause of hypertension is usually unknown and it may result from systemic inflammation related to tooth decay. 33333432: It is characterized by imbalances in angiogenesis, inflammation and endothelial dysfunction which cause the development of hypertension and proteinuria, sometimes progressing into a multisystem disorder. 34338559: The role of inflammation in the pathogenesis of hypertension is a well-known issue. 34550259: OBJECTIVE: Left atrium enlargement is common in hypertension due to left atrium inflammation. 34689174: Emerging evidence has supported a role of inflammation and immunity in the genesis of hypertension. 34736077: Hypertension is one of the important causes of cardiovascular diseases, and the imbalance of vascular homeostasis caused by oxidative stress and endothelial inflammation occurs throughout hypertension pathogenesis. 35281911: Additionally, the cold and hot Hibiscus extracts induced a cardioprotective effect through reducing necrosis, inflammation, and vacuolization that results from the induction of hypertension, an effect that was more prominent with the hot extract. 36521430: Overweight and obese (OW/OB) adults are at increased risk of hypertension due to visceral adipose tissue (VAT) inflammation. 36615704: This review aims to highlight the role of western diet-induced oxidative stress and inflammation in the pathogenesis of hypertension and the role of various types of diets in its prevention with reference to dietary approaches to stop hypertension (DASH) diet. 37623703: Inflammation, hypertension, and negative heart health outcomes including cardiovascular disease are closely linked but the mechanisms by which inflammation can cause high blood pressure are not yet fully elucidated. 38039843: PE is a clinical syndrome characterized by hypertension secondary to systemic inflammation, endothelial dysfunction, and syncytiotrophoblast stress leading to hypertension and multiorgan dysfunction. 10869806: Further, as inflammation is reported to play a prominent role is AD pathogenesis, IL-6, a known mediator of inflammation, is another candidate gene proposed to be associated with the risk of AD. 11715204: They could have a role in the neurotoxicity observed in AD because of the inflammatory reaction they generate. 11738475: Further, in diseases such as progressive supranuclear palsy, Huntington's, Alzheimer's and Parkinson's diseases, the aberrant activation of TGases may be caused by oxidative stress and inflammation. 11754998: The limited number of studies that have investigated chemokine and chemokine receptor expression in Alzheimer's disease (AD) brain and in cell culture models seem to support a role for inflammation in AD pathogenesis. 11755000: Biochemical, genetic, and epidemiological evidence indicates that inflammation is an essential part of the pathogenesis of Alzheimer's disease. 12099698: Transforming growth factor-beta-1 (TGF-beta), a key regulator of the brain responses to injury and inflammation, has been implicated in upregulating the expression of the Alzheimer amyloid precursor protein (APP) and Alzheimer's disease (AD) pathogenesis. 12973747: Moreover, doses leading to similar brain/serum levels provided neuroprotection in animal models relevant for neurodegeneration in AD such as neurotoxicity produced by inflammation in the NBM or beta-amyloid injection to the hippocampus. 15473667: Expression of the NF-kappaB-dependent genes responsible for inflammation, such as TNF-alpha, IL-1beta, and nitric oxide synthase (NOS), contributes to chronic inflammation which is a major cause of neurodegenerative diseases (i.e. Alzheimer's disease). 15644140: But simultaneous with the arrival of a more complex view of microglia, evidence that inflammation plays a causal or exacerbating role in AD etiology has been boosted by genetic, physiological, and epidemiological studies. 15665405: These then cause a cytokine cascade and microlocalized inflammation in the CNS, that in time results in clinical Alzheimer's disease. 15681802: Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD), consisting of the activation of both microglia and astrocytes. 15748779: The importance of the role of inflammation has been suggested in the pathogenesis of Alzheimer's disease (AD). 16192374: Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD). 16384684: The initial stages of Alzheimer's disease pathology in the neocortex show upregulation of cell cycle proteins, adhesion and inflammation related factors, indicating the early involvement of inflammatory and regenerating pathways in Alzheimer's disease pathogenesis. 16478525: Several lines of evidence suggest that enhanced oxidative stress, inflammation, and apoptosis play important roles in the pathogenesis of AD. Mutations in the PS-1 and APP genes, which increase production of the highly amyloidogenic amyloid beta-peptide (Abeta42), are the major causes of early onset familial AD. 16602061: DEVELOPMENT: Inflammation is considered an important, although secondary, element in the pathogenesis of AD. 16787834: In vivo, doses leading to similar brain/serum levels produce neuroprotection in animal models relevant for neurodegeneration in Alzheimer's disease such as neurotoxicity produced by inflammation in the NBM or beta-amyloid injection to the hippocampus. 17027528: Although the precise molecular and cellular relationship between AD and inflammation remains unclear, interleukins and cytokines might induce activation of signaling pathways leading to futher inflammation and neuronal injury. Epidemiologic data as well as clinical trial evidence suggest that nonsteroidal anti-inflammatory drug (NSAID) use may decrease the incidence of AD, further supporting a role for inflammation in AD pathogenesis. 17262990: The importance of inflammation in the pathogenesis of AD was indirectly confirmed by epidemiological investigations that revealed a decreased incidence of AD in subjects using anti-inflammatory drugs, especially the non-steroidal anti-inflammatory drugs (NSAIDs). 17767011: Inflammation is also believed to be integral to the pathogenesis of AD. Amyloid-beta peptides (Abeta), generated by proteolysis of the beta-amyloid precursor protein (APP) by beta- and gamma-secretases, play an important role in the pathogenesis of Alzheimer disease (AD). 17949824: Increasing evidence supports a propensity towards inflammation in Alzheimer's disease (AD) pathogenesis. 19914323: A large body of evidence suggests the importance of inflammation and oxidative or nitrosative stress in Alzheimer's disease (AD) pathogenesis. 20011709: The importance of inflammation in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease, is increasingly being recognized. 20160456: OBJECTIVES: To show that the interest in inflammation in Alzheimer's disease (AD) is not only an early event in the history of AD but that inflammation is also an early event in the pathogenesis of AD. 20195797: How the regulation of inflammation loses its effectiveness during AD pathogenesis remains largely unclear. 20205641: Morbidities of aging and Alzheimer's disease (AD) have been related to defective functions of both T cells and macrophages leading to brain amyloidosis and inflammation. 20933033: The Abeta aggregate-induced neurotoxicity, inflammatory reactions and oxidative stress are linked strongly to the etiology of AD. 21143138: This strongly indicates that inflammation plays a central role in the aetiology of AD. 21567187: Inflammation including microglial activation may contribute in AD pathogenesis, and biomarkers for this process may thus be of value to study AD pathogenesis and might facilitate development of therapies targeting these cells. 21920632: Inflammation is believed to be integral to the pathogenesis of Alzheimer's disease (AD). 21951392: Beta-amyloid (Abeta) plaques and local inflammation are central to the pathogenesis of Alzheimer's disease. 22342162: Inflammation within the CNS is part of the pathogenesis of neurodegenerative diseases, in particular Alzheimer's disease, multiple sclerosis and Parkinson's disease. 23046210: There is a great deal of evidence suggesting an important role for systemic inflammation in the pathogenesis of Alzheimer's disease. 23533697: Although much attention has been devoted concerning the contribution of the microscopic lesions, senile plaques, and neurofibrillary tangles to the disease process, inflammation has long been suspected to play a major role in the etiology of AD. 23566485: BACKGROUND: Immune activation and inflammation represent critical factors in the pathogenesis of Alzheimer's disease (AD) and are associated with increased blood concentrations of markers like neopterin and the kynurenine to tryptophan ratio (Kyn/Trp). 24369524: The presence of activated microglia and astrocytes in the vicinity of amyloid plaques in the brains of Alzheimer's disease (AD) patients and mouse models implicates inflammation as a contributor to AD pathogenesis. 24384767: Amyloid beta or Abeta plaques and neurofibrillary tangles define AD pathologically but do not fully explain it, because dementia may also be caused by inflammation resulting in neuronal, axonal synaptic loss and dysfunction. 24413537: Alzheimer's disease may result from low-grade inflammation of the brain, and the characteristic amyloid beta may be a protective response. 24557039: Immune activation and inflammation, likely triggered by amyloid-beta (Abeta) deposition, play a remarkable role in the pathogenesis of Alzheimer's disease (AD), which is the most frequent cause of dementia in the elderly. 24631395: The current study was designed to further our understanding of peripheral inflammation-induced AD-like pathology, by administering polyinosinic:polycytidylic acid (poly I:C), a viral mimetic. 25051986: BACKGROUND: Aging is characterized by a low-grade systemic inflammation that contributes to the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). 25554493: Substantial evidence from epidemiologic, pathologic, and clinical reports suggests that vascular factors are critical for the pathogenesis of AD. In Alzheimer's disease (AD), large populations of endothelial cells undergo angiogenesis due to brain hypoxia and inflammation. 26103884: There is relatively little information about inflammation in the DS brain and how the genetics of DS may alter inflammatory responses and modify the course of AD pathogenesis in this disorder. 26587902: BACKGROUND: The critical role of neuro-inflammation and oxidative stress in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD) has become evident. 26899953: Clusterin (CLU) is recognized as a secreted protein that is related to the processes of inflammation and immunity in the pathogenesis of Alzheimer's disease (AD). 26910914: Neuro-inflammation is associated with activation of astrocyte and amyloid-beta (Abeta) generations that lead to pathogenesis of Alzheimer disease (AD). 26913031: In this article, we consider how current imaging techniques can help to unravel new inflammation mechanisms in the pathogenesis of AD and identify novel therapeutic strategies to treat the disease by interfering with leukocyte trafficking mechanisms. 27010693: BACKGROUND: One of the factors that contribute to Alzheimer's disease (AD) is the DNA damage caused by oxidative stress and inflammation that occurs in nerve cells. 27357286: Inflammation is becoming increasingly recognized as an important contributor to Alzheimer's disease (AD) pathogenesis. 27412235: Inflammation is one of the main causes of Alzheimer's disease (AD). 27829994: In conclusion, astrocytes have been shown to exert a direct role in Abeta clearance and undergo functional impair associated with inflammation in the pathogenesis of AD. 28460142: AgNP exposure can increase amyloid beta (Abeta) deposition in neuronal cells to potentially induce Alzheimer's disease (AD) progression. This study suggested that AgNP exposure might cause Abeta deposition and inflammation for subsequent neuronal cell apoptosis to potentially induce AD progression. 28977138: Innate immunity and inflammation in Alzheimer's disease pathogenesis. 29249963: A working hypothesis links extrinsic inflammation as a secondary cause of AD. 29393440: Although the pathologic mechanism remains to be fully elucidated, inflammation has been shown to be critical in the pathogenesis of AD. 29562537: The production of soluble amyloid-beta oligomers (AbetaOs) and the activation of inflammation are two important early steps in the pathogenesis of Alzheimer's disease (AD). 29628886: Furthermore, the CCR might be mechanistically linked to inflammation, a critical factor in the AD etiology according to the genetic evidence. 30403186: OBJECTIVE: The dysregulation of neuro-inflammation is one of the attributes of the pathogenesis of Alzheimer's disease (AD). 30564548: The cognitive impairment that is a hallmark of AD may be caused by inflammation in the brain triggered and maintained by the presence of Abeta protein, ultimately leading to neuronal dysfunction and loss. 30661858: Inflammation increases beta-amyloid burden and is thought to drive Alzheimer's disease pathogenesis. 30777084: Given the role played by inflammation in AD pathogenesis and the established efficacy of IFNbeta1a in the treatment of inflammatory diseases of the central nervous system such as multiple sclerosis, its use may be a viable strategy to inhibit the pro-inflammatory cytokine and oxidative stress cascade associated with Abeta deposition in the hippocampus of AD patients. 30929586: BACKGROUND: An imbalance of free radicals and antioxidant defense systems in physiological processes can result in protein/DNA damage, inflammation, and cellular apoptosis leading to neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). 30968773: Evidence also suggests that inflammation may lead to atherosclerosis, Alzheimer's, hypertension, stroke, cysts and cancers. 31233762: According to the critical role of inflammation in pathogenesis of AD and memory deficits, a cytokine with anti-inflammatory properties like interferon beta (IFNbeta), currently used to slow down disease progression and protect against cognitive disturbance in multiple sclerosis, might be also an effective treatment in AD condition. 31312547: A central role for inflammation has been implicated in the pathogenesis of AD. 31451750: Regulator of calcineurin 1 (RCAN1) is a multifunctional protein involved in neurodegeneration, mitochondrial dysfunction, inflammation and protein glycosylation, and plays an important role in the pathogenesis of Down syndrome and Alzheimer's disease. 31680874: Accumulating evidences suggest an active role of inflammation in the pathogenesis of AD. 31865964: We believe this review will provide new insights into biomarker candidates for the early diagnosis of AD with systemic relevance to inflammation during AD pathogenesis. 31867568: Human and animal studies have shown that chronic immune response and inflammation are important factors in the pathogenesis of AD. 32444542: Tenuifolin Attenuates Amyloid-beta42-Induced Neuroinflammation in Microglia Through the NF-kappaB Signaling Pathway.BACKGROUND: Inflammation and oxidative stress are believed to play an important role in the pathogenesis of Alzheimer's disease (AD). 32606694: Background: beta-Amyloid (Abeta) induces oxidative stress and inflammation of microglial cells, thus leading to Alzheimer's disease. 32765394: Thus, ORC may exert a protective role in AD through attenuating the damage caused by inflammation and oxidative stress. 32781098: Evidence suggests that hyperglycemia induces oxidative stress, mitochondrial dysfunction, inflammation and excitotoxicity, all of which play important roles in the onset and progression of AD pathogenesis. 32916195: Chronic airway allergy induces pro-inflammatory responses in the brain of wildtype mice but not 3xTgAD mice.The effects of systemic inflammation on the pathogenesis of Alzheimer's disease (AD) are not clarified, both beneficial and deleterious effects being reported. 33422142: BACKGROUND: Both serotonergic signalling disruption and systemic inflammation have been associated with the pathogenesis of Alzheimer's disease (AD). 33737171: INTRODUCTION: Systemic inflammation has been increasingly implicated in the pathogenesis of Alzheimer's disease (AD), yet the mechanistic and temporal specificity of this relationship is poorly understood. 33881288: PURPOSE: Systemic inflammation is characteristic for the pathogenesis of Alzheimer's disease (AD) and is responsible for the accumulation of its disease-specific Tau-protein and beta-amyloid plaques. 33977208: Here, we explain how vascular dysfunction mechanistically contributes to thrombosis as well as inflammation and neurodegeneration in AD pathogenesis. 34023945: Chronic exposure to metals like aluminium and copper causes accumulation of Abeta plaques, promotes oxidative stress, neuro-inflammation, and degeneration of cholinergic neurons results in AD-like symptoms. 34025357: Recent studies have shown that inflammation plays early and perhaps causal roles in the pathogenesis of AD related to NVU damage, possibly in part by overactivating the aspartic acid protease activity of beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1), which until now has almost solely been studied in the context of the beta-amyloid cascade. 34032945: BACKGROUND: Numerous studies have indicated the role of inflammation in the pathogenesis of Alzheimer's disease (AD). 34245502: It was noted, that the capacities of the tenuigenin to decrease the secretion of beta amyloid and to protect of neurons from damage by already made beta ameloids, to inhibit the processes of the tau proteins' hyperphosphorylation and inflammations in microglia, as well as increase the main synaptic transmission can be used by the development of effective therapeutic drugs aimed to reduce the pathogenesis of Alzheimer's disease. 34260075: Inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). 34340010: Increasing evidence has placed inflammation and immune dysfunction at the center of the pathogenesis of Alzheimer's disease (AD). 34384901: Although the mechanisms are still not fully elucidated, studies have revealed that these highly conserved ncRNAs are important modulators of gene expression, amyloid-beta production, tau phosphorylation, inflammation, synaptic plasticity and neuronal survival, all features considered central to AD pathogenesis. 34403662: CONCLUSION: CircLPAR1 promotes Abeta25-35-induced apoptosis, inflammation, and oxidative stress via miR-212-3p/ZNF217 axis, suggesting a new insight into the pathogenesis of AD. 34856902: Inflammation in the CNS - understanding various aspects of the pathogenesis of Alzheimer's disease. 35145898: Objective: Sustained inflammation, which could be promoted by Abeta aggregation and tau hyperphosphorylation, is a critical player in Alzheimer's disease (AD) pathogenesis. 35327563: This review highlights the neuroinflammatory and neuroprotective role of epigallocatechin-3-gallate (EGCG): the medicinal component of green tea, a known nutraceutical that has shown promise in modulating AD progression due to its antioxidant, anti-inflammatory, and anti-aging abilities. Using Alzheimer's disease (AD) as the archetype, the pathological findings include the aggregation of Amyloid Beta (Abeta) peptides, mitochondrial dysfunction, synaptic degradation caused by inflammation, elevated reactive oxygen species (ROS), and cerebrovascular dysregulation. 35601620: Background: Inflammation and immune dysfunction play significant roles in the pathogenesis of Alzheimer's disease (AD)-related dementia. 36204826: Secondly, we outlined key aspects of glial cell-associated inflammation in Alzheimer's disease pathogenesis and provided the latest evidence on the roles of microglia and astrocytes in Alzheimer's disease pathology. 36340795: Combining animal pharmacodynamic experiments with network pharmacology analysis, we confirmed the importance of inflammation in pathogenesis of AD, clarified the pharmacodynamic characteristics of QZZD in treating AD, and proved its neuroprotective effects through the regulation of TNFR1-ERK1/2-NF-kappaBp65 signaling pathway, which might provide reference for studies on treatment of AD in the future. 36675125: SIRT3 downregulation leads to mitochondrial dysfunction, neuroinflammation, and inflammation, potentially triggering factors of AD pathogenesis. 36982996: This review is aimed at summarizing the effects of dietary supplementation on cognitive decline, neuroinflammation and oxidative stress in AD-like animal models with a focus on neuroinflammation induced by lipopolysaccharide (LPS) injection, which mimics systemic inflammation in animals. Evidence suggests that systemic inflammation, dysregulation of the immune response and the resulting neuroinflammation and neurodegeneration play a significant role in AD pathogenesis. 37251647: Recent advances highlight that inflammation is critical to Alzheimer Disease (AD) pathogenesis. 37332353: Cumulative studies have shown inflammation as one of the main contributors to the pathogenesis of AD, leading to the recognition of a specific role of neuroinflammation synergic with the Abeta and NFTs cascades. 37337817: Specifically, we have shown that acrolein, acting as a diffusive factor of secondary injury, is both critical and sufficient in promoting inflammation (TNF-alpha) and Abeta42 aggregation, two known contributors of AD pathogenesis. 38157740: It suggests that the therapeutic effect of nervonic acid on AD is likely to be produced by ameliorating inflammation. 8712791: Abundant circumstantial evidence implicates inflammation in the pathogenesis of AD. 8892340: The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenesis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD. 8892348: Recent evidence suggests that inflammation in the central nervous system plays an important role in the pathogenesis of Alzheimer's disease. 8996832: Largely this review presents current opinions which support the concept that inflammation and similar immune mechanisms need to be considered as participating in AD pathogenesis. 9545438: The essential role of inflammation and induced gene expression in the pathogenic pathway of Alzheimer's disease. 9550286: It has been suggested that inflammation may be a possible cause of Alzheimer's disease (AD). 9651139: Several converging lines of evidence suggest that beta-amyloid and inflammation may be linked in the pathogenesis of Alzheimer disease (AD), but the mechanism of beta-amyloid neurotoxicity is unclear. 16918352: We demonstrated in rodents that stimulation of sensory neurons reduces hypertension, stress-induced gastric mucosal injury, reperfusion-induced liver injury, and endotoxin-induced shock responses by attenuating inflammatory responses such as increases in both tissue levels of tumor necrosis factor (TNF) and tissue accumulation of neutrophils. 18653232: The prominent symptoms of this syndrome are hypertension, proteinuria and oedema, resulting from an exaggerated aseptic systemic inflammatory response, triggered by placental factors shed into the maternal circulation. 19080338: CONCLUSIONS: These findings suggest an enhanced inflammatory response in the organs of SHR, which might play a key role in pathogenesis of hypertension and secondary organ complications. 25102200: Recently, it has become evident that the immune system and inflammatory response are also essential in the pathogenesis of hypertension. 26640237: As inflammatory responses and migration of smooth muscle in peripheral vascular wall are key mechanisms for the pathogenesis of hypertension, we hypothesized that vaspin could prevent the development of hypertension in in vivo hypertensive animal model. 32701602: Actions of immune cells in the hypertensive kidney.PURPOSE OF REVIEW: Inflammatory processes play a critical role in the pathogenesis of hypertension. 34412079: OBJECTIVES: Maternal systemic and placental inflammatory responses participate in the pathogenesis of hypertensive disorders of pregnancy including preeclampsia, a pregnancy-specific syndrome, although the role of inflammation remains unclear. 34992205: Inflammatory processes occupy an important place in the pathogenesis of hypertension. 36245645: Emerging evidence suggests that high concentrations of extracellular sodium can directly trigger an inflammatory response in antigen-presenting cells (APCs), leading to hypertension and vascular and renal injury. 37083315: The biocompatible Nb2C MXenzyme is featured with multiple enzyme-mimicking activities, involving superoxide dismutase, catalase, glutathione peroxidase, and peroxidase, inducing cytoprotective effects by resisting oxidative stress, thereby alleviating inflammatory response and reducing blood pressure, which is systematically demonstrated in the stress-induced hypertension rat model. 38396672: Arterial hypertension is the result of an inflammatory process that results in the remodeling and thickening of the vascular walls, which is associated with an immunological response. 12923064: In most neurodegenerative disorders, including multiple sclerosis, Parkinson's disease, and Alzheimer's disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated microglia and its cytotoxic agents play a crucial pathologic role. 15817469: In most neurodegenerative disorders, including multiple sclerosis, Parkinson disease, and Alzheimer disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated astrocytes and microglia and their cytotoxic agents play a crucial pathological role. 15880353: Several lines of neuroimmunological evidence correlate the development of the inflammatory responses of the brain with the formation of amyloid plaques associated with the pathogenesis of neurodegenerative disorders such as Alzheimer's disease. 17048151: However, Abeta/amyloid deposition is likely necessary but not sufficient to cause AD, and other putative downstream pathologies, including the aggregation of phospho-tau in neurofibrillary tangles, synaptic and neuronal loss, and glial and inflammatory responses, are likely equally important to AD pathogenesis. Alzheimer's disease (AD) is the most commonly diagnosed etiology of dementia and may be caused by the progressive accumulation and deposition of neurotoxic Abeta/amyloid plaques and aggregates in brain with aging-the amyloid hypothesis of AD. 18539391: The expression level of cortical glial fibrillary acidic protein (GFAP) increased in an age-related manner, in particular in 2-month PS cDKO mice, suggesting that the interaction relationship between oxidative stress and inflammatory response may be closely associated with the underlying loss-of-function pathogenesis of AD. 19557827: In addition, innate inflammatory responses, such as those mediated by microglia, are integral to the pathogenesis of AD. 19650431: It regulates blood pressure and inflammatory response, takes part in the pathogenesis of Alzheimer disease, influences cellular proliferation and differentiation, as well as neoplastic progression. 19996595: BACKGROUND/AIMS: Abnormal inflammatory response has been associated to the pathogenesis of Alzheimer's disease (AD) and may be a marker of an ongoing neurodegenerative process. 21683531: However, the underlying mechanism of how inflammatory response induces AD is unknown. 24052108: AD probably results from the inflammatory response induced by extracellular Abeta deposits, which later become enhanced by aggregates of tau. It proposes that abnormal production of beta amyloid protein (Abeta) is the cause of AD and that the neurotoxicity is due to Abeta itself or its oligomeric forms. 24561250: Accumulating evidence demonstrates that inflammasomes, which cleave precursors of interleukin-1beta (IL-1beta) and IL-18 to generate their active forms, play an important role in the inflammatory response in the CNS and in AD pathogenesis. 25620241: The biology of NF-kappaB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. 27351675: Our findings suggest that oxidative stress and inflammatory responses could result in abnormal SET gene expression, contributing to the tauopathy in AD pathogenesis. 28253985: Extensive research has revealed that multiple cellular pathways involved, including amyloid beta production, mitochondrial structural and functional changes, hyperphosphorylation of Tau and NFT formation, inflammatory responses, and neuronal loss in AD pathogenesis. 29667667: Accumulating evidence has shown that activated microglia cause inflammatory immune response, which could lead to neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. alpha-Cyperone, one of the main ingredients of Cyperus rotundus oil, has been reported to possess anti-inflammatory activity in activated macrophages. 29676229: Viral induced oxidative and inflammatory response in Alzheimer's disease pathogenesis with identification of potential drug candidates: A systematic review using systems biology approach. 30646475: The convergence of gut-derived inflammatory response together with aging and poor diet in the elderly contribute to the pathogenesis of AD. 32452370: Infection of the brain with various types of pathogens, and the resulting inflammatory response, is becoming increasingly important in our understanding of the etiology of Alzheimer's disease (AD). 32975365: Evidence that in Down syndrome (DS), a population markedly predisposed to develop early onset AD, increased APP gene dose is necessary for both AD neuropathology and dementia points to normalization of the levels of the amyloid precursor protein (APP) and its products as a route to further define AD pathogenesis and discovering novel treatments. NEW/UPDATED HYPOTHESIS: We hypothesize that the increase in APP gene dose in DS initiates a process in which increased levels of full-length APP (fl-APP) and its products, including beta-CTF and possibly Abeta peptides (Abeta42 and Abeta40), drive AD pathogenesis through an endosome-dependent mechanism(s), which compromises transport of neurotrophic signals. Moreover, upregulation of fl-APP protein and products may drive downstream events that dysregulate tau homeostasis and inflammatory responses that contribute to propagation of AD pathogenesis. 33105802: Remarkably, the significant increase in expression of Lcn2 , S100a8 , S100a9 and also Saa3 and Ch25h , was found in AD brains suggesting that early changes of immune-response genes evoked by mild SIR could be crucial in AD pathogenesis. 34456729: Toxic Abeta oligomers (AbetaOs) can trigger inflammatory response and play an important role in the pathogenesis of AD. 35944080: Moreover, MT1-MMP was described as a key player in cancer progression and it is involved in various inflammatory processes, as well as in the pathogenesis of Alzheimer's disease (AD). 36145197: Moreover, based on thioflavin-T-based fluorometric assays, we elucidated that coumestrol effectively prevented self-aggregation of amyloid beta (Abeta), which induces an inflammatory response in the central nervous system (CNS) and is a major cause of Alzheimer's disease (AD). 36165619: Upstream lipid and metabolic systems are potential causes of Alzheimer's disease, Parkinson's disease and dementias. Using microglia as an example, we review data that suggest increased lipid concentrations cause dysfunctional inflammatory responses to immune challenges, leading to Alzheimer's disease, Parkinson's disease and dementia. 36286438: Neuroinflammation is a condition associated with several types of dementia, such as Alzheimer's disease (AD), mainly caused by an inflammatory response to amyloid peptides that induce microglial activation, with subsequent cytokine release. 36394096: The GO and KEGG enrichment analyses revealed that TCFW mainly acted on oxidative response, inflammatory response, insulin secretion, amyloid fibril formation, neurodegenerative pathway-multiple diseases, Alzheimer's disease, longevity regulation pathway, PI3K-Akt signaling pathway, MAPK signaling pathway, etc, which were the main pathogenesis of AD. 37416769: beta-amyloid binds to microglia Dectin-1 to induce inflammatory response in the pathogenesis of Alzheimer's disease. 38201258: An increasing amount of basic scientific data and clinical studies underscore the importance of inflammatory processes and subsequent glial activation in the pathogenesis of AD. 1078794: Hypertension caused by infusion of phenylephrine gave intermediate results, as did hypotension induced by either nitroprusside or hemorrhage during the ischemic period. 1242631: In our experiments, hypertension was produced by injection or infusion of hypertensive drugs. 1282597: In Wistar-Kyoto rats, BQ123 (10.0 mg/kg) reversed the hypertension produced by an infusion of ET-1 (0.01 nmol/kg/min). 15059935: The present study suggests that CCR2 expression in monocytes has a critical role in vascular inflammation and remodeling in Ang II-induced hypertension, and possibly in other forms of hypertension. Hypertension was induced by infusion of angiotensin II (Ang II) into wild-type mice, CCR2-deficient (CCR2-/-) mice, and bone marrow-transferred mice with a leukocyte-selective CCR2 deficiency (BMT-CCR2-/-). 1592449: These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. Salt-dependency of endothelin-induced, chronic hypertension in conscious rats. 1592467: Captopril prevents chronic hypertension produced by infusion of endothelin-1 in rats. These results indicate that endothelin-induced hypertension may involve stimulation of the renin-angiotensin system but not an increase in circulating angiotensin II concentration. 16289267: The present study was undertaken to determine if plasma infusion-induced hypertension increased fetal placental flow in proportion to the driving pressure across the fetal placental circulation. 1647798: The icv infusion of RU28318, a selective mineralocorticoid antagonist, at doses which are ineffective when administered sc, inhibits the development of hypertension produced by the sc infusion of aldosterone or deoxycorticosterone, as well as that produced by the oral administration of a licorice derivative and of a high salt diet in the Dahl S/JR rat. 17255211: In summary, hypertension due to infusion of a low dose of ANG II was accompanied by generalized peripheral vasoconstriction. Investigation of the mechanisms by which chronic infusion of an acutely subpressor dose of angiotensin II induces hypertension. 18084722: METHODS-RESULTS: Hypertension was induced by infusion of Ang-II (200 ng/kg/day) for 3 weeks. 1973355: Acute hypertension was induced using infusions of epinephrine during the control period and later propranolol (1.5 mg/kg) plus atropine (0.2 mg/kg). Effects of muscarinic and beta-adrenergic blockade on the aortic elastic response to epinephrine induced acute hypertension in conscious dogs. 20150548: Acute hypertension was produced by daily injections of angiotensin II in some mice with chronic hypertension to produce ICH. METHODS: Chronic hypertension was produced by infusion of angiotensin II and an inhibitor of nitric oxide synthase in drinking water in SOD1 transgenic (SOD1Tg) mice, SOD1-deficient (SOD1(-/-)) mice, and their respective wild-type littermates. 20736136: This work addresses this issue, using complete Freund's adjuvant (CFA)-induced monoarthritis in different models of hypertension: Spontaneous (spontaneously hypertensive rats, SHR), induced by infusion of angiotensin II (ANG) or 1,3-dipropyl-8-sulfophenylxanthine (DPSPX, an adenosine receptors' antagonist), and renal artery ligation (RAL). 21646597: The present study tested the hypothesis that IkappaBalpha and IkappaBbeta may have different roles in modulating cardiovascular inflammation and fibrosis, using a model of angiotensin II infusion-induced hypertension in wild-type mice and IkappaBbeta knock-in mice, in which the IkappaBalpha gene is replaced by IkappaBbeta cDNA (AKBI). 2190924: Chronic hypertension produced by infusion of endothelin in rats. These results indicate that elevated blood levels of endothelin could produce a maintained hypertension without sodium or water retention and that the hemodynamic basis for the increased mean arterial pressure is similar to that seen in most other forms of experimental and clinical hypertension. 2225435: These included systemic hypertension produced by an infusion of phenylephrine, cross-clamping of the descending thoracic aorta, and manual, superior displacement of the transverse aortic arch (arch elevation), either alone or in conjunction with the cross-clamp. 22371360: Radiotelemetric assessment of blood pressure revealed that HTN induced by infusion of systemic \slow-pressor\ doses of Ang II was abolished in mice with null mutations in EP(1)R or COX-1 but not COX-2. 23581476: EXPERIMENTAL APPROACH: Male Sprague Dawley rats were chronically instrumented with pulsed Doppler flow probes to measure regional haemodynamic responses to retigabine under control conditions and during acute hypertension induced by infusion of angiotensin II and arginine vasopressin. 23887740: Inhibition of platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis. Taken together, our results indicate Ang II infusion-induced hypertension stimulated platelet activation and platelet-leukocyte conjugation, which initiated inflammatory responses that contributed to cardiac fibrosis. Inflammation promotes the development of cardiac fibrosis and heart failure induced by hypertension. 24429674: METHODS: In the first portion of the study, rats received either an AngII infusion (400ng/kg/min) for 4 weeks, leading to hypertension with high circulating AngII, or an aldosterone (ALDO, 0.75 MUg/h) infusion for 4 weeks, leading to hypertension with low/normal circulating AngII. 25093805: Gbeta3-deficient mice were normal as judged by body weight gain by age or by feeding with high-fat diet (HFD); glucose tolerance and insulin sensitivity; baseline blood pressure and angiotensin II infusion-induced hypertension. 2542400: Rapid haemodynamic response to adrenocorticotrophin and the role of peripheral resistance in adrenocorticotrophin-induced hypertension in conscious sheep. The haemodynamic effects associated with the onset of hypertension induced by infusion of adrenocorticotrophin (ACTH) were investigated in sheep. The onset of ACTH-induced hypertension in sheep is characterized by very rapid haemodynamic changes with an increase in cardiac output and a relative increase in CTPR after an initial peripheral vasodilatation. These results indicate that constriction of the peripheral vasculature is essential for the onset and maintenance of ACTH-induced hypertension in the sheep, and that the vasoconstriction does not involve a specific Ca21+-dependent mechanism because minoxidil was as effective as nisoldipine in abolishing the pressor response to ACTH. The development of ACTH-induced hypertension was prevented by both nisoldipine, a calcium channel blocker, and minoxidil, a vascular smooth muscle relaxant. 25551569: METHODS: In C57BL/6-mice, hypertension was induced by infusion of 600 ng/kg * min angiotensin II. 25921924: These results suggest that HDAC6 may be a valuable therapeutic target for the treatment of hypertension-induced kidney fibrosis and inflammation. Hypertension was induced by infusion of ANG in mice. 2831143: Acute hypertension was induced by infusions of angiotensin performed 1) during the control period, 2) after propranolol (1.5 mg/kg), 3) after atropine (0.2 mg/kg), and 4) after propranolol plus atropine. 28436023: The aim of the present study was to determine the effects of metformin on angiotensin II (Ang II) infusion-induced hypertension in vivo. Activation of AMP-activated protein kinase by metformin ablates angiotensin II-induced endoplasmic reticulum stress and hypertension in mice in vivo. 28986310: Recently, a highly selective SGK1 inhibitor, EMD638683, was developed, though whether EMD638683 can prevent hypertension-induced cardiac fibrosis and the mechanisms by which this inhibitor may alter the disease process remain unknown. Using a murine Angiotension II (Ang II) infusion-induced hypertension model we found that EMD638683 treatment inhibited cardiac fibrosis and remodeling, with significant abatement of cardiac inflammation. 2985872: The plasma concentrations of 17 alpha-hydroxyprogesterone (17 alpha OHP) and 17 a'20 alpha-dihydroxy-4-pregnen-3-one (17 alpha 20 alpha OHP) have been measured in sheep during 5 days of ACTH administration at 20 micrograms/kg/day a rate of infusion known to produce hypertension. Calculation of the blood production rate of both steroids during ACTH treatment confirms that the rates of infusion of 17OHP (3.0 mumol/h) and 17 alpha 20 alpha OHP (1.5 mumol/h) used to produce hypertension, when infused together with the other major ovine adrenocortical steroids, produced plasma concentrations in the range as found following administration at a rate to increase blood pressure. 3021942: When renal perfusion pressure is prevented from increasing in various forms of experimental hypertension, caused by infusion of mineralocorticoids, angiotensin II, vasopressin, or norepinephrine and adrenocorticotrophic hormone (ACTH), sodium and water retention continues until ascites, pulmonary oedema and circulatory collapse occur within a few days. 3170609: Hypertension induced by mineralocorticoids or infusion of angiotensin II caused a marked suppression of kidney FABP expression, whereas amounts of heart FABP in kidney were unchanged. 34176379: Methods : C57BL/6 mice received an Ang II (1.1 mg/kg/day with a minipump) infusion for 2 weeks to induce hypertension. 452852: In 12 rats following administration of HRP, hypertension was induced by an infusion of angiotensin. 6658963: Hypertension was produced by infusion of phenylephrine to a diastolic blood pressure of 100 mm Hg. 6859220: Hypertension was produced by infusion of angiotensin II into rats for 1 or 4 hours; some rats were treated with heparin and others not. 7485485: To explore the relationship between insulin resistance and hypertension, we examined whether acute induction of hypertension can engender insulin resistance. For this purpose we measured rates of insulin-mediated glucose uptake in awake unstressed rats with the euglycemic hyperinsulinemic (12 microns.kg-1.min-1) clamp technique during infusions of saline alone or after induction of hypertension by bolus administration of NG-monomethyl-L-arginine (L-NMMA, 30 and 15 mg/kg), a competitive inhibitor of nitric oxide synthase. Insulin resistance after hypertension induced by the nitric oxide synthesis inhibitor L-NMMA in rats. 7802450: An optimal range of elevation level and stable maintenance of hypertension induced by the infusion of angiotensin II was essentially required to obtain a good response. 8089609: Since the administration of placental angiotensinase was effective in lowering blood pressure in rats with hypertension induced by the infusion of angiotensin II, placental proteases are possibly involved in the refractory response to exogenously infused angiotensin II. 8492856: After arterial hypertension, caused by the infusion of angiotensin II, where there was loss of myogenic tone, an increased low-frequency CVPT was accompanied by a positive phase shift (P < 0.01). 9404419: The influence of nonspecific blockade of endothelin receptors by bosentan (30 mg/kg per day, gavage) was assessed on hypertension induced by infusion of angiotensin II (AngII 200 ng/kg/min sc for 10 days) in rats. 31914623: Using an acute model of AD induced by the intracerebroventricular injection of amyloid-beta oligomers (oAbeta), we analyzed cellular and behavioral hallmarks of AD, GR signaling pathways, processing of amyloid precursor protein, and enzymes involved in Tau phosphorylation. 31991177: Sixty male adult Wistar rats were randomly divided into 6 groups (n = 10 per group) as follows: 1; control, 2; sham, 3; Abeta, 4; pre-treatment (vinpocetine + Abeta): oral gavage administration of vinpocetine at 4 mg/kg for 30 days followed by intracerebroventricular (ICV) injection of Abeta, 5; treatment (Abeta + vinpocetine): Abeta ICV injection followed by vinpocetine administration for 30 days, 6; pre-treatment + treatment (vinpocetine + Abeta + vinpocetine): vinpocetine administration for 30 days before and 30 days after AD induction. 32048245: Sixty-three rats were divided into nine groups: (1) healthy, (2-4) sham, and (5-9) AD models: (5) AD was induced by intracerebroventricular injection of amyloid beta (Abeta) 1-42. 32488543: Induction of AD was performed in ovariectomized female rats with high-fat high fructose diet (HFFD) feeding after 4 weeks following D-galactose injection (150 mg/kg). 32681248: This study aimed to investigate the protective effect of GSPE on the cognitive and synaptic impairments of AD using a sporadic AD rat model induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) (ICV-STZ). 33383443: Hence, rat model of AD was induced by intra-hippocampal injection of beta-amyloid 1-42 . 33715084: AD was induced by intra-cerebroventricular injection of Abeta1-42 peptide. 33974953: AD was induced by the intra-cerebroventricular injection of Abeta1-42 peptide. 34000331: We examined the efficacy of L. glauca in a mouse model of AD, which was induced by intrahippocampal injection of Abeta 1-42 . 34802394: This study investigated the neuroprotective effect of green tea (GT) on cognitive disorder, inflammation, and oxidative stress in the streptozotocin (STZ)- induced AD model. AD was induced by the injection of STZ (3 mg/kg, bilaterally, ICV). 34929632: This study aimed to determine the effect of 4 weeks of aerobic rehabilitation exercise (RhExe) on the genes expression of BDNF and TGF-beta1 in the hippocampus tissue of rats with the AD induced by injection of amyloid-beta (Abeta 1-42 ). 34992853: Here, we investigated whether natural products from Chrysophyllum perpulchrum as catechin and two dimeric procyanidins (catechin + hexose) could prevent progression of oxidative stress and cognitive changes using an AD-like rat model induced by Abeta 1-40 injection into the hippocampal CA1 subfield. 35281502: Impact of Donepezil on Brain Glucose Metabolism Assessed Using [ 18 F]2-Fluoro-2-deoxy-D-Glucose Positron Emission Tomography Imaging in a Mouse Model of Alzheimer's Disease Induced by Intracerebroventricular Injection of Amyloid-Beta Peptide. 35527550: METHODS: Rats were randomly assigned to the control (C), experimental periodontitis (P), Alzheimer's disease (AD), and experimental periodontitis with streptozotocin-induced AD (AD-P) groups. In the AD-P group, AD was induced by intracerebroventricular injection of streptozotocin after 6 weeks of experimental periodontitis induction. Experimental Periodontitis Deteriorates Cognitive Function and Impairs Insulin Signaling in a Streptozotocin-Induced Alzheimer's Disease Rat Model. OBJECTIVE: To assess the impact of experimental periodontitis on cognitive function deficits in a rat model of streptozotocin-induced AD and determine the mechanisms underlying these effects. 35532618: Protective Effect of L-Arginine in an Animal Model of Alzheimer's Disease Induced by Intra-Hippocampal Injection of AlCl3. 35556434: The streptozotocin (STZ) -induced AD model mimics respiratory problems seen in humans and exhibits neuronal hyperactivity in the nucleus tractus solitarii (nTS), the central integration site for respiratory afferents in the brainstem. AD was induced by intracerebroventricular injection of 2 mg/kg STZ in 6-week old male Sprague Dawley rats. 36271966: AD was induced by an intracerebroventricular (ICV) injection of streptozotocin (STZ). 36438603: AD was induced by intrahippocampal injection of amyloid-beta (1-42, 6 MUg), and DON was orally administrated (4 mg/kg) for 21 days. Given the promising data on the additive effect of combination therapy with donepezil (Aricept), an acetylcholinesterase inhibitor (AChEI), and regarding the similar neuronal mechanisms through which donepezil (DON) and environmental enrichment (EE) exert their enhancing effects on cognition; we asked whether simultaneous treatment with two paradigms in amyloid-beta-induced AD rats may lead to greater protection against the cognitive impairments than either treatment individually. 36442692: The aim of this study was evaluated the effects of 2-(4-(methylthio)phenyl)-3-(3-(piperidin-1-yl)propyl) thiazolidin-4-one (DS12) on memory and neurochemical parameters in a model of AD induced by an intracerebroventricular injection of streptozotocin (STZ). 36927298: In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat's model of Alzheimer's disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Abeta). 36982996: This review is aimed at summarizing the effects of dietary supplementation on cognitive decline, neuroinflammation and oxidative stress in AD-like animal models with a focus on neuroinflammation induced by lipopolysaccharide (LPS) injection, which mimics systemic inflammation in animals. Evidence suggests that systemic inflammation, dysregulation of the immune response and the resulting neuroinflammation and neurodegeneration play a significant role in AD pathogenesis. 37895841: Dapagliflozin/Hesperidin Combination Mitigates Lipopolysaccharide-Induced Alzheimer's Disease in Rats. The aim of this study was to elucidate the potential ameliorative effects of dapagliflozin and/or hesperidin on Alzheimer's disease (AD) induced by lipopolysaccharide (LPS) injection in rats. 37970437: AD was produced by injection of amyloid-beta (1-42, 6 ug) intrahippocampally, and a daily treadmill for 3 consecutive weeks was used for EX animals. 37978479: This study aimed to investigate the effect of Brazilian green propolis on cognitive impairment using a mouse model of Alzheimer's disease (AD) induced by intracerebroventricular injection of amyloid beta (Abeta) 25-35 . The groups were pretreated with vehicle and propolis at a dose of 100, 300 and 900 mg/kg body weight for 8 days, then AD-like phenotypes were induced by intracerebroventricular (ICV) injection of Abeta 25-35 . 38091207: We administered Abeta 1-42 oligomers in rats via intracerebroventricular (i.c.v.) injection to induce AD-like conditions. 10851121: Blood pressure in saline-injected animals recovered quickly (within 5 min), whereas hetastarch injections caused hypertension to be maintained for much longer, for over 40 min in the most extreme case. 11743995: Subsequent bilateral microinjection of kynurenate, a non-selective ionotropic excitatory amino acid receptor antagonist (50 mM, 100 nl), into the RVLM significantly attenuated the sympathoexcitation and hypertension evoked by injection of bicuculline. 1242631: In our experiments, hypertension was produced by injection or infusion of hypertensive drugs. 12554635: Renal cortical phenol injection provokes acute sympathetic nervous system-dependent hypertension and a shift of proximal tubule Na(+)/H(+) exchanger isoform 3 (NHE3) and Na(+)-P(i) cotransporter type 2 (NaPi2) to apical microvilli. 13317317: [Demonstration of the difference of mechanism of hypertension produced by carotid occlusion and of hypertension produced by adrenalin injection]. 14636847: CONCLUSIONS: Under the condition of acute hypertension induced by AII, leukocytes moved faster in the total choroidal circulation (from arteries to veins) compared to their velocity under the condition of normal blood pressure. Experimental acute hypertension was induced by the intravenous drip injection of angiotensin II (AII). On the other hand, the respective mean velocities in acute hypertension induced by AII were 13.50+/-1.82, 0.81+/-0.09, and 10.54+/-3.91 mm/s. Blood velocities might increase in the total choroidal circulation at an early stage in acute hypertension induced by AII, resulting in increased choroidal blood flow. 15404434: [Arterial hypertension produced by cisternal injections of sodium citrate]. 15870062: Thus, the aim of the present work was to study the retinal glutamate/glutamine activity in eyes with hypertension induced by intracameral injections of hyaluronic acid (HA). 1633282: Kainic acid injection in NTS evokes hypertension and c-fos expression in spinal cord. 1730453: Other models (such as partial renal infarct hypertension, post-mineralocorticoid-salt hypertension, and hypertension induced by repeated injections of angiotensin II) also may have primary or secondary immunologic factors contributing to their etiology. 1910032: The results indicate that hypertension induced by systemic ET-1 injection is less effective than hypertension induced by continuous systemic AII infusion in increasing tumor blood flow; AII is probably a suitable agent as a safe and effective enhancer of tumor blood flow. 192391: The same stimulation of the nerve during hypertension caused by noradrenaline injection led to the fall of arterial pressure and tachycardia. 19841522: CONCLUSIONS: Co-administration of vitamin C and E does not have an additive beneficial effect on reducing the kidney damage and hypertension compared to either vitamin C or E alone in DOCA-salt-induced hypertension. Unilateral nephrectomy was carried out in the study groups and hypertension was induced by deoxycorticosterone injection and 1% sodium chloride and 0.2% potassium chloride added to the drinking water. INTRODUCTION: We assessed whether co-supplementation of vitamins C and E has additive beneficial effects on reducing the kidney damage and attenuation of the arterial pressure elevation compared to administration of either vitamin C or vitamin E alone in deoxycorticosterone acetate-salt-induced hypertension. Reduction of kidney damage by supplementation of vitamins C and E in rats with deoxycorticosterone-salt-induced hypertension. 20150548: Acute hypertension was produced by daily injections of angiotensin II in some mice with chronic hypertension to produce ICH. METHODS: Chronic hypertension was produced by infusion of angiotensin II and an inhibitor of nitric oxide synthase in drinking water in SOD1 transgenic (SOD1Tg) mice, SOD1-deficient (SOD1(-/-)) mice, and their respective wild-type littermates. 23283357: Using an adoptive transfer animal model of PE, we provide in vivo evidence that the injection of IgG from women with PE, but not IgG from normotensive individuals, resulted in hypertension, proteinuria, and a reduction in aldosterone production from 1377 +/- 272 pg/mL to 544 +/- 92 pg/mL (P<0.05) in pregnant mice. 23302598: HT was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly for 4 weeks, whereas apelin was administered (200 MUg/kg i.p.) for 17 days. 2465061: In all experiments, labelled neurones were found in the same restricted region of the PAG at which DLH injection evokes hypertension and behavioural signs of the defence reaction. 25665476: Hypertension was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly, 4 weeks, whereas intraperitoneal apelin was administered (200 ug.kg-1) for 17 days. 26550192: Hypertension was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly, 4 weeks, whereas intraperitoneal ozone was administered (1.1 mg/kg) for 10 days. 26823951: After establishing a baseline, hypotension and hypertension were induced by injection of sodium nitroprusside (SNP) and phenylephrine (PE), respectively, and DeltaHR versus DeltaMAP were recorded as a measure of baroreflex sensitivity (BRS). 28346001: Hypertension was induced by intraportal injection of microspheres (10 to 15 mg/kg) at 5-day intervals via the catheter. 3763434: It is concluded that both intrathecal and intracerebroventricular vasopressin-induced hypertension appears to be mediated by the sympathetic system and that the spinal cord is more sensitive than the supraspinal sites to vasopressin in regulating autonomic functions. Intrathecal injection of arginine vasopressin in rats at a dose as small as 10 ng produced dose-dependent hypertension and tachycardia. New evidence for neuronal function of vasopressin: sympathetic mediation of intrathecal vasopressin-induced hypertension. Intracerebroventricular injection of arginine vasopressin also induced hypertension and tachycardia, but 600 ng was needed. 469730: In both fetal and adult sheep, actue hypertension due to I.V. injection of angiotensin II was not associated with a consistent and progressive bradycardia, such as was seen with acute hypertension caused by phenylephrine. 5914258: Their discharge was inhibited during hypertension caused by injections of adrenaline and during inflation of the lungs, but was increased during tracheal occlusion, stimulation of peripheral chemoreceptors and irritation of the larynx. They were activated during hypertension due to adrenaline and often by tracheal occlusion, chemoreceptor stimulation, laryngeal irritation and lung inflation. 6235459: From these studies, it is concluded that the injection of homodimaprit produces lesions in the preoptic area, resulting in hypertension that is maintained by excessive activation of the sympathetic nervous system. 6529980: AD-1211, as well as pentazocine and morphine, blocked the reflex hypertension caused by injection of both bradykinin and bradykinin plus PGE1 into the splenic artery of dogs. 6685202: Zomepirac sodium inhibited the reflex hypertension caused by an injection of bradykinin into the splenic artery of anaesthetized dogs, but not that by injection of bradykinin plus PGE1. 755652: Bilateral injections of adrenaline into the anterior preoptic area (POA) and areas surrounding the AH had little or no effect on blood pressure and heart rate, while injections into the posterior hypothalamus (PH) induced tachycardia and hypertension followed by a smaller fall in blood pressure. 7802751: Inadvertent epinephrine injection induced ventricular dysrhythmias, hypertension, hypotension and pulmonary oedema. 8024010: The SNC stimulation-induced hypertension, tachycardia, and increased striatal DA release were attenuated by prior destruction of the nigrostriatal DA system produced by intramedial forebrain bundle injection of 6-hydroxydopamine and by prior blockade of postsynaptic DA receptors produced by intra-CS injection of DA receptor antagonists, haloperidol or pimozide. 8238454: In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). 8705318: The DR stimulation-induced hypertension, tachycardia, or increased hypothalamic 5-HT release were attenuated by prior destruction of the ascending serotonergic system produced by ICV injection of 5,7-dihydroxytryptamine and by prior blockade of postsynaptic serotonergic receptors produced by intrahypothalamic injection of 5-HT2 antagonists, cyproheptadine and ketanserin. 9440240: Intravenous (i.v.) injection of scorpion venom (0.5 mg/kg) into 12 rats induced arterial hypertension and severe lung oedema, whereas i.v. injection of scorpion venom into 16 rats previously injected with commercial heparin induced arterial hypertension, but only a slight lung oedema. 15151831: CONCLUSION: The differentially displayed proteins in the brain identified between the rats with intrahippocampal amyloid beta injection and control rats may provide further insight into the pathogenesis of Alzheimer's disease and useful clues for developing new drugs for its treatment. 18687381: The rat model of Alzheimer's disease used in the present study was induced by the intracerebroventricular (ICV) injection of streptozotocin (STZ) using a stereotaxic instrument. 20030829: CONCLUSIONS: These findings indicate efficacy for NPC transplantation in an animal model of AD with effects consistent with cellular actions to attenuate inflammatory reactivity induced by intrahippocampal peptide injection. 20384276: Rats with AD-like cognitive deficiency was induced by injection of ibotenic acid into Nucleus Basalis of Meynert (NBM) bilaterally (5 microg 0.5 microL(-1), each side). 20838863: A nonhuman primate model of Alzheimer's disease generated by intracranial injection of amyloid-beta42 and thiorphan. 20933058: The present work explored the anti-neuroinflammation effects of Ginseng Rb1 in a rat model of Alzheimer disease produced by ventricle injection of Abeta1-42. 21689771: The present study utilized a mouse model of AD induced by intrahippocampal injection of AbetaO (10 MUM) to investigate the effects of Gami-Chunghyuldan (GCD), a standardized multi-herbal medicinal formula, on the presentation of memory deficits and neurohistological pathogenesis. 22235318: The current study was designed to further investigate the protective effect of the RCE on neurogenesis in a rat model of Alzheimer's disease (AD) induced by an intracerebroventricular injection of streptozotocin (STZ), and to determine whether this neuroprotective effect is induced by the antioxidative activity of salidroside. 22562026: METHODS: Two weeks after induction of AD by injection of Amyloid-beta1-40 into CA1 area of rat hippocamp, Y-maze and single-trial passive avoidance tests were used to show deficit of learning and memory abilities. 23061885: This study aimed to show that the rat model of sporadic Alzheimer's disease (sAD) generated by the intracerebroventricular (icv) injection of a sub-diabetogenic dose of streptozotocin (icvSTZ) is characterized by brain mitochondrial abnormalities. 23156675: The intranasal administration of glutamate antibodies in the dose of 300 microg/kg one hour after damage on the level of mRNA expression of Dffb gene which codes caspase-activated DNase which participates in intranucleosome fragmentation of genome DNA in apoptosis was investigated in experimental Alzheimer's disease induced by injection of neurotoxic fragment of beta-amyloid protein Abeta25-35 in Meynert basal magnocellular nuclei on rats. 23244235: We investigated the effect of thalidomide on AD-like cognitive deficits caused by intracerebroventricular injection of streptozotocin (STZ). 23726868: Short-term and long-term treatments with sodium hydrosulfide and/or Tabiano's spa-water significantly protected against impairment in learning and memory in rat models of AD induced by brain injection of beta-amyloid1-40 (Abeta) or streptozotocin, and in an AD mouse model harboring human transgenes APPSwe, PS1M146V and tauP301L (3xTg-AD mice). 24648641: [Purpose] This study examined the effect of the application of transcranial direct current stimulation (tDCS) on neurologic recovery and cognitive function of rats with Alzheimer-like dementia induced by scopolamine injections. 24678498: The rat model of Alzheimer's disease was induced by the intracerebroventricular (ICV) injection of Abeta25-35, using a stereotaxic instrument. 24877042: The rat model of Alzheimer's disease was induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) using a stereotaxic instrument. Treadmill exercise alleviates impairment of spatial learning ability through enhancing cell proliferation in the streptozotocin-induced Alzheimer's disease rats. Decreased cell proliferation with decrement of BDNF and TrkB expressions in the hippocampus were observed in the STZ-induced Alzheimer's disease rats. 25290208: Perindopril, an angiotensin converting enzyme inhibitor, has been reported to improve learning and memory in a mouse or rat model of Alzheimer's disease (AD) induced by injection of beta-amyloid protein. 25714979: This study aimed to investigate the neuroprotective effects of different extract fractions from AGR against Alzheimer disease-like symptoms induced by Amyloid Beta (Abeta) 1-42 intra-hippocampal injection. 25849905: In the present study, we investigated the effects of hippocampal BDNF in a rat model of AD produced by a ventricle injection of amyloid-beta1-42 (Abeta1-42). 25881906: Characterization of Cerebral Damage in a Monkey Model of Alzheimer's Disease Induced by Intracerebroventricular Injection of Streptozotocin. 26166589: OBJECTIVE: To evaluate the effects of Catechin (CAT) on memory acquisition and retrieval in the animal model of sporadic alzheimer's disease (sAD) induced by intracerebroventricular (icv) injection of streptozotocin (STZ) in passive avoidance memory test. 26386305: The selective sigma1 agonist PRE-084, or the non-selective sigma1 drug ANAVEX2-73 was combined with the acetylcholinesterase inhibitor donepezil or the NMDA receptor antagonist memantine in the nontransgenic mouse model of AD-like memory impairments induced by intracerebroventricular injection of oligomeric Abeta25-35 peptide. 26511841: In the present study, we tested PUE in a sporadic AD (SAD) mouse model which was induced by the intracerebroventricular injection of streptozotocin (STZ). 27023127: Intracerebroventricular Injection of Amyloid-beta Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits. 27516988: CONCLUSION: The results indicate that chronic administration of frankincense has the potential to improve dementia type of AD induced by i.c.v injection of streptozotocin in a time-dependent manner. 28101460: AD was induced by the injections of streptozotocin (3mg/kg, bilateral intracerebroventricular) at days 1&3. 28158298: Adult male ddY mice were used in this study, and an animal model of AD was induced by intracerebroventricular (ICV) injection of Abeta1-42. 28255862: Fourty adult male Wistar rats were randomly assigned to 5 groups:(n = 8 rats/group): group 1, control, consumed an ordinary diet, group 2 consumed a HFD for 8 weeks, then received phosphate-buffered saline (PBS) via intrahippocampal (IHP) injection, group 3 consumed HFD for 8 weeks, then received beta-amyloid (Abeta)1-42 via IHP injections to induce AD, group 4 consumed HFD for 8 weeks, then received Abeta1-42, and was treated by thymol (30 mg/kg in sunflower oil) daily for 4 weeks, and group 5 consumed HFD for 8 week, then received Abeta1-42 after what sunflower oil was administered by oral gavage daily for 4 weeks. 28397428: Twelve rats with Alzheimer's disease, induced by STZ injection (3 mg/kg) into both lateral ventricles using a stereotaxic frame (bilaterally ICV-STZ), were divided into 2 groups 5 days after the STZ injection: one treated with rhEPO 5000 (IU/kg/day, i.p.) and the other with 0.9% NaCl (1 mL/kg/day, i.p.) for 2 weeks. 28511119: Hence, A HPLC-QTOF-MS based plasma metabonomics approach was applied to investigate the neuroprotective effects of breviscapine on intracerebroventricular injection of aggregated Abeta 1-42 induced AD mice for the first time in the study. 29104777: These results are fully consistent with the data obtained in animal models of Alzheimer's disease induced by the injection of the beta-amyloid (betaA) fragment 25-35 into the giant-cell nucleus basalis of Meynert or by co-injection of the betaA fragment 25-35 and ibotenic acid into the hippocampus, and the model of ischemia stroke (chronic bilateral occlusion of carotids, 2VO). 29174415: Mucin-type O-glycosylation has been associated with inflammation of brain tissues in AD, thus in this work, we aimed at identifying changes in the glycosylation profile generated by the injection of Abeta25-35 into the CA1 of the hippocampus of rats, using histochemistry with lectins. 29270738: Our previous study has identified that injection of soluble H.pylori filtrate could induce AD-like pathologic changes and cognitive impairment in SD rats. 29493157: This study was aimed to investigate the protective effect and mechanism of beta-asarone on the animal model of Alzheimer's disease(AD) which was induced by intracerebroventricular injection of Abeta1-42 combined cerebral ischemia. 29710724: Moringa Oleifera Alleviates Homocysteine-Induced Alzheimer's Disease-Like Pathology and Cognitive Impairments. Homocysteine (Hcy) injection for 14 days was used to induce AD-like pathology. 29881705: Materials and Methods: Hippocampal injection of amyloid beta (Abeta) was used to induce Alzheimer's disease in male Wistar rats, followed by intra peritoneal administrations of 5 and 10 mg/kg thymoquinone on a daily basis for 4 weeks. 29948724: Here, we evaluated the effect of a 4-week moderate treadmill exercise on spatial memory via central and peripheral Abeta clearance mechanisms following developed AD-like neuropathology induced by intra-hippocampal Abeta1-42 injection in male Wistar rats. 30178892: The protective effect of betulinic acid on microvascular responsivity and protein expression in alzheimer disease induced by cerebral micro-injection of beta-amyloid and streptozotocin. 30412728: In our study, model mice with AD induced by intracerebroventricular injection of Abeta1-42 were used to determine the role of TEC on memory retrieval. 30701598: This paper aims to investigate the effects of KF on cognitive function impairment and neurodegeneration in the mouse model of Alzheimer's disease induced by intracerebroventricular (ICV) injection of Abeta1-42 . 30760053: Administration of hCG ameliorated the lowered density of hCG receptor-ir neurons in the cerebellum and prefrontal cortex in STZ-induced AD rats. We investigated the effects of different doses of hCG on hCG receptor density in the prefrontal cortex and cerebellum in a rat model of STZ-induced AD. AD was induced by intracerebroventricular injection of 3 mg/kg STZ. 30814820: Conclusion: Aerobic and resistance exercise could improve recognition memory and decrease AChE activity in Abeta-induced AD in rats. AD was induced by intracerebroventricular injection of Abeta25-35 peptide. 30822517: Herein, we investigated the neurogenesis potential of quercetin in a rat model of Alzheimer's disease induced by amyloid-beta injection. 31325424: This study investigated the neuroprotective effects of curcumin loaded lipid-core nanocapsules (LNC) in a model of Alzheimer's disease (AD) induced by intracerebroventricular injections of beta-amyloid1-42 (Abeta1-42) peptide in aged female mice, and compared these effects with those from free curcumin. 10101484: Also primary endothelial injury induces hypertension and atherogenesis. The main injury factor is hypertension, which provides to endothelium disfunction with vasopressors level growth which induces hypertension. 11397021: These included the use of Dacron instead of vein because of 3 vein patch blowouts, invasive postoperative monitoring of blood pressure, and the use of intravenous beta-blockers to control hypertension, because of 4 hyperperfusion injuries. 11399644: Recent studies have suggested that subtle microvascular and tubulointerstitial injury in the kidney can cause salt-sensitive hypertension. To test this hypothesis, we determined whether the mild renal disease induced by transient blockade of nitric oxide (NO) synthesis would result in salt-sensitive hypertension and whether prevention of the renal injury by coadministration of the immunosuppressive agent mycophenolate mofetil (MMF) would block the development of salt sensitivity. Mycophenolate mofetil prevents salt-sensitive hypertension resulting from nitric oxide synthesis inhibition. L-NAME treatment resulted in acute hypertension and the development of mild renal injury. 11956996: These findings suggest that hypertension activates endothelial cells to increase the expression of adhesion molecules and cytokines, and induces neutrophil and monocyte adhesion and migration, resulting in endothelial cell injury and increased permeability of endothelial cells, which results in hypertensive arterial disease. 12388425: Responses of proximal tubule sodium transporters to acute injury-induced hypertension. 12966249: Autonomic dysreflexia occurs in the majority of patients with injuries above the sixth thoracic vertebra and causes sudden, severe hypertension. 14581313: It is caused by spinal reflex mechanisms that remain intact despite the patient's injury, leading to hypertension. 15142637: Today, endothelial injury is more often precipitated by distinctly modern stressors such as hypertension, smoking, diabetes, and dyslipidemia. 15231850: These findings suggest an impairment of erythrocyte membrane physical-chemical properties in overweight and obese people as a consequence of oxidative injury that might be part of a pathogenetic mechanism responsible for obesity-related pathologies such as atherosclerosis and hypertension. 15509134: The antioxidant properties demonstrated in this mechanism contribute to the drug's antihypertensive action and thus, may reduce the risk of injuries inflicted by reactive oxygen species involved in the pathogenesis of hypertension. 16374423: Loss of renal kallikrein, produced by tubulointerstitial injury, may participate in the pathogenesis of the hypertension observed in this model. 16390865: Phenol injury-induced hypertension stimulates proximal tubule Na+/H+ exchanger activity. 1664085: Such parenchymal injury may lead to arterial hypertension, and renal failure when bilateral. 16928620: Recent evidence has suggested that subtle acquired tubulointerstitial injury may cause a defect in sodium excretion function, thus leading to salt-sensitive hypertension. 18852387: We also questioned whether neonatal O(2) injury causes long-term renal damage, important in the pathogenesis of hypertension. 19118493: Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. 19641713: CONCLUSIONS: The duration of alcohol ingestion is important in the induction of hypertension and the associated NO and antioxidant depletion, and oxidative tissue injury. The time response of alcohol-induced hypertension and associated tissue oxidative stress response has not been fully explored. 20088639: Traumatic injury of renal arteries is rare and can induce renal dysfunction and hypertension. 20807613: In the case of hypertension-attributed kidney disease, it remains unclear if the hypertension is a contributing cause or a consequence of glomerular injury. 22745791: VEGF inhibition can promote renal vascular and parenchymal injury, causing proteinuria, hypertension and thrombotic microangiopathy. 25432379: Endothelial injury or dysfunction leads to multiple cardiovascular diseases, such as atherosclerosis, myocardial infarction, stroke, hypertension and peripheral vascular disease. 25560433: Premature depletion of progenitors due to prematurity or postnatal loss of nephrons due to injury causes chronic kidney disease and hypertension. 26150439: Recent evidence indicates that salt-sensitive hypertension can result from a subclinical injury that impairs the kidneys' capacity to properly respond to a high-salt diet. 26936874: In summary, congenital solitary kidney rats are highly susceptible to the induction of hypertension compared with uninephrectomized rats, suggesting that low nephron endowment is an important driver of elevated blood pressure, hastening nephron injury through the transmission of elevated systemic blood pressure and thereby accelerating decline in kidney function. 27760997: Notably, salt loading increases renal Rac1 activity in several models of salt-sensitive hypertension, which, in the presence of aldosterone, synergistically activates MR signaling, causing hypertension and kidney injury. This crosstalk pathway promotes glomerular podocyte injury, and is also involved in the pathogenesis of hypertension. 2839626: Endothelial injury and platelet activation may be involved in the pathogenesis of hypertensive vascular disease. 2922776: After a mild injury, induced moderate hypertension (121-140 mm Hg) improved spinal cord blood flow significantly, whereas hypotension decreased it in a linear fashion. Even extreme hypertension (161-180 mm Hg) induced by adrenaline did not significantly increase spinal cord blood flow at T1 but caused hyperemia at C6 due to loss of autoregulation. 30976074: However, there was no direct invasion by the two organisms causing endothelial cell injury, leading to speculation regarding the other mechanisms that may lead to HTN. 31676114: BACKGROUND: Hypertension with hyperaldosteronism could be associated with stroke attributable to endothelial injury. 4053303: Hyperplastic growth response of vascular smooth muscle cells following induction of acute hypertension in rats by aortic coarctation. This study examines the growth response of vascular smooth muscle cells following induction of acute hypertension in rats by partial ligation of the abdominal aorta between the renal arteries. It is suggested that a non-denuding form of endothelial \injury\ may play an important role in the proliferative growth response of smooth muscle cells following induction of coarctation hypertension. 7784725: Since the MAP was elevated in only those groups that received injury in the upper pons, we concluded that injury in the upper pons can lead to hypertension following i.v. administration of pancuronium. 7840303: Cortical blood flow increased dramatically 3-15 s following injury-induced hypertension in both the cocaine and saline groups (approximately 230-260%), but then fell below preinjury values within minutes. 8467426: These results suggest that hemodilution with DCLHb decreases focal ischemic injury, and is most effective when given in a manner that induces hypertension. 8990373: Of the 31 recipients of KNW, 18 received kidneys declined for reasons of advanced age, defined as > or =60 years (including 8 who also had a history of hypertension, 4 who also had >10% sclerosed glomeruli on biopsy, and 3 also declined based upon donor quality because of acute injury), 8 for donor quality alone (e.g., prolonged hypotension), 3 on the basis of biopsy results alone, and 2 for anatomic abnormalities. 9630451: Furthermore, it was proposed that early alterations in MCTP-induced lung injury leading to hypertension were associated with a similar inhibition of EC proliferation. 11462768: The amyloid beta-peptides have been implicated in the excitotoxic mechanism of neuronal injury in the pathogenesis of Alzheimer's disease. 12099698: Transforming growth factor-beta-1 (TGF-beta), a key regulator of the brain responses to injury and inflammation, has been implicated in upregulating the expression of the Alzheimer amyloid precursor protein (APP) and Alzheimer's disease (AD) pathogenesis. 16159194: Peroxynitrite (ONOO(-)), formed from the reaction of superoxide ((*)O(2)(-)) and nitric oxide ((*)NO), induces cellular and tissue injury, resulting in several human diseases such as stroke, Alzheimer's disease, and atherosclerosis. 16355213: Angiogenesis factors, especially vascular endothelial growth factor, are now known to have roles in the birth of new neurons (neurogenesis), the prevention or mitigation of neuronal injury (neuroprotection), and the pathogenesis of stroke, Alzheimer's disease and motor neuron disease. 16534775: CONCLUSION: This study showed that oxidative injuries could be involved in the pathogenesis of AD, as well as indicating that some antioxidant might be associated with the cognitive functions in AD. OBJECTIVES: It has been suggested that oxidative injuries have an important role in the pathogenesis of Alzheimer's disease (AD). 17602566: ONOO- induces cellular and tissue injury, resulting in several human diseases such as Alzheimer's disease, atherosclerosis, and stroke. 19950527: CONCLUSION: R. rosea extract can protect rats against cognitive deficits, neuronal injury and oxidative stress induced by intracerebroventricular injection of streptozotocin, and may be used as a potential agent in treatment of neurodegenerative diseases such as AD. 22540007: In addition, DG could alleviate lipid peroxidation and partially restore the mitochondrial function in Abeta(1-42)-induced AD mice. Therefore, these results demonstrated that DG could attenuate Abeta(1-42)-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improved cognitive impairment in Abeta(1-42)-induced AD mice, indicating that DG exerted potential beneficial effects on AD. Furthermore, DG significantly decreased the escape latency and search distance and increased the target crossing times of Abeta(1-42)-induced AD mice in the Morris water maze test. 23877934: Increasing evidence has demonstrated that white matter (WM) disruptions, due to the injury of the axon and myelin, play an important role in the pathogenesis of Alzheimer's disease (AD). 25362039: BACKGROUND: It has been suggested that oxidative injuries have a role in the pathogenesis of Alzheimer's disease (AD). 26166438: Studies have revealed that astrocyte response to gross tissue damaging injury leads to anisomorphic astrogliosis reinforcing a cascade of events, eventually increasing the pathogenesis of AD and many other neurodegenerative disorders. 26221414: In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration. 27793193: Recent diffusion tensor imaging studies in AD suggest that increased diffusion in the fornix secondary to p-MAPT-related axonal injury could serve as a predictive biomarker of the risk of disease progression. 28702899: INTRODUCTION: Oxidative injury to the brain and aging are theoretical co-causes of Alzheimer's Disease (AD). 29630554: While plasma NFL may not reflect NAL in individuals with normal global cognition, the current observations indicate that onset of axonal injury, reflected by increased plasma NFL, within the preclinical phase of AD may contribute to the pathogenesis of AD. 29978424: Pretreatment of neurons with Klotho protein can avoid neuronal injury related to the toxic amyloid-beta and glutamate, centrally related to the pathogenesis of Alzheimer's disease (AD), in order that Klotho protein could play a neuroprotective role in AD patients. 3561662: The results do not support the hypothesized roles of blood-brain barrier disruption or of immunologically-mediated injury of the central nervous system in the pathogenesis of AD. 7777136: Increasing evidence supports the involvement of amyloid beta-peptide (A beta) and an excitotoxic mechanism of neuronal injury in the pathogenesis of Alzheimer's disease. 9883847: Excitotoxicity, a form of neuronal injury in which excessive activation of glutamate receptors results in cellular calcium overload, has been implicated in the pathogenesis of Alzheimer disease (AD), although direct evidence is lacking. 11198152: The mechanism that relates insulin to blood pressure and the role of insulin in the pathogenesis of arterial hypertension have not been clearly defined. 11327624: Thus, the evidence summarized here supports an important role for insulin and the sympathetic nervous system in the pathogenesis of obesity-related hypertension. 12546272: The metabolic syndrome may be viewed as a state of insulin-counterregulatory overdrive: counterregulatory hormones and fatty acids chronically duel with insulin, causing a cascade of biochemical interactions resulting in insulin resistance, hypertension, and dyslipidemia. 15226099: Insulin infusion induces endothelin-1-dependent hypertension in rats. 17132536: Renal D1 receptor function was studied in insulin-induced hypertension in male Sprague Dawley rats. 1730459: Moreover, insulin-induced hypertension was associated with a shift of renal pressure natriuresis, since sodium balance was maintained at elevated arterial pressures. These observations indicate that chronic hyperinsulinemia in rats produced hypertension that was not salt-sensitive and not dependent on sodium retention or increased renin secretion. 1752728: Several studies have been performed to determine if plasma insulin concentration bears a relationship with blood pressure and may be a causative factor in the genesis of hypertension. 1881501: Insulin as a cause of sodium retention and hypertension. 2185153: These observations provide no evidence that chronic hyperinsulinemia or interactions between insulin and plasma catecholamines cause hypertension in normal dogs. 2227116: Higher insulin concentrations in drug-treated hypertensive patients might result from the treatment rather than contribute to the pathogenesis of hypertension. 2455613: In vitro action of insulin on erythrocyte sodium transport mechanisms: its possible role in the pathogenesis of arterial hypertension. 25364368: Diabetes mellitus is a group of metabolic disorders in which the blood glucose is higher than normal levels, due to insufficiency of insulin release or improper response of cells to insulin, resulting in high blood pressure. 2649514: These studies indicate that glomerular capillary hypertension in diabetes is an acutely reversible consequence of insulin deficiency and not the result of renal hypertrophy. 2687519: On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE. 28738763: Finally, lixisenatide may be best used as an adjunct therapy for patients who are inadequately controlled with other diabetic medications, or select group of patients at risk of insulin induced obesity, hypertension or heart failure. 28971990: Hyperinsulinemia has been hypothesized to cause hypertension in obesity, type 2 diabetes, and metabolic syndrome through a renal mechanism. Thus, by developing a novel approach for chronic, continuous renal artery insulin infusion, we provided new evidence that insulin causes hypertension in rats through actions initiated within the kidney. 8345807: To determine whether insulin modulates ET levels in vivo and whether this effect is important in the pathogenesis of obesity-associated hypertension, we measured circulating immunoreactive ET-1 levels during euglycemic hyperinsulinemic clamps (20 mU/m2.min-1 for 120 minutes) in eight obese women (body mass index, 36 +/- 1 kg/m2) before and after 10 weeks on an 800-kcal/d protein-sparing liquid diet. 8707382: The resistance of various tissues to the vasodilator and metabolic effects of insulin may be an important risk factor in the genesis of hypertension observed in several pathological states. 8972890: Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats. This study tested whether combined alpha1- and beta-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. 9095092: These results indicate that insulin-induced hypertension in rats depends on angiotensin II and suggest that a reduction in glomerular filtration rate contributes to the shift in pressure natriuresis. Insulin-induced hypertension in rats depends on an intact renin-angiotensin system. This study tested the dependence of insulin-induced hypertension in rats on a functional renin-angiotensin system. 9369270: This observation is of potential interest with respect to the interaction of Ang II and insulin, eg, in the genesis of hyperinsulinemia and hypertension. 9484757: The improvement of hypertension observed in KP recipients suggests a key role of glucose and insulin metabolism on pathogenesis of diabetic hypertension. 9719048: Angiotensin receptor blockade blunts hyperinsulinemia-induced hypertension in rats. These results indicate that angiotensin type 1 receptors play a determinant role in the pathogenesis of insulin-induced hypertension in rats. The study was conducted to examine the effects of the angiotensin subtype 1 and 2 receptor antagonists (losartan and PD123319, respectively) on blood pressure (BP) and renal excretory function in chronic hyperinsulinemia-induced hypertension in rats. 9869010: OBJECTIVE: To investigate the role of angiotensin II in the pathogenesis of hyperinsulinemia-induced hypertension in rats. CONCLUSIONS: Angiotensin converting enzyme inhibition or angiotensin II type 1 receptor antagonism can prevent and reverse insulin-induced hypertension in rats, suggesting that angiotensin II itself or an angiotensin II-dependent mechanism has an etiological influence in the pathogenesis of this hypertension model. When the insulin-induced hypertension had become established (systolic blood pressure increased from 132+/-3 to 155+/-2 mmHg 4 weeks after the infusion, P< 0.05 ), subsequent fosinopril or losartan treatment for 2 weeks reversed the elevated systolic blood pressure and heart rate to the control levels. 10354294: BACKGROUND: Insulin resistance and hyperinsulinemia induce glomerular hypertension and hyperfiltration, which may result in glomerulosclerosis. 10422304: This would be especially so in the case of membrane transporters and insulin resistance which may be a consequence, or a cause, of high blood pressure, but which give rise to lipid metabolism alterations. 10466472: BACKGROUND: It has been suggested that hyperinsulinemia and insulin resistance participate in the pathogenesis of hypertension, in part by activating sympathetic activity. 10582537: Several lines of evidence suggest that insulin resistance and/or hyperinsulinemia may play an important role in the pathogenesis of hypertension. 10616862: The higher risk of later developing type 2 diabetes and hypertension in women who have a history of gestational diabetes is explicable by their poorer profile on variables associated with insulin metabolic syndrome, and appears to be attributable to insulin resistance. 10652907: Hypertension, in a sizable number of patients, though not all, is associated with and possibly caused by insulin resistance. 10707568: Insulin resistance syndrome is the theory that glucose intolerance, hyperinsulinemia, increased very low density lipoprotein triglyceride level, decreased high density lipoprotein cholesterol level, and hypertension are proposed consequences of insulin resistance. 10736756: Insulin resistance syndrome is the theory that glucose intolerance, hyperinsulinemia, increased very low density lipoprotein triglyceride level, decreased high density lipoprotein cholesterol level, and hypertension are proposed consequences of insulin resistance. 10933578: Insulin resistance may cause a metabolic syndrome but whether insulin resistance causes hypertension is very controversial. 11057433: OBJECTIVE: To clarify the role of insulin resistance and hyperinsulinaemia in the pathogenesis of obesity-related hypertension. 11265132: [Effects of ethanol on the nervous and vascular systems: the mechanisms of alcohol-induced hypertension]. The effects of ethanol on the nervous and vascular systems in relation to the mechanisms of alcohol-induced hypertension proposed so far are reviewed here. More detailed and integrated mechanisms for alcohol-induced hypertension, which is not a homogeneous disease, remain to be clarified. 8) The difference in the genetic polymorphism of acetaldehyde dehydrogenase among Japanese people may not be directly related to development of alcohol-induced hypertension. 7) Long-term heavy drinking often results in the development of insulin resistance and glucose intolerance, which in turn triggers hypertension. 11384694: CONCLUSION: These findings are consistent with the hypothesis that insulin resistance precedes the clinical onset of hypertension in pregnancy, and may be important in the etiology of hypertension. 11475857: Obesity, insulin resistance and hyperinsulinaemia are responsible for hypertension in diabetes mellitus type 2. 12393073: Insulin resistance may be a factor in the etiology of hypertension, and habitual alcohol intake may modify this relationship. 12529486: OBJECTIVE: Rats with ventromedial hypothalamic lesion (VMH) are massively obese with endogenous hyperinsulinemia, insulin resistance, low sympathetic activity, and high parasympathetic activity, which are likely to induce hypertension. 12608549: BACKGROUND: Insulin resistance has been reported to induce hypertension. 12757656: OBJECTIVE: To investigate whether insulin resistance is the common route for hereditary and environmental factors to cause hypertension. CONCLUSIONS: Insulin resistance is a common route for hereditary and environmental factors to induce hypertension. 1285941: To investigate the hypothesis that insulin resistance plays a role in the etiology of hypertension and hyperlipidemia, we measured serum lipid levels, the fasting glucose/insulin ratio, and the insulin response to oral glucose (GTT) in a group of young obese subjects (n = 21) with hypertension and normal glucose tolerance and in normotensive subjects (n = 36) with normal glucose tolerance, matched for age and body mass index. 12877071: There are several mechanisms about high blood pressure induced by insulin resistance in type 2 diabetes. High blood pressure was partially caused by the endothelial dysfunction. 12877072: Further studies on Wistar fatty rat are expected to elucidate the mechanism of hypertension induced by insulin resistance and suggest on approach to treat hypertension in obese or type 2 diabetes. 1347538: A number of biologic actions of insulin lend credence to the hypothesis that insulin resistance can produce hypertension, perhaps by stimulating a hyperkinetic circulation. 15185899: Diabetic patients have an increased risk of coronary disease partly due to a higher frequency of associated risk factors including hypertension and hyperlipidemia but also from specific risks largely resulting from insulin resistance, hyperinsulinemia and hyperglycemia. 15254581: Metabolic complications in PPARgamma deficiency, such as hypertension, have been considered to be secondary to insulin resistance. 1541035: This insulin resistance and the resulting hyperinsulinaemia are now recognised as common background factors that may be responsible for hypertension, hyperlipidaemia, decreased thrombolysis and also impaired glucose tolerance and diabetes. 15975995: Because defects at the level of IRS1 may underlie at least some forms of insulin resistance, sodium retention, facilitated by hyperinsulinemia through the IRS1-independent pathway, could be an important factor in pathogenesis of hypertension in insulin resistance. 1612069: It was only recently, however, that Reaven, DeFronzo, and Ferrannini with techniques to quantitate insulin resistance suggested that this represents a common factor in this group of disorders and that hyperinsulinemia resulting from insulin resistance could be the cause of the hypertension, dyslipidemia, and atherosclerosis. 16179890: Insulin resistance (IR) has profound, negative effects on the function of arteries and arterioles throughout the body and leads to arterial hypertension and vascular occlusive diseases such as heart attacks and strokes. 16355015: Of these elements, obesity may play the most important and pivotal role in creating the conditions that lead to hypertension in the metabolic syndrome. The cause of hypertension in the metabolic syndrome is complex and multifactorial and all of the elements of the metabolic syndrome, including obesity, insulin resistance, and the characteristic dyslipidemia probably are involved in mediating changes ultimately resulting in hypertension and modifying its course. 1658839: This article reviews mechanisms by which hyperinsulinemia, insulin resistance, or both may lead to hypertension. 16815981: In summary, testosterone is essential in vivo for the development of endothelial dysfunction and hypertension secondary to insulin resistance, suggesting a facilitatory role for testosterone in increasing BP in fructose-fed male rats. 16929378: To the extent that insulin resistance leads to hyperglycemia, dyslipidemia and hypertension, this association is not surprising. 16989076: This review discusses the mechanisms by which hyperinsulinemia and/or insulin resistance may lead to hypertension. 17213573: Insulin resistance up-regulates the local RAS which contributes to the pathogenesis of hypertension, heart failure, and atherosclerosis. 17254516: Insulin resistance upregulates the renin-angiotensin system (RAS), which contributes to the pathogenesis of hypertension, heart failure, and atherosclerosis. 17267845: In later gestation maternal metabolic manifestations of the metabolic syndrome, such as gestational hypertensive disorders and diabetes, become clinically recognized because of the increased insulin resistance in obese compared with nonobese women. 1733245: These findings do not support a role for peripheral insulin resistance in the genesis of hypertension in SHR. 1930926: In those with type 2 diabetes insulin resistance and hyperinsulinaemia may play a part in the pathogenesis of hypertension independent of obesity. 19348235: Insulin resistance up-regulates the renin-angiotensin-aldosterone system (RAA system) by various mechanisms, which contributes to the pathogenesis of hypertension and atherosclerosis. 19360315: Feeding rats with a high-fructose diet induced insulin resistance, leading to hypertension or metabolic disorders. 19487712: Emerging evidence supports a paradigm shift in our understanding of the renin-angiotensin-aldosterone system and in aldosterone's ability to promote insulin resistance and participate in the pathogenesis of the metabolic syndrome and resistant hypertension. 19603071: The objective of this study was to determine whether hypertension specifically affects the plasma lipidome independently and differently from the effects induced by obesity and insulin resistance. CONCLUSIONS/SIGNIFICANCE: Top-down shotgun lipidomics demonstrated that hypertension is accompanied by specific reduction of the content of ether lipids and free cholesterol that occurred independently of lipidomic alterations induced by obesity and insulin resistance. 19633817: These data suggest that the kidneys could be actively participating in the pathogenesis of insulin resistance-induced hypertension through the arachidonic acid CYP 450-RhoA/Rho kinase pathway(s). Renal protein expression for the cytochrome P (CYP) 450 arachidonic acid metabolizing enzymes has been shown to be altered in other models of diet-induced hypertension. 19801534: It causes insulin resistance that in turn leads to diabetes, hypertension and cardiovascular abnormalities. 2045166: Although controversy exists as to the role insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension, data are presented from both obese and nonobese subjects that strongly suggests that selective insulin resistance and hypertension are directly related. 2076856: It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. 21286851: Consequently, we believe that the decrease in oxidative stress after 1 month of CPAP treatment in these patients is not contributing much to IR genesis, though it could be related to the hypertension etiology. 21958881: Substantial evidence suggests that a large portion of the population have suboptimal levels of vitamin D, which may adversely affect the cardiovascular (CV) system, including increasing levels of parathyroid hormone, activating the renin-angiotensin-aldosterone system, and increasing insulin resistance, thus leading to hypertension and left ventricular hypertrophy, metabolic syndrome/diabetes mellitus, systemic inflammation, and increased risk of atherosclerosis and CV disease events. 22248781: The most important consequences of insulin resistance in children include increased incidence of type 2 diabetes, atherogenic dyslipidemia and arterial hypertension, which lead to increased cardiovascular risk. 22322931: [Insulin resistance-induced hypertension and perivascular nerves-an approach to elucidate the mechanisms involved]. 23745744: Insulin resistance-induced hypertension and a role of perivascular CGRPergic nerves. Therefore, to elucidate the mechanisms of insulin resistance-induced hypertension, we investigated that the effects of hyperinsulinemia or hyperglycemia on vascular responses mediated by perivascular nerves including sympathetic adrenergic nerves and calcitonin gene-related peptide (CGRP)-containing nerves (CGRPergic nerves). In this article, we show evidence that insulin resistance-induced hypertension could be resulted from increased density and function of sympathetic nerve, and decreased density and function of CGRPergic nerves. Furthermore, our findings provide a new insight into the research of therapeutic drugs for insulin resistance-induced hypertension. 24358774: The serum NO levels of three different doses FGF21 treatment group were significantly higher than that of the model control group [(7.32 +/- 0.11), (7.24 +/- 0.13), (6.94 +/- 0.08) vs. (6.56 +/- 0.19) micromol x L(-1), P < 0.01], and the degree of improvement showed obvious dose-dependent manner, indicating that FGF21 can significant increase serum NO in fructose-induced hypertension rat model and improve endothelial NO release function. [Therapeutic effect of fibroblast growth factor 21 on hypertension induced by insulin resistance]. This study is to evaluate the therapeutic effect of fibroblast growth factor 21 (FGF21) on hypertension induced by insulin resistance in rats and to provide mechanistic insights into its therapeutic effect. Thus, this study demonstrates that FGF21 significantly ameliorates blood pressure in fructose-induced hypertension model by relieving insulin resistance. 25481558: In this review, we discuss the development of insulin resistance during pregnancy, hormones and newly discovered factors associated with insulin resistance and secretion, lipid metabolism, and the pathogenesis of hypertension during pregnancy. 2569446: The role of insulin resistance and hyperinsulinemia in the etiology of fructose-induced hypertension was studied in male Sprague-Dawley rats. 26295295: Obesity, insulin resistance (IR), inflammation, and hyperandrogenism may lead to polycystic ovary syndrome (PCOS) and hypertension. 26631327: INTRODUCTION: Global sugar consumption has increased in the past 50 years; its abusive intake is responsible for peripheral insulin resistance, which causes the metabolic syndrome - obesity, diabetes mellitus, hypertension, and coronary heart disease. 27219878: However, the potential effect of UDCA on hypertension induced by type-2 diabetic insulin resistance has not been reported. 27884224: This article updates recent literature with a focus on the function of insulin resistance, obesity, and renin angiotensin aldosterone system-mediated oxidative stress on endothelial dysfunction and the pathogenesis of hypertension. 28162091: BACKGROUND: The pathophysiology of insulin resistance-induced hypertension and hyperlipidemia might entail differences in dementia risk in cases with hypertension and hyperlipidemia without prior diabetes mellitus (DM). 29093373: Chronic hyperinsulinemia in insulin resistance model rats caused significant increases in the function and distribution of perivascular sympathetic nerves and decreases in those of perivascular CGRPergic nerves, resulting in the development of hypertension (insulin resistance-induced hypertension). [Function of Perivascular Nerves in Insulin Resistance-induced Hypertension]. 30562438: Moreover, insulin resistance induces hypertension, hypertriglyceridemia and impaired glucose tolerance, and causes the metabolic syndrome. 31081518: * Insulin resistance plays a key role in the pathogenesis of hypertension. 33432967: A high salt intake exacerbates insulin resistance, evoking hypertension due to systemic perivascular inflammation, oxidative-nitrosative stress and endothelial dysfunction. 33480422: A high salt intake exacerbates insulin resistance, evoking hypertension due to systemic perivascular inflammation, oxidative-nitrosative stress and endothelial dysfunction. 35628624: Our aim is to summarize the main pathophysiological mechanisms through which IR causes HS and to highlight the specific principles of treatment of HS for children with DM. 36912156: CONCLUSIONS: Our results suggest that elevated insulin concentration at birth plays a critical role in the early life origins of hypertension and support the hypothesis implicating insulin resistance in the etiology of hypertension. BACKGROUND: Although insulin resistance is closely related to hypertension, the debate continues as to whether insulin resistance is a cause or a consequence of hypertension. 38096969: Hydrogen sulfide ameliorates hypertension and vascular dysfunction induced by insulin resistance in rats by reducing oxidative stress and activating eNOS. 38390815: Evidence suggests that insulin resistance might trigger high blood pressure (BP). 38504161: AIM: Insulin resistance (IR) may participate in the pathogenesis of hypertension by mediating low-grade systemic inflammation. 7485485: To explore the relationship between insulin resistance and hypertension, we examined whether acute induction of hypertension can engender insulin resistance. For this purpose we measured rates of insulin-mediated glucose uptake in awake unstressed rats with the euglycemic hyperinsulinemic (12 microns.kg-1.min-1) clamp technique during infusions of saline alone or after induction of hypertension by bolus administration of NG-monomethyl-L-arginine (L-NMMA, 30 and 15 mg/kg), a competitive inhibitor of nitric oxide synthase. Insulin resistance after hypertension induced by the nitric oxide synthesis inhibitor L-NMMA in rats. 7607722: These findings do not support a direct role for insulin resistance in the pathogenesis of the hypertension associated with abdominal obesity. 7624391: Thus it is concluded that insulin resistance and its associated abnormalities are of utmost importance in the pathogenesis of NIDDM, hypertension, and coronary heart disease. 7695182: Excess free fatty acid may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance, and hypertension and finally atherosclerosis. 7699923: Not only hyperglycemia but also hypertension, dyslipoproteinemia, and other factors due to insulin resistance resulting from visceral fat syndrome, might be responsible for the occurrence of atherosclerosis. 7700882: We have briefly reviewed the controversy regarding the role of insulin resistance and hyperinsulinemia in the pathogenesis of hypertension in an attempt to emphasize the evidence in support of this concept. 7725634: The hypothesis of insulin resistance in the pathogenesis of arterial hypertension as part of the hormonal metabolic X syndrome and our 5H syndrome resp. 7782934: Although controversy exists as to the role that insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension, data are presented that strongly suggest that selective insulin resistance and hypertension are directly related. 7859591: Excess free fatty acid may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. 7986471: Correlations between insulin resistance, hyperinsulinemia, and hypertension do not appear to be explainable by the concept that insulin resistance occurs secondary to hypertension. Although hyperinsulinemia and insulin resistance have been speculated to cause hypertension, most of the evidence supporting this hypothesis has come either from correlation studies or from short-term studies of the cardiovascular, renal, and sympathetic effects of insulin. 8158379: Nevertheless, whether insulin resistance and/or hyperinsulinemia itself contribute to the pathogenesis of hypertension is still unclear. 8206593: Hyperinsulinemia and insulin resistance are implicated in the etiology of hypertension, but the mechanisms involved have not been established. 8417411: Although controversy exists as to the role that insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension there are ample data from both obese and nonobese subjects strongly suggesting that selective insulin resistance, hyperlipidemia, and essential hypertension are directly related. 8568012: Hyperinsulinemia and insulin resistance may cause systemic hypertension through multiple mechanisms. 8576793: INSULIN RESISTANCE AND HYPERTENSION: Hypertension is often associated with insulin resistance, which may be the underlying cause of hypertension in many cases. 8581775: Excess free fatty acids may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. 8914427: Excess free fatty acid of the portal circulation may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. 9240760: These results suggest that insulin resistance is involved in the etiology of hypertension in NIDDM patients, and that this derangement has an important role for the progression of diabetic nephropathy. 9249996: Mechanisms of insulin resistance leading to hypertension: what we can learn from experimental models. 9493563: Evidence from chronic insulin infusion studies in rats suggests hyperinsulinaemia can increase BP under some conditions; however, conflicting evidence in humans and dogs leaves in question whether hyperinsulinaemia is a factor in hypertension induced by obesity. This derangement has also been proposed as a mechanism through which insulin resistance can cause hypertension. 17049785: Insulin resistance is central to Type II diabetes and is also implicated in the pathogenesis of Alzheimer's Disease (AD). 17982898: Central insulin resistance as a trigger for sporadic Alzheimer-like pathology: an experimental approach. 19705099: Accordingly, metabolic and cognitive disorders such as obesity, type 2 diabetes mellitus and Alzheimer's disease are associated with resistance of central nervous structures to the effects of insulin, which may derive from genetic polymorphisms as well as from long-term exposure to excess amounts of circulating insulin due to peripheral insulin resistance. 21435176: Possible implications of insulin resistance and glucose metabolism in Alzheimer's disease pathogenesis. 22201977: Growing evidence supports roles for brain insulin and insulin-like growth factor (IGF) resistance and metabolic dysfunction in the pathogenesis of Alzheimer's disease (AD). 22610992: Given the potential relationship between insulin resistance and pathogenesis of Alzheimer's disease (AD) in elderly life, we investigated the relationship between perinatal DEHP exposure and AD pathogenesis. 24333407: Impaired insulin signaling and insulin resistance in brain have been found to play an important role in the pathogenesis of AD. 25755673: CONCLUSIONS: The extracts of moderate and severe red peppers were found to prevent the memory deficit and exacerbation of insulin resistance by blocking tau phosphorylation and beta-amyloid accumulation in diabetic rats with experimentally induced Alzheimer's-like dementia. 26136993: In conclusion, the expression of BACE1 in the brain tissue of insulin-resistant rats increased, and IR was indicated to participate in the pathogenesis of AD. The aim of this study was to investigate the expression of beta-site APP-cleaving enzyme 1 (BACE1) in the hippocampal tissue of an insulin-resistant rat model, and thereby explore the roles of BACE1 and insulin resistance (IR) in the pathogenesis of Alzheimer's disease (AD). 26240147: Insulin resistance and neuroinflammation have emerged as two likely key contributors in the pathogenesis of Alzheimer disease (AD), especially in those sporadic AD cases compromised by diabetes or cardiovascular disease. 26268336: Impaired brain insulin signaling or brain insulin resistance and its role in the molecular pathogenesis of sporadic AD have been demonstrated. 27466310: Deficits in glucose, impaired insulin signalling and brain insulin resistance are common in the pathogenesis of Alzheimer's disease (AD); therefore, some scholars even called AD type 3 diabetes mellitus. 27810390: Agmatine ameliorates type 2 diabetes induced-Alzheimer's disease-like alterations in high-fat diet-fed mice via reactivation of blunted insulin signalling. The aim of this study was to investigate the ability of agmatine to treat AD induced by brain insulin resistance. Previous studies in high-fat diet-induced AD animal models have shown that brain insulin resistance in these animals leads to the accumulation of amyloid beta (Abeta) and the reduction in GSK-3beta phosphorylation, which promotes tau phosphorylation to cause AD. 27988872: Alzheimer's disease (AD) should be regarded as a degenerative metabolic disease caused by brain insulin resistance and deficiency, and overlapping with the molecular, biochemical, pathophysiological, and metabolic dysfunctions in diabetes mellitus, non-alcoholic fatty liver disease, and metabolic syndrome. 29132997: AIMS: Diabetes mellitus (DM) and impairments of glucose metabolism and insulin resistance in the brain have been suggested as a likely etiology of Alzheimer's disease (AD). 29163128: In this review, we will discuss insulin resistance as a contributing factor to the pathogenesis of AD, as well as the metabolic and bioenergetic disruptions linking insulin resistance and AD. 29712510: DISCUSSION: GCBE exerted neuroprotective effects against IR-induced AD mediated by alleviating IR and modulating brain insulin signaling cascade. 29951404: Disruption of insulin signaling cascade and insulin resistance can induce AD; and central insulin resistance causes systemic alterations in serum insulin, FBS levels, and lipid profile. 30364261: Increased risks for Alzheimer's disease (AD) are a well-recognized consequence of diabetes, insulin resistance (IR), and hyperinsulinemia. 30804755: We further highlight the deleterious consequences of Tau pathology-induced insulin resistance to the brain and/or peripheral tissues, suggesting that these are key events mediating cognitive decline in Alzheimer's disease (AD) and other tauopathies. 32829453: Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer's disease (AD). In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. 33164543: In this study, the probable role of insulin resistance in the pathogenesis of AD was investigated in patients with Type 2 Diabetes Mellitus (T2DM). OBJECTIVE: Recent evidence suggests that insulin resistance may play an important role in the pathogenesis of Alzheimer's disease (AD). 33552476: This model predicts that any condition leading to an increase of [Ca 2+ ] i may trigger central insulin resistance and explains why central insulin resistance is implicated in the pathogenesis of AD, with which glutamate excitotoxicity is a comorbid condition. 33816504: Insulin resistance is a kind of pathological state, which is important in the pathogeneses of type 2 diabetes mellitus (T2DM), gestational diabetes mellitus and Alzheimer's disease. 34524376: Disturbances in the action of GSK-3 enzyme may leads to various disease conditions that include insulin resistance leading to diabetes, neurological disease like Alzheimer's disease and cancer. 34609116: Insulin resistance is also a factor that contributes to pathogenesis of AD. The complications that are discussed in this article are diabetic nephropathy, diabetes induced cardiovascular disease, diabetic neuropathy, Diabetic Foot Ulcer (DFU) and Alzheimer's disease. The progression of AD can be due to the change in DNA methylation of CLOCK gene, followed with worsening of AD by APOE4 gene due to dyslipidaemia condition in T2DM patients. 34686782: CONCLUSION: The present paper proposes the hypothesis that hypercoagulation might amplify MetS associated insulin resistance, neuroinflammation, BBB disruption, and amyloid beta accumulation which eventually leads to AD. 35533773: Therefore, activation of alpha7nAChR through GTS-21 might be the potential target for the amelioration of central insulin resistance induced AD. 36118711: Overall, this pattern is reminiscent of neural abnormalities previously observed in Alzheimer's disease, suggesting that similar neurobiological mechanisms, secondary to insulin resistance and manifesting as NVC alterations, might be developing in T2DM pathology. 36162508: Taken together, our results suggest that CX3CL1-ICD may have translational potential for neuroprotection in Alzheimer's disease and for disorders resulting from insulin resistance. 36362376: The biological plausibility of the link between high adiposity, insulin resistance, and dementia is central for understanding AD etiology, and to form bases for prevention efforts to decrease the disease burden. 36404813: Objectives: Glucose intolerance and insulin resistance are hallmarks of metabolic syndrome and lead to Alzheimer's disease (AD). 36626931: In humans, central insulin resistance is at least part of the formal pathogenesis of AD. 36630734: PP2Calpha aggravates neuronal insulin resistance leading to AD-like phenotype in vitro. Our study thereby demonstrates escalation of hyperinsulinemia mediated neuronal insulin resistance leading to AD-like pathogenesis by PP2Calpha in vitro and hints a novel molecule, PP2Calpha, linking AD pathogenesis. 37985011: In conclusion, brain insulin resistance could lead to AD and vice versa. 32023431: Gut microbiota and neuroinflammation in pathogenesis of hypertension: A potential role for hydrogen sulfide. 32535221: Gut microbiota modulates stress-induced hypertension through the HPA axis. 32852030: Dysbiosis of gut microbiota has been implicated in the pathogenesis of hypertension. 33269431: Lately, the influence of early-life diet on gut microbiota leading to altered short chain fatty acid profiles has been discussed in the etiology of arterial hypertension. 33793332: There is mounting evidence to suggest that the gut microbiome plays an important role in the development and pathogenesis of hypertension. 34887530: Recent evidence suggests that the gut microbiota plays an important role in the development and pathogenesis of hypertension. 34970454: We reviewed the roles of neuroinflammation and gut microbiota and their interactions in the pathogenesis of hypertension and described the ascending signaling mechanisms behind the microbiota-gut-brain axis in detail. 35209934: DISCUSSION: Expanding upon our previous research on the role of the gut microbiota in the pathogenesis of hypertension, this study serves as a clinical translation advancement and explores the potential of fecal microbiota transplantation for treating hypertension. 35420126: Mounting evidence from animal and human studies indicates that the composition and metabolic profiles of the gut microbiota are linked to the pathogenesis of cardiovascular disease, particularly arterial hypertension, atherosclerosis, and heart failure. 35795187: By affecting these living cells, the gut microbiota can cause heart failure, atherosclerosis, hypertension, myocardial fibrosis, myocardial infarction, and coronary artery disease. 36027334: OBJECTIVE: Recent studies showed that the gut microbiota (GM) is involved in the regulation of blood pressure and the pathogenesis of arterial hypertension (AH). 37199902: Furthermore, studies on sex differences in gut microbiota, etiology of hypertension, and sex bias in prescription of antihypertensive medications have revealed promising avenues in sexual dimorphism-based precision medicine. 37853925: The imbalance of gut microbiota is thought to play an important role in the pathogenesis of hypertension. 32319677: However, studies related to gut microbiota have been mostly restricted to comparisons of amyloid deposits, while investigations on neurobehavioral changes and the pathogenesis of AD are limited. 32829453: Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer's disease (AD). In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. 32876860: Roles of Gut Microbiota in Pathogenesis of Alzheimer's Disease and Therapeutic Effects of Chinese Medicine. Roles of Gut Microbiota in Pathogenesis of Alzheimer's Disease and Therapeutic Effects of Chinese Medicine.Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by progressive cognitive impairment. Hence, the purpose of this review is to outline the roles of GM and its core metabolites in the pathogenesis of AD. 33814442: Recent studies showed that gut microbiota might play an important role in the pathogenesis of Alzheimer's disease (AD). 33829390: This review discusses the gut microbiota and epigenetics connection in the pathogenesis of AD and aims to highlight vast opportunities for diagnosis and therapeutics of AD. 33916001: Recent studies suggested that gut microbiota can influence AD progression; however, potential mechanisms linking the gut microbiota with AD pathogenesis remain obscure. Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, is a major cause of death and disability among the older population. 34365962: As supported by a growing amount of evidence in recent years, the gut microbiota plays an important role in the pathogenesis of Alzheimer's disease through the brain-gut-microbiota axis. 34384375: This study aims to investigate metabolic output of the dysbiosis of GMB in AD pathogenesis. 34411603: The initial stage of the involvement of gut microbiota in the pathogenesis of AD may be the dysfunction of the blood-brain barrier (BBB). 34520319: Finally, we discuss the possible interactions between SCRD and GM in AD pathogenesis, as well as several methodological improvements that are necessary for future research. 34735921: Recently, the roles of short-chain fatty acids (SCFAs), the main metabolites generated by fermentation of dietary fiber by gut microbiota, in the pathogenesis of AD have attracted considerable interest. 35070441: This article aims to review the leading-edge knowledge concerning potential roles of GM in AD pathogenesis and of probiotics in its treatment and prevention. 35213369: Gut Microbiota as a Hidden Player in the Pathogenesis of Alzheimer's Disease. 35248147: CONCLUSIONS: There is strong increasing evidence supporting a role for the gut microbiome in the pathogenesis of Alzheimer's disease, including effects on synaptic dysfunction and neuroinflammation, which contribute to cognitive decline. 35440320: As proposed by scientists and supported by a growing amount of evidence in recent years, the gut microbiota plays an important role in the pathogenesis of Alzheimer's disease via a constant bidirectional communication through the brain-gut-microbiota axis which is a multifunctional network involving the nervous system and the peripheral circulatory system. The Role of the Gut Microbiota and Microbial Metabolites in the Pathogenesis of Alzheimer's Disease. 35538829: RESULTS: Findings suggested that channels of free radicals, such as transition metal accumulation, and genetic factors are mainly accountable for the redox imbalance that assist to understand better the pathogenesis of AD and incorporate new therapeutic approaches. Here we reviewed some of the key findings that have shown the function of Abeta peptide, oxidative stress, free radical damage Triggering Receptors Expressed on Myeloid Cells 2 (TREM2), Nitric Oxide (NO), and gut microbiota in the aetiology of AD. 35634849: Accumulating evidence from experimental and animal studies also show potential effects of gut microbiome on AD pathogenesis. 35754271: BACKGROUND: Dysbiosis of gut microbiota has been reported to be enrolled in the pathogenesis of Alzheimer's disease (AD). 35992591: Aims: To explore the possible pathways of the involvement of gut microbiota in AD pathogenesis through metabolites and to identify new AD biomarkers. 36047913: Neuroinflammation and intestinal microbiota cause pathological progression of Alzheimer's disease (AD), leading to neurodegeneration and cognitive decline. 36578263: Evidence that the gut microbiota plays a key role in the pathogenesis of Alzheimer's disease is already un-ravelling. 36683147: The current study focused on uncovering the potential interactions among gut-derived Abeta in aging, gut microbiota, and AD pathogenesis. 36736919: Growing evidence suggests that the gut microbiome (GM) plays a pivotal role in the pathogenesis of AD through the microbiota-gut-brain axis (MGB). 36914812: Our findings demonstrate that gut microbiota mainly modulate the mutual transformation of microglial subtypes, which may lead to new insights into the pathogenesis of AD and MDD. 37511841: Convincing evidence has demonstrated the roles of GM in the pathogenesis of AD, which are partly mediated by modified microglial activity in the brain. 38031265: SCOPE: Recent studies have highlighted the vital role of gut microbiota in the pathogenesis of Alzheimer's disease (AD). 38452948: Recently, the role of gut microbiota has been implicated in the pathogenesis of AD. 38479921: Recent research has revealed that the gut microbiota (GM) plays an important role in the pathogenesis of AD through the microbiota-gut-brain axis. 38606018: Conclusion: Dietary vitamin A supplementation modulates the gut microbiota, intestinal permeability, inflammatory factors, and Abeta protein formation, offering insights into the pathogenesis of AD and potential therapeutic avenues for further exploration. 11575537: BACKGROUND: Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia, which may be altered when the efferent sympathetic fiber to the cardiovascular system is interrupted. 14758180: OBJECTIVE: In children, like in adults, tracheal intubation is a painful procedure that may induce hypertension, tachycardia, and other undesirable hemodynamic disorders. 17358099: The objective of this study was to compare the effects of esmolol with those of lidocaine (lignocaine) and fentanyl on prevention of tachycardia and hypertension caused by endotracheal intubation. 1931397: Laryngoscopy and tracheal intubation often cause hypertension and tachycardia, which may be exaggerated during rapid-sequence induction of anaesthesia. 1931398: Laryngoscopy and tracheal intubation often cause hypertension, tachycardia and arrhythmias, which may be exaggerated during rapid-sequence induction of anaesthesia. 19462810: Hypertension caused by tracheal intubation was successfully prevented by nicardipine, which was ineffective for intraoperative hypertension. 20075530: During induction of general anesthesia hypertension and tachycardia caused by tracheal intubation may lead to cardiac ischemia and arrhythmias. 22179601: PURPOSE: General anesthesia for cesarean delivery is frequently associated with hypertension and tachycardia caused by tracheal intubation, which may lead to cardiac ischemia in susceptible patients or may cause harm due to increased intracranial pressure. 2225292: Laryngoscopy and tracheal intubation often cause hypertension and tachycardia, which may be exaggerated during rapid-sequence induction of anaesthesia. 23248653: BACKGROUND: Hypertension and tachycardia caused by tracheal intubation can be detrimental in hypertensive patients. 25885723: CONTEXT: During induction of general anesthesia hypertension and tachycardia caused by tracheal intubation may lead to cardiac ischemia and arrhythmias. 25886336: CONTEXT: Laryngoscopy and endotracheal intubation activates the sympathetic nervous system, causing tachycardia and hypertension. 25886340: CONTEXT: Laryngoscopy and tracheal intubation produce sympathetic overdrive by catecholamine release resulting in hypertension and tachycardia. 26500981: BACKGROUND: Laryngoscopy and endotracheal intubation can cause hypertension and tachycardia which can result in myocardial ischemia or stroke in vulnerable people. 26622115: As conventional laryngoscopy guided endotracheal intubation evokes significant hypertension and tachycardia, we have used I-gel, second generation extraglottic airway device, in an attempt to overcome these drawbacks. 26905703: INTRODUCTION: Laryngoscopy and tracheal intubation causes significant sympathetic response resulting in hypertension and tachycardia. 26957684: BACKGROUND: Pressor response is a part of stress response caused by reflex sympathetic discharge due to direct laryngoscopy and tracheal intubation resulting in tachycardia, hypertension and arrhythmias. 30358284: Hypertension caused by tracheal intubation was successfully prevented by remifentanil. 31031490: Background: General anesthesia administration involves laryngoscopy and endotracheal intubation which are associated with the pressor response and can lead to tachycardia, hypertension, and arrhythmias, which can be deleterious in compromised patients and hence, this response needs to be suppressed. 9972756: IMPLICATIONS: In women with severe preeclampsia, rapid-sequence induction of general anesthesia and tracheal intubation can cause severe hypertension. 10093929: Role of free radicals and metal ions in the pathogenesis of Alzheimer's disease. 16267663: Two of the defining hallmarks of Alzheimer's disease (AD) are deposits of the beta-amyloid peptide, Abeta, and the generation of reactive oxygen species, both of which may be due to the Abeta peptide coordinating metal ions. 18289347: There is evidence that binding of metal ions like Zn2+ and Cu2+ to amyloid beta-peptides (Abeta) may contribute to the pathogenesis of Alzheimer's disease. 19540003: As for aluminum, a role for this ion in AD pathogenesis is still controversial. 19808086: AIM OF THE STUDY: To determine the effect of alcoholic extract of Bacopa monnieri on cognitive function and neurodegeneration in animal model of Alzheimer's disease induced by ethylcholine aziridinium ion (AF64A). 21209855: The metals hypothesis implicates redox-active copper ions in the pathogenesis of AD and the Cu(2+) coordination of various Abeta peptides has been widely studied. 21280585: The role of metal ions in Alzheimer's disease etiology is unresolved. 22452395: Abnormal interactions of Cu and Zn ions with the amyloid beta (Abeta) peptide are proposed to play an important role in the pathogenesis of Alzheimer's disease (AD). 23043377: The copper ion, Cu(2+), is found at high concentrations in plaques, but its role in AD etiology is unclear. 23416043: Several lines of evidence have supported the potential involvement of metal ions in the etiology of Alzheimer's Disease (AD). 23506614: Herein, we present current understanding on the roles of Abeta, tau, and metal ions, placing equal emphasis on each of these proposed features, as well as their inter-relationships in AD pathogenesis. 23793644: Abeta aggregation, possibly modulated by metal ions, is now considered as an important factor in AD aetiology. 23841511: The interaction of Cu(II) and Zn(II) ions with amyloid-beta (Abeta) plays an important role in the etiology of Alzheimer's disease. 24954589: Analysis of the literature suggests that the main factors of AD and PD pathogenesis (oxidative stress, structural disorders and aggregation of proteins, mitochondrial dysfunction, energy deficiency) that initiate a cascade of events resulting finally in the dysfunction of neuronal networks are mediated by the disbalance of Zn2+ and Cu2+. Disbalance of zinc (Zn2+) and copper (Cu2+) ions in the central nervous system is involved in the pathogenesis of numerous neurodegenerative disorders such as multisystem atrophy, amyotrophic lateral sclerosis, Creutzfeldt-Jakob disease, Wilson-Konovalov disease, Alzheimer's disease, and Parkinson's disease. 24970207: Metal ions, including copper and zinc, have been implicated in the pathogenesis of Alzheimer's disease through a variety of mechanisms including increased amyloid-beta affinity and redox effects. 25014537: Revealing molecular level details of subcomponents in metal ion coordination is critical in understanding the role of metal ions in Alzheimer's disease etiology. 25051063: Dysfunctional interaction of amyloid-beta (Abeta) with excess metal ions is proved to be related to the etiology of Alzheimer's disease (AD). 25633876: Metal ions may play a role in the etiology of neurodegenerative disorders such as AD, and in this work we explore the metal ion induced folding and aggregation of Bri2-23 using Hg(ii) and Ag(i) as spectroscopic probes with structural and ligand preferences similar to those of Cu(i), while not displaying redox activity under the experimental conditions. 25968625: Dysfunctional interactions of amyloid-beta (Abeta) with Zn and Cu ions are proved to be related to the etiology of Alzheimer's disease (AD). 27044837: Misbalance of zinc (Zn(2+)) ions in the central nervous system is involved in the pathogenesis of numerous neurodegenerative disorders such as Alzheimer's disease, Depression, and Epilepsy. 27591874: Al(3+) ions are the most probable etiological cause of Alzheimer's disease. 27591943: Dysfunctional interaction of amyloid-beta (Abeta) with excess metal ions is proved to be related to the etiology of Alzheimer's disease (AD). 29111371: The accumulation of the extracellular beta-amyloid (Abeta) aggregates with metal ions in conjunction with reactive oxygen species (ROS) is closely related to the pathogenesis of Alzheimer's disease (AD). 29596976: Abnormal interaction of amyloid-beta peptide (Abeta) and metal ions is proved to be related to the etiology of Alzheimer's disease (AD). 30882825: Copper ions have high relevance to AD pathogenesis, causing Cu(ii)-mediated Abeta aggregation and oxidative damage to neuronal cells. 32261634: Metal ions play an important role in amyloid aggregation and neurotoxicity in the AD pathogenesis. 32266063: Current understanding of metal ions in the pathogenesis of Alzheimer's disease. 33617717: The high concentration of zinc metal ions in Abeta aggregations is one of the most cited hallmarks of Alzheimer's disease (AD), and several substantial pieces of evidence emphasize the key role of zinc metal ions in the pathogenesis of AD. 34299316: In addition, since toxic aggregates of amyloid-beta (Abeta) have been proposed as one of the major causes of the disease, the mechanism of clearing Abeta is also required to be investigated to reveal the etiology of AD clearly. Dyshomeostasis of these redox-active metal ions in the brain could cause Alzheimer's disease (AD). 36082494: Aggregation and fibrillation of beta-amyloid peptides (Abeta) as well as accumulation of toxic metal ions have been believed to be the central events to cause Alzheimer's disease (AD). 11232594: This furthers the evidence that redox-active iron and subsequent Fenton reaction generating reactive oxygen are critical factors in the pathogenesis of AD. Multiple lines of evidence indicate that oxidative stress is an integral component of the pathogenesis of Alzheimer disease (AD). 16122736: Excess of iron in the brain has been implicated in the pathogenesis of several human neurodegenerative diseases, for example Alzheimer's disease and Parkinson's disease. 17029598: Hypercholesterolemia is a potential trigger of Alzheimer's disease, and is thought to increase brain levels of beta-amyloid (Abeta) and iron. 17408857: The decrease in loosely bound iron in mild-moderate AD patients may be associated with myelin breakdown seen in the beginning stages of AD and implicates that iron dysregulation is an early event in AD pathogenesis. Accumulating evidence implicates a role for altered iron and copper metabolism in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). 17628213: Iron is a reactive oxygen species and has been implicated in the pathogenesis of Alzheimer's disease (AD). 18376063: Recent studies also point to redox active metals such as iron, copper and zinc in mediating oxidative stress in AD pathogenesis. 19195795: Body iron stores that increase with age could be pivotal to AD pathogenesis and progression. This communication explores the temporal link between the age-associated increase in body iron stores and the age-related incidence of Alzheimer's disease (AD), the most prevalent cause of senile dementia. 21303349: Despite the crucial role of redox active metals like copper and iron in central biological reactions, their elevated levels are involved in the pathogenesis of Alzheimer's Disease (AD). Iron, copper, and zinc are some of the metals, which intensify this process and contribute for the pathogenesis of AD. 21514009: It is now accepted that transition metals, such as iron and copper, are involved in the pathogenesis of the Alzheimer's disease (AD) through their participation in toxic oxidative phenomena. 21902663: In addition, disruption of iron regulation plays a key role in the etiology of Alzheimer's disease, Parkinson's disease, Huntington's disease, Friedreich's ataxia and other neurological disorders, cancer (lung cancer, breast cancer, colon cancer), Fanconi anemia, stroke and ageing. 22746342: Disruption of iron regulation also plays a key role in the etiology of Alzheimer's disease (AD). 23887894: Better knowledge of the distribution of iron in the brains of Alzheimer's disease (AD) patients may facilitate the development of an in vivo magnetic resonance (MR) marker for AD and may cast light on the role of this potentially toxic molecule in the pathogenesis of AD. 24343096: In addition, it should be noted the important role that low molecular mass fractions of iron, copper, aluminium and cobalt appear to play in pathogenesis of Alzheimer. 25557378: Future investigation of CO and iron in the pathogenesis of Alzheimer's disease is warranted. 30598025: Moreover, it is already established that metals (particularly copper, zinc and iron) have a key role in the pathogenesis of AD. 10592123: Since the spastic artery is intrinsically resistant to hypertension, the marked increase in CBF during hypertension can be attributable to ischaemia following SAH. 13445909: [A new model of experimental hypertension induced by ischemia of the spleen]. 1378784: However, the long term use of these drugs has additional advantages, particularly with respect to their ability to slow Ca(++)-dependent processes involved in the formation of atherogenic lesions, partially antagonise the effects of the raised levels of circulating endothelin-1 encountered during ischaemia-induced heart failure and hypertension, and trap and immobilise oxyradicals. 14466940: Ischaemia of the brain as a cause of chronic hypertension in man. 14845060: [Experimental arterial hypertension produced by extrarenal ischemia]. 14865056: [Experimental arterial hypertension due to extrarenal ischemia]. 15334016: These findings led to the hypothesis that ischemia of the endothelial cells of Schlemm's canal induces hypertension in human eyes. 1721532: CONCLUSIONS: These data support the theory that some of the complications of severe GPH may follow organ damage due to prolonged tissue ischaemia. 17377512: Uteroplacental ischemia results in proteinuric hypertension and elevated sFLT-1. 19075097: Hypertension produced by placental ischemia in pregnant rats is associated with increased soluble endoglin expression. 19114880: Delayed ischemia is treated with combinations of volume expansion, induced hypertension, augmentation of cardiac output, angioplasty, and intra-arterial vasodilators. 21505354: Changes in cardiac structure in hypertension produced by placental ischemia in pregnant rats: effect of tumor necrosis factor blockade. 22647295: We have shown that adoptive transfer of CD4(+) T cells from placental ischemia (reduction in uteroplacental perfusion, RUPP) rats causes hypertension and elevated inflammatory cytokines during pregnancy. 22832532: These findings suggest that the timing during which placental insufficiency occurs may play an important role in determining the extent of alterations in angiogenic balance, fetal growth restriction, and the severity of placental ischemia-induced hypertension. 23460290: The present data indicate that treatment with pravastatin attenuates oxidative stress and lowers MAP in placental ischemia-induced hypertension, but may have negative effects on circulating angiogenic potential during pregnancy. Pravastatin attenuates hypertension, oxidative stress, and angiogenic imbalance in rat model of placental ischemia-induced hypertension. 23685261: Therefore, we hypothesized that complement activation is critical for placental ischemia-induced hypertension. Thus, these studies have identified a mechanistic link between complement activation and the pregnancy complication of hypertension apart from free plasma VEGF and have identified complement inhibition as a potential treatment strategy for placental ischemia-induced hypertension in preeclampsia. Complement activation is critical for placental ischemia-induced hypertension in the rat. We employed the reduced utero-placental perfusion pressure (RUPP) model of placental ischemia in the rat to induce hypertension in the third trimester and evaluated the effect of inhibiting complement activation with a soluble recombinant form of an endogenous complement regulator, human complement receptor 1 (sCR1; CDX-1135). 23785075: Here, we report in the reduced uterine perfusion pressure (RUPP) rat model that administration of oral sildenafil is effective in attenuating placental ischemia-induced hypertension during gestation. 2386205: Hypertension and progressive glomerular injury caused by focal glomerular ischemia. 24054401: Acute ischemia of the brainstem has been known to produce hypertension. 24668059: Here, we have utilized a relevant preclinical rodent model of placental ischemia-induced hypertension, the reduced uterine perfusion pressure (RUPP) model, to determine the effect of chronic placental ischemia on the underlying chorionic tissue and placental villi. 24704473: Placental ischemia could be an initiating event, but the linking mechanisms leading to hypertension and growth restriction are unclear. 24914197: Down but not out: an emerging role for the B-type endothelin receptor in placental ischemia-induced hypertension. 25150279: Although our previous studies demonstrated that inhibition of complement activation attenuates placental ischemia-induced hypertension using the rat reduced uterine perfusion pressure (RUPP) model, the important product(s) of complement activation has yet to be identified. 25411364: Increased renal ANG II reduces the responsiveness of the renal sensory nerves in physiological and pathophysiological conditions, including hypertension, congestive heart failure, and ischemia-induced acute renal failure. 2604012: Uteroplacental ischemia causes hypertension in various species but the mechanisms involved are not known. 26135305: Since neutrophils are associated with tissue injury and inflammation, we hypothesized that neutrophils are critical to placental ischemia-induced hypertension and fetal demise. Neutrophil Depletion Attenuates Placental Ischemia-Induced Hypertension in the Rat. Using the reduced uteroplacental perfusion pressure (RUPP) model of placental ischemia-induced hypertension in the rat, we determined the effect of neutrophil depletion on blood pressure and fetal resorptions. 26569331: A major theory with strong experimental evidence is that placental ischemia, resulting from inappropriate remodeling and widening of the maternal spiral arteries, stimulates the release of soluble factors from the ischemic placenta causing maternal endothelial dysfunction and hypertension. 2665522: Utero-placental ischemia is known to cause systemic hypertension in various species, but the mechanisms are unknown. 26831193: Placental Growth Factor Administration Abolishes Placental Ischemia-Induced Hypertension. 27588825: Previous studies in a rat model of placental ischemia-induced hypertension demonstrated that inhibiting complement activation attenuated increased maternal blood pressure with C3a and C5a identified as the important products of complement activation. Role of IgM and angiotensin II Type I receptor autoantibodies in local complement activation in placental ischemia-induced hypertension in the rat. The AT1 receptor antagonist losartan prevents placental ischemia-induced hypertension as well as AT1-AA interaction with AT1 receptors. 27789293: The prophylactic administration of H2 attenuated placental ischemia-induced hypertension, angiogenic imbalance, and oxidative stress. 2837560: We concluded that this was a case of secondary reninism--a case of hypertension secondary to the local ischemia at the entrapped glomeruli. 28381873: Likewise, continued studies have revealed a critical role for the complement arm of the innate immune system in placental ischemia induced hypertension and in preeclampsia. 28422842: RATIONALE: Page kidney is an uncommon condition that hypertension occurs secondary to microvascular ischemia and alternation of small-vessel hemodynamics due to external compression of renal parenchyma and activation of the renin-angiotensin-aldosterone system. 28472389: Carbon Monoxide Releasing Molecules Blunt Placental Ischemia-Induced Hypertension. 28828114: Such a compression in kidneys causes hypoperfusion and microangiopathic ischemia and activates renin-angiotensin-aldosterone system leading to hypertension. 29185370: Prior studies indicated that complement activation was critical for placental ischemia-induced hypertension in a rat model. 29212810: Interestingly, placental ischemia-induced hypertension in rats [reduced uterine perfusion pressure (RUPP) model] is abolished by ETA receptor blockade, suggesting a critical role for ET-1. 29534686: BACKGROUND: Page kidney phenomenon is caused by strong renal parenchymal compression and leads to renal hypoperfusion and microvascular ischemia, resulting in renal dysfunction and hypertension. 30229567: Adrenergic receptor blockade attenuates placental ischemia-induced hypertension. Although markers of sympathetic nervous activity are elevated in experimental models of placental ischemia-induced hypertension and women with PE compared with their normal pregnant counterparts, the importance of adrenergic receptor signaling in the development of hypertension in PE is unknown. Therefore, we tested the hypothesis that adrenergic receptor blockade attenuates the development of placental ischemia-induced hypertension in rats. In conclusion, these data implicate that placental ischemia-induced hypertension involves adrenergic receptor signaling to promote increases in blood pressure during PE. 3048154: Since free intracellular calcium is already ten times elevated in the myocytes in systemic hypertension, the myocardium may be more vulnerable to further calcium overload owing to the ischemia and necrotization is augmented. 30571561: These data indicate that while obese MC4R-def pregnant rats have higher blood pressure during pregnancy, placental ischemia-induced hypertension is attenuated in obese MC4R-def pregnant rats. Thus, obese women with abnormal MC4R signaling may be less susceptible to the development of placental ischemia-induced hypertension. Previously, we reported that placental ischemia-induced hypertension is dependent upon intact signaling of the sympathetic nervous system. Although blockade of MC4R may lead to increased body weight during pregnancy, we tested the hypothesis that placental ischemia-induced hypertension is attenuated in obese MC4R-deficient pregnant rats. Melanocortin-4 Receptor Deficiency Attenuates Placental Ischemia-Induced Hypertension in Pregnant Rats. 31397167: Overall, these data do not exclude a role for antibodies produced by B cells before depletion but indicate the presence of B lymphocytes in the last trimester of pregnancy is not critical for placental ischemia-induced hypertension.NEW & NOTEWORTHY The adaptive and innate immune systems are implicated in hypertension, including the pregnancy-specific hypertensive condition preeclampsia. Studies of others have provided evidence for the importance of lymphocytes in placental ischemia-induced hypertension; however, the contributions of B1 versus B2 lymphocytes are unknown. Role of B1 and B2 lymphocytes in placental ischemia-induced hypertension. We hypothesized that peritoneal B1 lymphocytes are important for placental ischemia-induced hypertension. 31571657: However, following P3 HI, the number of stress-induced Fos-positive 5-HT neurons was decreased significantly in the dorsal raphe ventrolateral, interfascicular and ventral nuclei compared with control animals exposed to restraint stress. 31729903: The glucagon-like peptide 1 receptor agonist liraglutide attenuates placental-ischemia induced hypertension. 31786977: When administered in a rat model of placental ischemia, SynB1-ELP-p50i partially ameliorated placental ischemia-induced hypertension and reduced placental TNF-alpha levels with no signs of toxicity. 33175587: Placental ischemia in preeclampsia (PE) results in hypertension and intrauterine growth restriction (IUGR). 33710923: Impact of hyperleptinemia during placental ischemia-induced hypertension in pregnant rats. We tested the hypothesis that hyperleptinemia during reduced uterine perfusion pressure (RUPP) exaggerates placental ischemia-induced hypertension. In contrast to our hypothesis, placental ischemia-induced hypertension was attenuated by leptin infusion. 36247865: Investigation of the Correlation between Cuff Inflatable Hypertension and the Difference in Interarm Diastolic Pressure Induced by Single Arm Ischemia. 37071439: Stable adrenomedullin analog mitigates placental ischemia-induced hypertension and fetal growth restriction in rats. In addition, studies using the RUPP model showed that ADE101 significantly reduces placental ischemia-induced hypertension and fetal growth restriction in a dose-dependent manner. 414679: The limited ischaemia (demonstrated by later arteriography) of the parenchyma at the pole of the kidney was responsible, during the following weeks, for severe hypertension with a raised level of circulating plasma renin, but one that was rapidly treatable. 5780690: Hypertension due to ischemia of one kidney. 5995711: [2 Cases of arterial hypertension caused by segmentary ischemia of a kidney. Favorable effect of nephrectomy]. 6098292: Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. 7018887: The present study was carried out on male rats, using three models of experimental hypertension: cerebroischemic, single clamp bilateral and combined, induced by ischemia of the brain and one of the kidneys. 7210750: The crisis of hypertension is always to be regarded as an emergency situation, since always irreversible lesions may be appear on the different organs as a sequel of the permanent vasoconstriction and ischaemia. 7376951: The vasopressor effect produced by isolated intraspinal hypertension may be the consequence of ischaemia of the spinal vegetative structures. 7631855: Ischemia-induced hypertension was generated in rats by infrarenal aortic cross clamping for 5 h after which plasma was obtained from femoral vein blood. 11132936: Therefore, it was concluded that the WM lesions in DAT are the result of ischemia rather than wallerian degeneration. 15681798: One of the logical approaches to this problem is to study the effects of ischemia and hypoxia on the metabolism of amyloid precursor protein, which plays one of the key roles in the pathogenesis of AD. 23319188: The identification of the genes involved in sporadic Alzheimer's disease induced by ischemia will enable to further define the events leading to Alzheimer's disease-related abnormalities. 23519520: The identification of the genes involved in Alzheimer's disease induced by ischemia will enable to further define the events leading to sporadic Alzheimer's disease-related abnormalities. 25232510: However, since May 1998, we know that a progressive ischemia in the medial temporal lobes and subcommissural regions can cause Alzheimer's disease; because, in contrast to this, its revascularization by means of omental tissue can cure or improve this disease. 27699087: Evidence from rodent and cell models show a number of neurotrophic and neuroprotective effects of guanosine preventing deleterious consequences of seizures, spinal cord injury, pain, mood disorders and aging-related diseases, such as ischemia, Parkinson's and Alzheimer's diseases. 33608912: Here, we review recent evidence that microglial phagocytosis of live neurons and synapses causes neurodegeneration in animal models of Alzheimer's disease and other tauopathies, Parkinson's disease, frontotemporal dementias, multiple sclerosis, retinal degeneration, and neurodegeneration induced by ischaemia, infection or ageing. 35903609: Because excess copper and zinc may be present in the synaptic clefts during ischemia, it is possible that secreted copper and copper-induced reactive oxygen species may enhance zinc neurotoxicity and eventually contribute to the pathogenesis of vascular type senile dementia. 36225888: Ischemia as a common trigger for Alzheimer's disease. 36892020: Cerebral ischemic injury, one of the leading causes of morbidity and mortality worldwide, triggers various central nervous system (CNS) diseases, including acute ischemic stroke (AIS) and chronic ischemia-induced Alzheimer's disease (AD). 37326114: Cerebral ischemic injury, one of the leading causes of morbidity and mortality worldwide, triggers various central nervous system (CNS) diseases, including acute ischemic stroke (AIS) and chronic ischemia-induced Alzheimer's disease (AD). 37357280: In AD, white matter hyperintensities (WMH) which are postulated to develop as a result of chronic ischemia from small vessel CVD are shown to play a role in the aetiology. 11092174: CONCLUSION: Renin-secreting juxtaglomerular tumor of the kidney (reninoma) is a very rare but curable cause of severe hypertension. 11928050: Juxtaglomerular cell tumor is an extremely rare neoplasm of the kidney that causes blood hypertension. 15703093: Juxtaglomerular cell tumor as a rare cause of hypertension in adults. 1628189: Juxtaglomerular cell tumour of the kidney as cause of hypertension: a case report. 17019534: We present a case of myocardial infarction in a young female with reninoma induced hypertension and myocardial bridging. Myocardial infarction in a young female with reninoma induced hypertension and myocardial bridging. 18192852: Reninoma is a tumor of the renal juxtaglomerular cell apparatus that causes hypertension and hypokalemia via hypersecretion of renin. 18242388: Juxtaglomerular tumors, or reninomas, are a rare cause of hypertension, almost always benign and accurately localized by a combination of biochemical tests and imaging. 19003641: Hypertension due to a reninoma (suspected on the basis of biochemical and clinical features, and exquisite sensitivity of hypertension to angiotensin-converting enzyme [ACE] inhibition, but not visible on imaging) was cured by laparoscopic nephrectomy. 1942353: Renin-secreting juxtaglomerular tumor causing severe hypertension: diagnosis by computerized tomography-directed needle biopsy. Renin-secreting tumors are a rare cause of severe hypertension accompanied by hypokalemia. 20434032: A juxtaglomerular cell tumor (JCT) is a rare, renin-secreting tumor of the kidney and can cause hypertension. 20453480: Reninoma is an uncommon cause of hypertension in a young adult and should be included in the differential diagnosis as a potential life-threatening and curable condition. 21871063: JGCT is a curable cause of hypertensive disease if it is discovered early and surgically removed, but may cause a fatal outcome usually by a cerebrovascular attack or may cause fetal demise in pregnancy. 22308872: Reninoma or juxtaglomerular cell tumor (JCT) of the kidney is a rare but curable cause of severe hypertension. 22490754: OBJECTIVE: Reninoma is a rare benign tumor of the renal juxtaglomerular cell apparatus that causes hypertension and hypokalemia via hypersecretion of renin, while it is extremely rare that reninoma induced hypertensive crisis with reversible posterior encephalopathy syndrome (RPES). 22607947: Reninoma is an extremely rare, renin-secreting, benign kidney tumor that can cause hypertension. We present a case of hypertension secondary to reninoma treated with laparoscopic nephron-sparing surgery in a 15-year-old girl and review some relevant published literature. Hypertension secondary to reninoma treated with laparoscopic nephron-sparing surgery in a child. 22981035: Newly developed hypertension due to juxtaglomerular cell tumor in pregnancy. 23607027: The juxtaglomerular cell tumor (JGCT) is a rare renal tumor characterized by excessive renin secretion causing intractable hypertension and hypokalemia. 24401674: BACKGROUND/AIM: Reninomas are rare juxtaglomerular tumours which can cause severe hypertension and hypokalaemia. 24556856: Renin-secreting juxtaglomerular cell tumor of the kidney causing severe hypertension and polyuria. 24926309: Juxtaglomerular cell tumor is a rare renin-secreting tumor associated with refractory hypertension in young females and is a possible cause of hypertension during pregnancy. 25611839: Here we present the first reported case in Argentina of a 21-year-old patient with arterial hypertension and hypokalaemia due to a renin-secreting juxtaglomerular cell tumour, which was diagnosed after seven years of development. Juxtaglomerular cell tumour as a curable cause of hypertension: case presentation. 26877959: Reninoma is a tumor of the renal juxtaglomerular cell apparatus that causes hypertension and hypokalemia because of hypersecretion of renin. 27316587: Hypertension due to juxtaglomerular cell tumor of the kidney. 30042049: Juxtaglomerular cell tumors are rare, generally benign, and they are one of the secondary surgically treatable causes of arterial hypertension. 30376707: Reninoma, a renin-secreting juxtaglomerular cell tumor, is a rare cause of severe hypertension, usually diagnosed in adolescents and young adults. 30527885: Juxtaglomerular cell tumors (JCTs), a rare but potentially curable cause of hypertension, are difficult to diagnose because they may be missed or misidentified as a cyst by computed tomography (CT). 36729016: Juxtaglomerular cell tumor (reninoma) as a cause of arterial hypertension in adolescents. 37963756: [A case of hypertension secondary to juxtaglomerular cell tumor in a young female patient]. 4071145: We have reported our experience at Duke University Medical Center with juxtaglomerular apparatus tumor, a rare but remediable cause of significant hypertension. 6362818: The authors describe a juxtaglomerular cell tumor (JGCT) which caused severe hypertension in a 58-year-old man. 8857975: Hypertension caused by left renal reninoma. 10023633: Although it is possible that the hyperuricemia could simply be the consequence of the renal disease, further studies are necessary to rule out a pathogenic role for uric acid in the development of renal disease and salt-dependent hypertension. 1012375: Family history of hypertension, kidney disorders, age, and weight are all predisposing factors to o.c. induced hypertension. 10226277: The loss of circadian blood pressure regulation is associated with the severity of essential hypertension and has been reported in hypertension due to renal disease. 10649899: [The captopril test--an aid in the detection of scarring nephropathy as a cause of arterial hypertension in children]. 10867664: METHODS: Fifteen healthy subjects 24-34 years old, 15 healthy subjects 68-80 years old, 25 hypertensive patients, 25 patients with hypertension and chronic renal failure (15 mild, 10 severe), and 12 patients with hypertension and chronic renal failure and acute renal insufficiency due to ischemic nephropathy underwent color Doppler sonography of both kidneys. 10989756: In conclusion, our data suggest that renal disease will be common cause of hypertension and also a selective factor for long term survival of hypertensives in a country where renal replacement therapy is not available. 11054344: Ischemic nephropathy is a long-term cause of hypertension and renal failure. 11190292: In the case of type 1 diabetes mellitus, hypertension is often the result of a underlying nephropathy. 11305806: BACKGROUND: Renal artery disease can cause both hypertension and renal failure, and color Doppler sonography (CDS) may be a good screening method to detect it. 11369824: Hypertension leads to renal disease through a series of mechanisms that seem to be exaggerated in African-Americans, who have a higher prevalence of both hypertension and end-stage renal disease than whites. Renal disease itself leads to hypertension, which in turn can contribute to progression of renal disease. 11479244: Does hypertension in type I diabetics result from nephropathy or metabolic alterations? 1223937: [Diagnostic and prognostic value of the separated renin in hypertension due to monolateral nephropathy]. 12267711: Risks of lupus that must be considered in choosing a contraceptive method include vascular accidents such as venous thrombosis and inflammatory lesions of the arteries, hypertension usually secondary to nephropathy or corticotherapy, metabolic disturbances, anomalies of hemostasis, initiation or exacerbation of the disease with use of combined OCs, and predisposition to infection. 12465655: Continuous use of a high-salt diet slowed the progression of radiation nephropathy, but eventually exacerbated radiation-induced hypertension and accelerated renal failure. 12996895: Human hypertension due to unilateral renal disease, with special reference to renal artery lesions. 13023322: [Arterial hypertension caused by unilateral nephropathy]. 13207856: Hypertension caused by unilateral renal disease. 13243908: [Arterial hypertension caused by unilateral nephropathy]. 13433477: Reversible hypertension due to renal artery disease. 13436929: Hypertension due to unilateral renal disease; with a report on a functional test helpful in diagnosis. 1344112: Hypertension due to renal arterial disease. 13515463: [Results of nephrectomy in hypertension caused by urological-type unilateral nephropathy]. 13756035: The diagnosis and treatment of hypertension due to unilateral renal disease. 13785667: Hypertension due to unilateral renal disease. 1379154: Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. 13811563: Unilateral renal disease as a cause of hypertension: its detection by ureteral catheterization studies. 13830742: [Solitary permanent arterial hypertension due to unilateral nephropathy--nephrectomy]. 13903997: A roentgenologic sign of unilateral renal disease as a cause of hypertension. 13925112: [Systemic arterial hypertension caused by unilateral nephropathy]. 13955297: [Preliminary research on the hypertension caused by kidney diseases]. 14096847: [CONSIDERATIONS ON A CASE OF ARTERIAL HYPERTENSION CAUSED BY UNILATERAL NEPHROPATHY]. 14102140: [ARTERIAL HYPERTENSION CAUSED BY RENAL ARTERY DISEASES]. 14102143: [TREATMENT OF ARTERIAL HYPERTENSION CAUSED BY RENAL ARTERY DISEASES]. 14119852: DIAGNOSIS OF HYPERTENSION CAUSED BY UNILATERAL RENAL ARTERY DISEASE. 14194062: [HYPERTENSIVE DISEASE CAUSED BY UNILATERAL NEPHROPATHY; DIAGNOSIS AND POSTNEPHRECTOMY DEVELOPMENT]. 14227448: HYPERTENSION IN CHILDHOOD DUE TO UNILATERAL RENAL DISEASE. 14291470: HYPERTENSION DUE TO UNILATERAL RENAL ARTERY DISEASE. 14299432: REMEDIABLE HYPERTENSION DUE TO UNILATERAL RENAL DISEASE: CORRELATION OF SPLIT RENAL-FUNCTION TESTS AND PRESSOR ASSAYS OF RENAL VENOUS BLOOD IN HYPERTENSIVE PATIENTS. 14328100: [HYPERTENSION DUE TO MONOLATERAL KIDNEY DISEASE. RECOVERY AFTER NEPHRECTOMY]. 14449357: Hypertension produced by unilateral renal disease. 14511965: Clinically undetected renal disease could be a rare cause of hypertension in pregnancy. 14689099: On the one hand, kidney disease provokes hypertension. 15299: The renal diseases which cause systemic hypertension in the first two decades of life differ from the adult in their incidence and etiology. 15485598: In contrast to the striking decline in mortality rates from both stroke and coronary heart disease, the prevalence of hypertension as a cause of end-stage renal disease (ESRD) has increased such that it is now the second most common cause of ESRD in the United States. Over the past several decades, it has become clear that hypertension is both a cause and a consequence of kidney disease. 16137544: Renal disease and even renal structural abnormalities (nephron underdosing) lead to hypertension. 167: There are different types of renal hypertension: hypertension due to parenchymal renal disease, renovascular hypertension, hypertension due to urological disease, hypertension of endstage renal disease. 16710820: Renal diseases are the most frequent causes of AH in children, but essential hypertension can also be detected early in life. 1701048: This ablation nephropathy (AbN) caused proteinuria, progressive renal failure, and hypertension. 17390717: Renovascular hypertension and renal hypertension are two major secondary forms of hypertension due to renal disease. 1792767: Results indicate that the functional state of the liver in vasorenal hypertension is disturbed as a result of the main renal disease and also under the effect of arterial hypertension as a destabilizing factor leading to disorders of the hemodynamics and furthering potentiation of lipid peroxidation processes in the body. 18320238: However, secondary causes of hypertension such as renal parenchymal diseases, congenital abnormalities and renovascular disorders still remain the leading cause of pediatric hypertension, particularly in children under 12 years old. 18713167: Ischemic nephropathy is not only a cause of hypertension but also an important cause of end-stage renal disease. 19158823: The presence of kidney disease is a common and underappreciated pre-existing medical cause of resistant hypertension. 19262237: The presence of kidney disease is a common and underappreciated preexisting medical cause of resistant hypertension. 19302426: The presence of kidney disease is a common and underappreciated preexisting medical cause of resistant hypertension. 20049319: Atherosclerotic renal artery disease is a common cause of hypertension and chronic kidney disease that may progress into end stage renal failure if not diagnosed and treated early. 20283462: Hypertension due to unilateral renal disease. 20325599: Hypertension due to Unilateral Renal Disease. 20964736: The aetiologies of renal diseases can affect cardiovascular outcomes, and the two major causes of end-stage renal disease, diabetes mellitus and hypertension, indeed do so. 20979962: The relationship between chronic kidney disease and hypertension remains enigmatic and a matter of considerable clinical and academic interest, with evidence suggesting that hypertension is both a cause and a consequence of kidney disease. 21067025: Patients with endocrine disease, pregnancy, coarctation of aorta, and renal disease leading to hypertension were excluded from the study. 21762366: Moreover, several factors and conditions that can interfere with blood pressure control such as excess sodium intake, obesity, diabetes, older age, kidney disease, and certain identifiable causes of hypertension were shown to be common among patients with resistance to antihypertensive treatment. 22278141: OBJECTIVES: Hypertension is both a cause and a consequence of kidney disease. 22480462: Kidney diseases are the most common causes of hypertension, prompting the search for a renovascular cause to start appropriate treatment. 23275987: The following covariates were entered into the Cox's model: sex, duration of hypertension before malignant phase, age, serum creatinine, stages 3 and 4 fundi, diastolic blood pressure, cardiac and neurological involvements, extrarenal atheromatous disease, aetiology of the malignant hypertension (primary, secondary to parenchymal nephropathy, and secondary to renovascular abnormalities), all these covariates being recorded during the initial admission; and mean diastolic blood pressure during the period the patients were observed. 23678314: The study included patients with primary or essential hypertension, and excluded patients with secondary hypertension, hypertension due to renal disease, pheochromocytoma, coarctation of the aorta, as a result of taking oral contraceptives, corticosteroids, and cocaine. 24051253: Hypertension was secondary to renal disease in three animals. 2412044: We conclude that i.v. ketanserin is effective in the acute management of severe hypertension, including hypertension secondary to renal disease. 25228801: Several factors and conditions interfering with blood pressure (BP) control, such as excess sodium intake, obesity, diabetes, older age, kidney disease, and certain identifiable causes of hypertension are common in patients resistant to antihypertensive treatment. 2580173: Because renal disease is a common cause of hypertension and the two conditions frequently coexist, in some patients agents that are eliminated by both renal and hepatobiliary routes may be more desirable than those eliminated almost exclusively by the kidneys, such as captopril. 25819380: OBJECTIVE: Renal disorders can cause hypertension, but less is known about the influence of hydronephrosis on blood pressure. 26281905: All the removed kidneys were nonfunctioning because of benign diseases: VUR (84), UPJO (38), MKDK (20), xanthogranulomatosis pyelonephritis (4), nephropathy causing uncontrollable hypertension (2) and nephrolithiasis (1). 2746999: [Studies on kallikrein activity in diabetic patient with hypertension caused by nephropathy]. 27780982: Pseudohypoaldosteronism type II (PHA II) is a renal tubular disease that causes hyperkalemia, hypertension, and metabolic acidosis. 28075529: The current study aimed to investigate whether or not race and SES alter the effects of diabetes, hypertension, and obesity on mortality due to renal disease. 2833821: The authors present the indices of blood pressure (BP), plasma renin activity, the concentration of aldosterone, cortisol, adrenocorticotropic and antidiuretic hormones in 56 patients with arterial hypertension resulting from kidney parenchymatous diseases before hemosorption and at varying time after it. [Changes in arterial pressure and concentration of several hormones in the blood effected by hemosorption in patients with arterial hypertension caused by parenchymatous diseases of the kidneys]. 30519668: Purpose: We report an update on a recently published case of uncontrolled hypertension secondary to immunoglobulin A (IgA) nephropathy resulting in massive bilateral retinal and choroidal infarction. 3056448: Systemic hypertension is both the cause and the consequence of renal disease. In contrast, systemic hypertension with afferent arteriolar vasodilatation leads to glomerular hypertension and is associated with structural injury. 31194119: Introduction: Diagnosis of superimposed preeclampsia in women with chronic kidney disease (CKD) is complicated by the presence of hypertension and proteinuria due to renal disease. 32828236: Blood pressure and kidney disease: chicken or egg (or both)?A recent study supports the concept that reduced kidney function causes higher blood pressure, but it found no evidence of causality in the opposite direction. 3321517: Different forms of adrenocortical hyperplasia revealed during histomorphological investigation, endocrine nephropathy of various degree and vascular changes of hypertensive genesis in the renal parenchyma were discussed as causes of residual hypertension. 3325889: Renal diseases with activation of the renin-angiotensin-system induce hypertension by augmentation of the total peripheral resistance. 33269815: OBJECTIVES: To analyze the potential differences between primary HTN and HTN secondary to renal diseases, in order to tailor diagnostic procedures to pediatric patients with suspicion of HTN. The patients with primary HTN were significantly older than those with HTN secondary to renal disease. The diagnostics of HTN secondary to kidney disease have revealed risk factors worsening the prognosis, including higher values of cholesterol or of parameters connected with DBP. CONCLUSIONS: As expected, HTN secondary to renal disease prevails in younger children, but primary HTN has become an emerging issue in teenagers. 33778424: In contrast, most patients with secondary HTN had been managed by the Nephrology Department, renal diseases being the leading cause of their HTN (46.3%). 33781840: Kidney disease, blood pressure determination, hypertension pathogenesis, and the renin angiotensin system (RAS) are inextricably linked. 34131993: Systemic hypertension (SH) in dogs typically occurs secondary to renal disease, diabetes mellitus, hyperadrenocorticism, malignant adrenal tumors, or various medications. 3530554: Three hundred twenty-three children with hypertension due to different kidney disorders were analysed. 35497107: All six patients had hypertension due to renal disease, except one girl with chemotherapy-induced hypertension. 36444523: Systemic hypertension (SH) in cats may occur secondary to renal disease, hyperthyroidism, or idiopathic causes. 36986445: The prognosis of hypertension leads to organ damage by causing nephropathy, stroke, retinopathy, and cardiomegaly. 37152513: Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiographic syndrome reported in children with hypertension due to renal diseases, immunosuppression after solid organ transplant, cytotoxic agents for chemotherapy, and many others rare instances. 37915683: In the pediatric population, the most common cause is hypertension caused by renal disease or different drugs. 3813293: Hypertension due to a unilateral nephropathy, when studied on a statistic level, does not induce any atheromatous lesion nor heart ponderal hypertrophy more acute than essential high blood pressure. 38435: [Hypertension due to unilateral parenchymatous nephropathy (author's transl)]. 38641998: INTRODUCTION: Immunoglobulin A (IgA) nephropathy is a common immune-mediated kidney disease leading to high blood pressure and may progress to kidney failure. 3887903: Discussed in particular are the prevalence of hypertension in various forms of renal parenchymal disease at various levels of renal function, pathogenesis of hypertension in renal parenchymal disease, and the course of hypertension in these diseases. 3997234: Plasma chromogranin A concentration was higher in subjects with essential hypertension (n = 32) than in normal controls (n = 18; 198 +/- 32 versus 129 +/- 12 ng/ml [mean +/- SEM]; p less than 0.05), and was also elevated in subjects with hypertension secondary to renal parenchymal disease (n = 9; 192 +/- 36 ng/ml; 0.05 less than p less than 0.1) and those with pheochromocytoma (n = 11; 1614 +/- 408 ng/ml; p less than 0.01). 4001724: The delayed manifestations are not present in early life and include the following: endocrinopathies: diabetes, thyroid disease, and growth hormone deficiency; deafness; ocular damage: glaucoma, keratic precipitates, keratoconus, corneal hydrops, and absorption of the cataractous lens; vascular effects: fibromuscular proliferation of the intima, sclerosis of arteries, systemic hypertension secondary to renal disease, and subretinal neovascularization; and progressive rubella panencephalitis. 4355135: The follow-up was 5 to 10 years in the four groups of hypertensive patients (essential hypertension, malignant hypertension, hypertension secondary to renal parenchymatous disease and hypertension caused by, or associated with, renal artery obstruction). 507289: Aortography proved the presence of renal artery disease and renal vein renin assay established its significance in the etiology of the patients' hypertension. 5608317: [Possibilites and limits of renal functional and hemodynamic study for the differential diagnosis of hypertension due to unilateral nephropathy]. 6025390: Nephrectomy for hypertension due to unilateral renal disease. 632367: Nineteen patients with severe essential hypertension or hypertension due to renal parenchymal disease were treated with intravenous clonidine. 661889: Renin activities (measured after the subjects were standing) were also lower in patients with essential hypertension and hypertension due to renal disease (P less than 0.01 and P less than 0.02, respectively). 6763143: In addition to its established role in RAS, mild activation of the renin-angiotensin system may also be important for the pathogenesis of hypertension caused by unilateral RPD. 7018775: Thus our results document a limited prognostic value of renal venous renin determination in patients with hypertension due to unilateral renal disease. 7694340: The influences of renal function and mass on the catabolism of serum gastrin were studied in 27 patients with hypertension caused by unilateral parenchymal renal disease (77.8%), renal artery stenosis (11.1%) and essential hypertension (11.1%). 796975: In about 15% of cases hypertension is caused by renal diseases, including unilateral and bilateral parenchymatous nephropathies, renal artery stenosis and renin producing tumors. 8125561: Renal artery disease is an important cause of both renal failure and hypertension. 8254782: From 1970 to 1990, 57 patients 50 years old or younger were treated for hypertension caused by atherosclerotic renal artery disease. 8404957: This work suggests that a screening investigation with a low radiation burden can be carried out at most institutions; if the investigation is positive, there will be a high index of suspicion that renovascular disease is the cause of the hypertension. In children over 1 year of age, renal disease is the commonest cause of hypertension. 8571752: Hypertension can be a cause as well as a consequence of renal disease. 8629871: Therefore, hypertension is both a cause and a consequence of renal disease, and it may be difficult to distinguish them clinically. Renal parenchymal disease is a common but often unrecognized cause of hypertension. 8821841: Atherosclerotic renal artery disease is an important secondary cause of hypertension. 8865987: She developed complications of diabetes mellitus which included retinopathy resulting in legal blindness, nephropathy resulting in end-stage renal disease, and chronic hypertension. 8952809: Essential hypertension would appear to be as much a renal disturbance related to the intake of sodium as hypertension secondary to renal disease. 9143784: Hypertension secondary to renal disease was studied in non-pregnant and pregnant ewes to determine whether there were any changes in arterial pressure and the distribution of cardiac output and, in particular, whether uteroplacental blood flow was affected. 9158501: CONCLUSION: The association between simple renal cysts and higher arterial BP probably arises from underlying renal disease causing both. 9428448: The unique association of hypertensive ESRD with atherosclerosis suggests that atherosclerosis is a risk factor for chronic renal failure and that a primary renal microvascular disorder may lead to both hypertension and progressive renal insufficiency. 9494784: Besides renal biopsy, which is impractical, especially in epidemiologic research, there are virtually no measures available that can distinguish genuine PIH from hypertension due to latent renal disorder, chronic hypertension, or genetic susceptibility. 9642252: Progressive renal diseases lead to prolonged glomerular hypertension, which induces the proliferation of mesangial cells. 9683055: Regarding the relationship between urinary albumin and blood pressure, microalbuminuria seems to be an early indicator of renal disease, causing high blood pressure in some instances, whereas it looks like the consequences of renal damage produced by severe hypertension in other instances. 9685796: In all cases kidney disease was the cause of arterial hypertension. 9748735: Renal disease is the cause of hypertension in about 5% of all hypertonics. 11054344: Ischemic nephropathy is a long-term cause of hypertension and renal failure. 11566959: Thus, omapatrilat not only markedly reduces the blood pressure in this model of renal failure-induced hypertension but may also prevent the abnormal compensatory stimulation of the vasodilator activity of the peripheral sensory nervous system. 12650046: Renal failure due to a large intranephric cyst obstructing the right ureter and renal artery was the suggested cause of the systemic hypertension. 15603326: On the case of 45 years old female with occasionally recognised renal failure, significant proteinuria and hypertension, without clinical symptoms of ATS we present problem of differentiation of atherosclerotic and hypertension cause of nephropathy. 15726214: Hypertension is both cause and consequence of renal failure, but the precise nature and prevalence of hypertensive nephrosclerosis as a cause of renal failure remains controversial. 19142019: BACKGROUND AND AIMS: Glomerular diseases are the third leading cause of kidney failure worldwide, behind only diabetes and hypertension. 20356704: However, any of the above listed signs found in isolation can be a tell tale sign of PE and must therefore prompt for the identification of a possible fetal effect The differential diagnosis of PE includes essential hypertension and hypertension secondary to a pre-existing renal failure. 2181693: The cause of hypertension in this patient with tuberous sclerosis appeared to be the result of volume expansion due to renal failure. 22964493: The effect of electroacupuncture on insulin-like growth factor-I and oxidative stress in an animal model of renal failure-induced hypertension. CONCLUSION: These findings suggest that the anti-hypertensive mechanism of EA could be related to the effects of oxidative stress on IGF-I in RF-induced hypertension. METHODS: We stimulated the Zusanli (ST36) and Taixi (KI3) acupoints in a rat model of RF-induced hypertension. BACKGROUND/AIMS: The present study was performed to demonstrate the effect of electroacupuncture (EA) and acupuncture on renal failure (RF)-induced hypertension. 32664062: CASE CONCERNS: A 27-year-old Chinese Han male with a history of hypertension and proteinuria, admitted to our hospital because of renal failure with MHT and thrombocytopenia. 33254542: Increased blood volume contributes to hypertension in obesity just as it does in hypertension secondary to renal failure. 6547112: Experimental evidence indicates that arginine vasopressin (AVP) may contribute to the rise of blood pressure (BP) in hypertension induced by renal failure and sodium overload. 7954538: Hypertension and oedema resulting from sodium retention are the main indications for diuretic treatment in patients with chronic renal failure. Pathophysiology and treatment of hypertension and oedema due to renal failure. 8125561: Renal artery disease is an important cause of both renal failure and hypertension. 8608665: Left ventricular hypertrophy (concentric and eccentric), which can be due to hypertension and anemia, is commonly observed in ESRD patients and has been shown to be a predictor of cardiac morbidity and mortality in these patients. Renal failure itself obviously is a prerequisite in the pathogenesis of r-HuEPO-induced hypertension, since it was never observed in anemic patients without renal disease. Normalization, though, is generally not achieved and in patients with r-HuEPO induced hypertension the increase of blood pressure may oppose the beneficial effects of r-HuEPO treatment on cardiac hypertrophy. 9033698: Myocardial hypertrophy due to volume and pressure overload is common in hemodialysis patients because renal failure is usually responsible for arterial hypertension. 10682193: If hypertension is secondary to chronic renal failure of any etiology, it can be recognized from biochemical assays for blood urea nitrogen and creatinine. 11338095: Atheromatous renovascular disease (ARVD) is a common cause of hypertension and chronic renal failure (CRF). 11849400: Almost no data exist regarding hypertension secondary to chronic renal failure. 12616031: ARVD is a common cause of hypertension and chronic renal failure (CRF), and it is one of the most common renal diagnoses in elderly patients accepted on to dialysis programmes with end-stage renal failure (ESRF). 12817064: Glomerular hypertension results in glomerular capillary wall stretch, endothelial damage and a rise in protein glomerular filtration. AH is also a well known consequence of chronic renal disease, and at the same time one of the main factors which causes diabetic and/or non-diabetic chronic renal failure progression. 13129740: OBJECTIVE: To observe the therapeutic effects of valsartan on hypertension secondary to chronic renal diseases. 14071629: METHYLDOPA IN TREATMENT OF HYPERTENSION DUE TO CHRONIC RENAL DISEASE. 1451118: Diurnal change of plasma atrial natriuretic peptide (ANP) concentration was investigated in 12 patients with hypertension due to chronic renal failure (CRF) and in 12 patients with essential hypertension (EH) of comparable degree. 15027587: Risk is considered to be high among patients with chronic hypertension, women with a past history of preeclampsia, diabetes (class D, F, R), patients with active systemic disease or with antiphospholipid antibodies or women with lupus or renal lesions and/or proteinuria as well as chronic kidney disease resulting in proteinuria, hypertension and renal insufficiency. 15789534: This high prevalence is not completely explained by usual CKD causes like diabetes or hypertension. 17534470: As either the cause or the consequence of CKD, hypertension is an important independent factor determining the rate of loss of renal function. 17851470: Chronic kidney disease (CKD) is a key cause of hypertension and a potent independent risk for cardiovascular disease. 18245745: CRF was the most common cause leading to hypertension. 18319559: Rare case of choroidal hemorrhage complicated with hypertension due to chronic renal failure. 19496385: Truly drug-resistant hypertension is commonly caused by chronic kidney disease, obstructive sleep apnea, or hyperaldosteronism, all of which can lead to fluid retention. 19878707: RESULTS: CRF resulted in hypertension, proteinuria, renal tissue lipid accumulation, up-regulation of scavenger receptor A1 (SR-A1), acyl-CoA cholesterol acyltransferase-1 (ACAT1), carbohydrate-responsive element binding protein (ChREBP), fatty acid synthase (FAS), acyl-CoA carboxylase (ACC), liver X receptor (LXR), ATP binding cassette (ABC) A-1, ABCG-1, and SR-B1 and down-regulation of sterol responsive element binding protein-1 (SREBP-1), SREBP-2, HMG-CoA reductase, PPAR-alpha, fatty acid binding protein (L-FABP), and CPT1A. 20049319: Atherosclerotic renal artery disease is a common cause of hypertension and chronic kidney disease that may progress into end stage renal failure if not diagnosed and treated early. 2006993: Loss of nocturnal decline of blood pressure in hypertension due to chronic renal failure. 20308607: Hypertension is both a cause and a consequence of chronic kidney disease, but the prevalence of chronic kidney disease throughout the diagnostic spectrum of blood pressure has not been established. 2085873: Our data demonstrate that the circadian rhythms of blood pressure and heart rate are altered also in hypertension due to chronic renal failure. 21224027: High blood pressure can be both a cause and a consequence of chronic kidney disease and will contribute to an unfavorable renal and cardiovascular (CV) prognosis. 21423678: Drug-induced hypertension, obstructive sleep apnoea, primary aldosteronism, and chronic kidney disease represent the most common secondary causes of resistant hypertension. 21435622: The most common causes of these problems are CDS, osteoarthritis, systemic hypertension (commonly secondary to chronic kidney disease or hyperthyroidism), hyperthyroidism (even without hypertension), deafness, and brain tumors. 21747971: Hypertension is both an important cause and consequence of chronic kidney disease. 23344662: Current evidence supports the notion that chronic kidney disease is a cause of chronic hypertension, even in the absence of detectable changes in glomerular filtration rate. 23591024: Existing epidemiologic and clinical trial data suggest that the blood pressure in patients with hypertension at high risk for cardiovascular events because of coronary artery disease, diabetes mellitus, chronic kidney disease, stroke, or heart failure should be reduced to <140/90 mm Hg in patients younger than 80 years and the systolic blood pressure be reduced to 140-145 mm Hg if tolerated in patients aged 80 years and older. 23677781: Systemic hypertension is an increasingly diagnosed disorder in dogs and cats and frequently occurs secondary to chronic kidney disease. 24103894: Chronic kidney disease (CKD) is the most costly disease covered by Medicare, and two common causes of CKD, diabetes and hypertension, are increasing worldwide. 24522942: Hypertension secondary to chronic kidney disease prevails in earlier childhood and obesity-related primary hypertension in adolescence. 24920147: Systemic hypertension is an increasingly diagnosed disorder in dogs and cats and frequently occurs secondary to chronic kidney disease. 25093157: RESULTS: Chronic kidney disease even in its early stages can cause hypertension and potentiate the risk for cardiovascular disease. 25126300: BACKGROUND: Chronic kidney disease is prevalent in the United States, and diabetes and hypertension cause up to two thirds of all new cases. 25416656: Chronic kidney disease (CKD), in particular, has been long considered a frequent underlying cause of resistant hypertension, however, recently, direct epidemiologic data for this entity in patients with CKD were brought to light again, suggesting an even higher prevalence of resistant hypertension (approximately 20%-35%) among such individuals. 25708823: Because chronic kidney diseases lead to hypertension and cardiac failure, we investigated the changes in apelin receptor gene expression in the myocardium and aorta of rat models of kidney disease hypertension. 26064513: Hypertension was thought to be secondary to CKD as she had scarred echogenic kidneys due to known reflux nephropathy. 26295257: CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation. 26558187: Pre-treatment considerations in childhood hypertension due to chronic kidney disease. 27188117: We describe our experience with a 15-year-old girl receiving anesthesia during one-stage bilateral nephrectomy for treatment-resistant hypertension due to chronic renal failure. 27496485: Recently chronic kidney disease and renalase metabolism of endogenous catecholamines are thought to make major contribution to the pathogenesis of hypertension. 2759900: Five years after the diagnosis of hypertension, the dog was euthanatized because of chronic renal failure secondary to pyelonephritis. 27873228: Chronic kidney disease (CKD) is both a common cause of hypertension and CKD is also a complication of uncontrolled hypertension. 27917928: Rats underwent 5/6 nephrectomy for 8 weeks, which induced CKD and hypertension. Renal Denervation Improves the Baroreflex and GABA System in Chronic Kidney Disease-induced Hypertension. 28435002: Systemic arterial hypertension secondary to chronic kidney disease in two captive-born large felids. 28875847: Hypertension is the second leading cause of CKD after diabetes and is strongly related to morbidity and mortality. OBJECTIVE: Since there is a strong relation between hypertension and CKD, and hypertension seems to lead to cardiovascular diseases, which have epidemic proportions in CKD, this review article discusses the etiology of hypertension and the existing optimal therapies that contribute to the hypertension and heart rate management. Since this relation exists and hypertension leads to cardiovascular diseases, the management of hypertension and increased heart rate should be a main therapeutic target in these patients. 29228345: Mechanisms and mediators of hypertension induced by erythropoietin and related molecules. Animal studies show the primary importance of chronic kidney disease in the genesis of EPO-induced hypertension. EPO-induced hypertension, at least in part, appears to be independent of an increase in hemoglobin, because experiments show that hemoglobin may be increased by EPO without an increase in blood pressure (BP) by simply treating the animals with EPO-binding protein and that treatment with EPO in the setting of iron deficiency may not increase hemoglobin but may still increase BP. Preclinical studies show deranged regulation of the nitric oxide, endothelins and porstanoids and the sympathoadrenal and renin-angiotensin pathways as causes of EPO-induced hypertension. Human studies suggest that EPO administration is also associated with increased responsiveness to catecholamines and angiotensin II on vascular tissue; in addition, hypoxia-induced vasodilation may be impaired in those with EPO-induced hypertension. However, experimental data are not consistent across studies and better mechanistic designs are needed, especially in patients with chronic kidney disease, to dissect the precise mechanism of EPO-induced hypertension. The purpose and focus of this review is to critically evaluate the mechanisms of EPO-induced hypertension. 2934412: Chronic renal failure is frequently associated with volume overload, resulting in hypertension and, in some cases, congestive heart failure. 30276536: Comparison of echocardiographic changes in children with primary hypertension and hypertension due to mild to moderate chronic kidney disease. 31366298: Furthermore, chronic kidney disease precipitates vascular risk factors that can lead to atherosclerosis, hypertension, atrial fibrillation, and diabetes. 31764582: Selective afferent renal denervation mitigates renal and splanchnic sympathetic nerve overactivity and renal function in chronic kidney disease-induced hypertension. 4053363: A 46-year-old black man with diabetes mellitus and hypertension was hospitalized because of myocardial ischemia and chronic renal failure. 9607208: LZ therapy normalized plasma MDA and significantly ameliorated CRF-induced hypertension. 10785847: Renal transplantation provides interesting insights into the pathogenesis of hypertension. 11791036: The genetic predisposition of the recipients to hypertension does not modify the rate and the extent of the arterial pressure rise induced by an SHR kidney graft. 2105587: Is renal transplantation useful for the understanding of the pathogenesis of hypertension? 2318524: Our data indicate that secondary damage to the renal grafts caused by high perfusion pressure before transplantation can induce hypertension in recipients of these kidneys. Hypertension in rats induced by renal grafts from renovascular hypertensive donors. 25873808: Transplant renal artery stenosis (TRAS), the most common vascular complication of kidney transplantation, can lead to heart failure, uncontrolled hypertension, and irreversible dysfunction of the transplanted kidney. 30134838: BACKGROUND: Transplant renal artery stenosis (TRAS) is a serious complication after renal transplantation, leading to hypertension, deterioration in renal function, and/or graft loss. 3889670: Hypertension secondary to renal transplantation was studied in our experimental model in the rat. 4573117: [Kidney transplantation in dogs. An operative method for treating experimentally induced vasorenal hypertension]. 7715893: Severe renal artery stenosis (RAS) is a relatively uncommon complication following renal transplantation but is a curable cause of hypertension which demands reliable early diagnosis to reduce morbidity, mortality and graft loss. 8266761: Although iliac artery stenosis is a rare complication after renal transplantation, it can be the cause of hypertension and renal dysfunction. 8846507: Renal cross-transplantation studies also indicate the principal role of the kidney as the primary organ responsible for the genesis of hypertension. 8862301: UNLABELLED: Severe renal artery stenosis (RAS) is a relatively uncommon complication after renal transplantation but is a curable cause of hypertension, which demands reliable early diagnosis to reduce morbidity, mortality and graft loss. 12899778: [Role of leptin in the pathogenesis of obesity-related hypertension]. 14749502: Of particular importance is the putative role of leptin in the causation of hypertension via an activation of the sympathetic nervous system and a direct effect on the kidneys, resulting in increased sodium reabsorption leading to hypertension. 15051422: Oxidative stress, nitric oxide production, and renal sodium handling in leptin-induced hypertension. NO deficiency and abnormal renal Na+ handling may contribute to leptin-induced hypertension. 15156072: Abnormal renal sodium retention and vasoconstriction associated with NO deficiency may contribute to leptin-induced hypertension and to blood pressure elevation in hypertensive obese individuals. Up-regulation of renal Na+, K+-ATPase: the possible novel mechanism of leptin-induced hypertension. 15171372: [Involvement of leptin in the pathogenesis of hypertension and hypertensive target-organ damage]. 15886421: Antioxidant treatment is effective in leptin-induced hypertension and should be considered in controlling blood pressure in hyperleptinemic obese individuals. 18282556: Transactivation of epidermal growth factor receptor in vascular and renal systems in rats with experimental hyperleptinemia: role in leptin-induced hypertension. We examined the role of epidermal growth factor (EGF) receptor in the pathogenesis of leptin-induced hypertension in the rat. 18690414: Renal antioxidant enzymes and glutathione redox status in leptin-induced hypertension. 19378230: CONCLUSION: Higher activity of sympathetic nervous system and higher levels of leptin in hypertensive women after menopause may suggest their participation in the pathogenesis of hypertension in this group of patients. 21694920: Resistance to leptin results in excess signaling to hypothalamic sympathetics leading to hypertension. 24002404: Increased leptin secretion may be responsible for sympathetic nervous system overactivity and hypertension, while reduced omentin may have an important permissive role in the development of atherogenic processes. 14749504: The fact that chronic leptin administration or overexpression of leptin produces hypertension supports the concept that the hemodynamic actions of leptin are due predominantly to sympathetic activation. 15913657: These results indicate that oxidative stress-induced NO deficiency is involved in the pathogenesis of leptin-induced hypertension. 16612235: Here, current knowledge about the role of leptin in the regulation of blood pressure and in the pathogenesis of arterial hypertension is presented. 17283868: Leptin has attracted attention as a possible cause of hypertension in obese persons. 17984669: Leptin antagonist reverses hypertension caused by leptin overexpression, but fails to normalize obesity-related hypertension. CONCLUSION: Central overexpression of leptin leads to hypertension that can be reversed by a leptin antagonist. 18056787: These findings provide support for roles for leptin and the ET system in the pathogenesis of obesity-associated hypertension. 18206959: These data indicate that: (1) ERK, activated by oxidative stress, is involved only in the early phase of leptin-induced BP elevation, (2) the later phase of leptin-induced hypertension is characterized by excessive NO inactivation by superoxide, (3) the time-dependent shift from ERK to O(2)(-)-NO dependent mechanism may be associated with reduced SOD/GPx ratio, which favors formation of O(2)(-) instead of H(2)O(2). 21286276: Leptin, an adipose tissue hormone which regulates food intake, is also involved in the pathogenesis of arterial hypertension. 23883674: The review focuses on a critical analysis of the concept of selective leptin resistance (SLR) and the role of leptin in the pathogenesis of obesity-induced hypertension in both experimental animals and humans. Finally, I review perplexing data on the effects of leptin on sympathetic activity and BP in humans and its role in human obesity-induced hypertension. 24171506: When leptin and leptin receptor genes were considered together, synergistic interaction was observed between the two genes leading to hypertension, while the polymorphism at leptin gene and obesity was correlated. 26953321: Leptin Induces Hypertension and Endothelial Dysfunction via Aldosterone-Dependent Mechanisms in Obese Female Mice. Together, these data demonstrate that leptin induces hypertension and endothelial dysfunction via aldosterone-dependent mechanisms in female mice and suggest that obesity leads to cardiovascular disease via sex-specific mechanisms. We hypothesized that leptin induces hypertension and endothelial dysfunction via aldosterone-dependent mechanisms in females. 27049292: With recent studies linking leptin and angiotensin signaling, we hypothesized that nGR-induced nLep deficiency increases adult leptin sensitivity; leading to leptin- or stress-induced hypertension, through a pathway involving central angiotensin II type 1 receptors. 31545149: Leptin induced hypertension in C57BL/6J mice, which was abolished by CB denervation, Trpm 7 blockers, and Trpm7 small hairpin RNA applied to CBs. OBJECTIVE: To examine if leptin induces hypertension acting on the CB Trpm7. CONCLUSIONS: We conclude that leptin induces hypertension acting on Trmp7 in CB, which opens horizons for new therapy. RATIONALE: Obesity leads to resistant hypertension and mechanisms are poorly understood, but high plasma levels of leptin have been implicated. Leptin Induces Hypertension Acting on Transient Receptor Potential Melastatin 7 Channel in the Carotid Body. 10321259: Liquorice-induced hypertension is an example of an acquired defect in dehydrogenase activity of 11 beta HSD, caused by glycyrrhetinic acid. 10773616: Prolonged ingestion of liquorice is a well-known cause of hypertension due to hypermineralocorticoidism. 11028416: [Steroid hormone- and licorice-induced hypertension]. 11230376: Aldosterone receptor antagonism normalizes vascular function in liquorice-induced hypertension. The present study investigated the effects of the aldosterone receptor antagonists spironolactone and eplerenone on endothelial function in liquorice-induced hypertension. 11425780: Renal activity of 11beta-HSD is decreased in patients with apparent mineralocorticoid excess (SAME), licorice-induced hypertension, and essential hypertension. CONCLUSIONS: Chronic ET(A) receptor blockade normalizes blood pressure, prevents upregulation of vascular ET-1, and improves endothelial dysfunction in 11beta-HSD inhibitor-induced hypertension and may emerge as a novel therapeutic approach in cardiovascular disease associated with reduced 11beta-HSD activity. 11682659: CONCLUSIONS: In GA-induced hypertension, both aldosterone receptor antagonism and endothelin receptor antagonism normalize blood pressure and improve renovascular function and, thus, may represent a new therapeutic approach in cardiovascular disease associated with impaired 11beta-HSD2 activity. The present study investigated the effect of the aldosterone receptor antagonist spironolactone in comparison with the endothelin ET(A) receptor antagonist darusentan on renovascular endothelial function in liquorice-induced hypertension. Influence of aldosterone vs. endothelin receptor antagonism on renovascular function in liquorice-induced hypertension. 11797564: [Licorice-induced high blood pressure]. 12416071: [Ambulatory 24-hour blood pressure monitoring in a case of liquorice-induced hypertension]. We report on the use of ambulatory blood pressure monitoring in a young female with liquorice-induced hypertension. 1476186: We have found that the infusion of both glycyrrhizic acid, an active principle of licorice, and carbenoxolone, a synthetic analogue, into a lateral ventricle of the brain [intracerebroventricular (icv)] of a rat, at a dose less than that which has an effect when infused subcutaneously, produces hypertension. While the oral administration caused saline polydipsia and polyuria typical of chronic systemic mineralocorticoid excess, the icv licorice derivatives produced hypertension without affecting saline appetite. Furthermore, the hypertension produced by the oral administration of carbenoxolone or glycyrrhizic acid is blocked by the icv administration of RU 28318, an MR antagonist, at a dose below that which has an effect on blood pressure when infused subcutaneously. They also suggest that more is involved in licorice-induced hypertension than only inhibition of 11 beta-HSD. 17016026: Typical adverse effects of Shakuyaku-kanzo-To (SKT), an herbal medicine containing licorice, is a licorice-induced pseudoaldosteronism with hypokalemia and hypertension. 17320224: Excessive intake of licorice can cause hypokalemia and hypertension and generally, the onset and severity of symptoms depend on the dose and duration of licorice intake, as well as individual susceptibility. 18237050: [Hypertension due to liquorice and liquorice tea consumption]. 18256580: Consumption of large quantities of liquorice can cause hypokalemia and hypertension. 18380391: [Hypertension due to liquorice and liquorice tea consumption]. 18438069: [Hypertension due to liquorice and liquorice tea consumption]. 19707475: This article appraises physiological and pharmacological effects on health of liquorice, critiques products containing liquorice, describes a typical case report of liquorice-induced hypertension, and appraises oral effects from consumption of liquorice products. 20007258: Carrying a mutation in HSD11B2 is, conversely, a genetic risk factor for licorice-induced hypertension or AME state. 20597806: Licorice-induced hypertension and common variants of genes regulating renal sodium reabsorption. CONCLUSIONS: Defects of the 11betaHSD2 gene do not constitute a likely cause for licorice-induced hypertension. METHODS: Finnish subjects (n = 30) with a previously documented incident of licorice-induced hypertension were recruited for the study using a newspaper announcement. The frequency of these ENaC variants was significantly higher in subjects with licorice-induced hypertension (6/30 i.e. 20%) than in blood donors (11/301 i.e. 3.7%, P = 0.002). AIM: To study if gene alterations affecting renal sodium reabsorption associate with susceptibility to licorice-induced hypertension. 22487411: [Liquorice-induced hypertension and hypokalaemia]. Consumption of large amounts of liquorice can cause hypertension and hypokalaemia. 2326827: Ingestion of licorice or treatment with chemical derivatives of glycyrrhetinic acid (GA), an active principle of licorice, can cause hypertension, sodium retention, and hypokalemia. 2394832: A 11 beta-OHSD deficiency has been invoked as a cause of the syndrome of apparent mineralocorticoid excess, and 11 beta-OHSD inhibition by liquorice has been invoked to explain the hypertension induced by this drug. They reinforce the notion that a defect in 11 beta-OHSD plays a major role in the syndrome of apparent mineralocorticoid excess and liquorice-induced hypertension. 25945908: It is already known that the ingredients of licorice may induce hypertension. 28276791: Licorice can cause hypertension and hypokalemia due its effects on cortisol metabolism. We report a case of jelly bean ingestion that highlights the presentation, pathophysiology and management of licorice-induced hypertension. 29538199: Licorice and glycyrrhizin induced hypertension has been widely reported, yet licorice and glycyrrhizin induced hypertensive crisis has been rarely known. LESSONS: Licorice and glycyrrhizin induced hypertension due to pseudo-hyperaldosteronism has been widely reported, yet only 3 cases reported that excessive consumption of licorice could lead to hypertensive emergencies. 30298226: Liquorice-induced hypertension with severe hypokalemia and rhabdomyolysis is a rare condition and the initial presentation with acute muscle paralysis is still more unusual. 3889147: Exchangeable sodium in our patient with licorice-induced hypertension was increased to a comparable extent as in primary hyperaldosteronism. Body-sodium and blood volume in a patient with licorice-induced hypertension. 6884644: We describe the case of a young woman affected by systemic high blood pressure, in whom the clinical history and laboratory data (hypokalaemia, low plasma renin activity and negligible aldosterone levels) were consistent with the hypothesis of liquorice-induced hypertension. This unusual persistence of liquorice-induced hypertension supports the hypothesis that liquorice facilitated the phenotypic development of a hypertensive state in a patient with a family history positive for that disease. 7623371: The results indicate that liquorice-induced hypertension might be more common than has been appreciated and it important for medical doctors to be on the alert for this effect in both the prevention and treatment of hypertension. 8070427: Deficient 11 beta-dehydrogenase activity provides a novel pathogenetic mechanism for hypertension, and current research suggests that several common forms of hypertension can be explained by the mechanisms that operate in licorice-induced hypertension. Licorice-induced hypertension and syndromes of apparent mineralocorticoid excess. 8544895: Liquorice-induced hypertension--a new understanding of an old disease: case report and brief review. The literature on liquorice-induced hypertension is briefly reviewed with emphasis on the biochemical features of this mineralocorticoid excess syndrome. 8994882: Licorice induces high blood pressure by inhibiting an SDR in the kidney, and appears to combat ulcers by inhibiting another in the stomach. 9029719: Deficiency of the 11 beta-HSD2 isoform, as described in the syndrome of apparent mineralocorticoid excess and following liquorice (glycyrrhetinic acid) or carbenoxolone ingestion, results in hypertension in which cortisol acts as a potent mineralocorticoid. 9683905: In licorice-induced hypertension glycyrrhetinic acid, the active substituent of licorice, inhibits 11 beta-HSD2 resulting in an acquired hypermineralocorticoid state. 9888533: Licorice induces high blood pressure by inhibiting an SDR in the kidney. 1071714: This study describes the changes observed in the rat microcirculation in vivo in the transparent tissue chamber of the rat back, during the florid hypertension produced by ligation of the rat aorta between both renal arteries. 1184305: The present study has been concerned with blood pressure, renal functions and the microscopic changes of the kidney during permanent hypertension induced by unilateral ligation of the renal artery. 13045646: [Partial kidney infarct and hypertension due to the ligation of accessory blood vessels]. 13071310: [Partial kidney infarct and hypertension as a consequence of ligation of accessory vessels. II]. 14403696: [Experimental studies on the problem of contralateral renal fixation in unilateral kidney ligation-induced hypertension]. 14956518: [Partial kidney infarction and hypertension caused by ligation of accessory blood vessels]. 16355448: This research investigated the anti-hypertension effect of the traditional Chinese medicine (TCM) ju-ling-tang (JLT) on an animal model of hypertension induced by unilateral renal artery ligation. 19166202: In this study, rabbits were used and the model of pre-hepatic portal hypertension (PHT) was induced by partial ligation of portal vein in two steps. 1924410: To determine the biochemical and hemodynamic responses to aortic ligation, and to assess the survival rate after the induction of hypertension, 90 normotensive rats were subjected to surgical constriction of the abdominal aorta. 1940031: In anesthetized and artificially ventilated rats, passive or reflex hypertension was produced by ligation of the abdominal aorta (12 rats), or sudden lowering of the cutaneous temperature to 25-30 degrees C achieved by exposure to cold water (26 rats), respectively. 20968096: In the present study, we analyzed the release of atrial and brain natriuretic peptides in the myocytes of the right atrium in rats by the quantitative morphometric method using double immunocytochemical labeling of atrial granules comprising NP in vasorenal hypertension induced by the renal artery ligation. 21376106: Changes in patterns of cerebral blood flow and hypertension induced by surgical ligations of selected arteries exert significant hemodynamic stress to weaken vessel walls, primarily at sites of basilar bifurcation. 24382264: Rats with pre-hepatic portal hypertension because of partial portal vein ligation develop minimal hepatic encephalopathy (MHE) with hyperammonemia, impaired blood-brain barrier, mild brain edema, and severe mitochondrial changes in the hippocampus. 25599976: FTIR was used to monitor biochemical changes in plasma caused by PAH as compared with the systemic hypertension induced by partial ligation on the left artery and with the control group. 26870333: Beagle dog models of HPS and PoPH were induced by chronic common bile duct ligation and Sephadex microspheres, respectively. 27824106: Peripheral and spinal 5-HT receptors participate in cholestatic itch and antinociception induced by bile duct ligation in rats. 2895070: The purpose of this study was to assess the role of kinins in the acute antihypertensive effect of the converting enzyme inhibitor (CEI) enalaprilat in rats with severe hypertension induced by aortic ligation between both renal arteries. 2959234: [Arterial hypertension, myocardial hypertrophy and disorders of cardiac rhythm induced by ligation of the left coronary artery in the rat]. 30431106: Aortic constriction induces hypertension and cardiac hypertrophy via (pro)renin receptor activation and the PLC-beta3 signaling pathway. Hypertension and cardiac hypertrophy were induced by partial abdominal aortic ligation in Sprague-Dawley rats. 3053893: The reflex responses of heart rate (HR) to bolus injection and infusion of phenylephrine and nitroglycerine were studied in rats with one-kidney, one clip (1-K, 1C) hypertension and hypertension produced by aortic ligation. 31295531: Pre-hepatic portal-hypertension was induced by partial portal vein ligation (PPVL). 31419795: METHODS: Female Sprague Dawley rats were subjected to bilateral ovariectomy; the ligation of the left common carotid, the right external carotid, and the right pterygopalatine arteries; induced systemic hypertension; and the administration of a lysyl oxidase inhibitor. 32120907: The most common techniques to induce cerebral aneurysms were surgical ligation of the common carotid artery with subsequent induction of hypertension by ligation of the renal arteries, followed by elastase-induced creation of IAs in combination with corticosterone- or angiotensin-induced hypertension. 3346048: Hypertension induced by aortic ligation between the renal arteries resulted in rapid elevations in circulating humoral factors and blood pressure. 37473803: Hypertension was induced by left renal artery ligation in all groups except the Sham control group. 38242036: Here, we investigated the anti-inflammatory and reno-cardiac protective effects of a polyphenol-rich fraction of bergamot (BPF) in an experimental model of hypertension induced by unilateral renal artery ligation. 3938404: The effect of the converting enzyme inhibitor captopril (5 mg (kg bwt)-1) on systemic and renal haemodynamics has been studied in conscious rats in which a progressive hypertension has been induced by progressive aortic ligation (AL) between the renal arteries, and in a sham-operated (SO) group. 4053303: Hyperplastic growth response of vascular smooth muscle cells following induction of acute hypertension in rats by aortic coarctation. This study examines the growth response of vascular smooth muscle cells following induction of acute hypertension in rats by partial ligation of the abdominal aorta between the renal arteries. It is suggested that a non-denuding form of endothelial \injury\ may play an important role in the proliferative growth response of smooth muscle cells following induction of coarctation hypertension. 4317470: [Changes of the pressoactive substance extractable from both kidneys of rats with hypertension induced by complete ligation of the aorta between the renal arteries]. 4464749: Renal function and morphology in hypertension induced by ligation of one renal artery in the rat. 4677444: [Changes in the blood pressure level during disturbed higher nervous system activity in dogs with experimental hypertension induced by two-stage ligation of 3 out of 4 major cerebral arteries]. 4681177: [Higher nervous activity in dogs with experimental hypertension induced by 2-stage ligation of 3 or 4 major cerebral arteries]. 4728259: Hypertension resulting from ligation of segmental renal vessels. 5148332: Renin activity of renal venous blood in experimental hypertension induced by ligation of one renal artery in dogs. 5474477: Permanent hypertension induced by ligation of one renal artery in the dog. 5507768: [Course of chronic cerebroischemic hypertension in rabbits caused by ligation of branches of carotid arteries above the carotid sinuses]. 6005419: [Experimental hypertension in dogs produced by ligation of three major cerebral arteries]. 6372495: Partial ligation of the rat aorta between the renal arteries induces acute hypertension with atrophy of the left (ischemic) kidney, intense stimulation of juxtaglomerular cell (JGC) secretory activity, and significant increases in renal cortical renin activity, in plasma renin activity, and in the plasma levels of angiotensin I (AI) and angiotensin II (AII). 6753490: Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. 7136755: Hypertension was induced by ligation of the thoracic aorta. 7282395: Acute arterial hypertension was induced by ligation of the aorta. 7660412: METHODS: Cerebral aneurysms were induced in rats by ligation of the unilateral common carotid artery, producing hypertension. 7660414: METHODS: Cerebral aneurysms were induced in rats by both the ligation of the unilateral common carotid artery and induced hypertension. 9575886: We chose this model, as opposed to that produced by renal artery branch ligation, because the latter causes exuberant hypertension (HTN), which independently affects NO metabolism. 9701119: METHODS: Cerebral aneurysms were induced in rats by means of the combination of ligation of the unilateral common carotid artery and induced hypertension. 12419469: These results support the hypothesis that oxidative damage to lipid, protein, and DNA is an important early event in the pathogenesis of AD. 12668899: Since apoE is a regulator of lipid metabolism, it is reasonable to assume that lipids such as cholesterol are involved in the pathogenesis of AD. 15270198: Although early studies recognized the loss of cholesterol and other lipids in the brain, these findings have been poorly connected with AD pathogenesis, despite the identification of the epsilon4 allele of APOE as a major risk factor in AD. 16344479: Thus, the lipid- and receptor-binding regions in apoE4 fragments act together to cause mitochondrial dysfunction and neurotoxicity, which may be important in Alzheimer's disease pathogenesis. 21605030: Apo E is the major component of lipoprotein particles in the brain that mediate transport of cholesterol and other lipids between neurons and glial cells, indicating an implication of cerebral lipid metabolism in the pathogenesis of AD. Importantly, mutations in the genes of APP and the two homologous PS proteins are a major cause of familial early onset AD, indicating that the metabolism of APP and generation of Abeta play critical roles in the initiation of the disease. 22367100: This review summarizes the current state of our knowledge of the influence of cholesterol and lipid pathways in AD pathogenesis in vitro and in vivo. 24575399: This review summarizes lipid alterations found in AD postmortem brains, AD transgenic mouse models, and the current understanding of how lipids influence the molecular mechanisms leading to AD and A beta generation, focusing especially on cholesterol, docosahexaenoic acid (DHA), and sphingolipids/glycosphingolipids. 24894353: Here, we review ApoE-lipid interactions, as well as the roles that lipids may play in the pathogenesis of AD. Evidence suggests that the ApoE protein, a major lipid transporter, plays a key role in the pathogenesis of AD, and its role in both normal and aberrant lipid metabolism warrants further extensive investigation. 24898654: The probable auto-antigenic role of lipids (anti-ganglioside antibodies) in the pathogenesis of Alzheimer's disease. 28002106: As the brain has a high lipid content, lipidomics may offer novel insights into the underlying pathogenesis of Alzheimer's disease. 29522770: SIGNIFICANCE: Therefore, this solid lipid nanoparticle of quercetin can be used as future nanomedicine for various neurodegenerative disorders like Alzheimer and Parkinson disorders due to its potential anti-oxidative, anti-lipid peroxidative and acetylcholinesterase inhibitory actions. 29526709: This, we believe, will refocus our thinking on the influence of lipids and open new approaches in delineating the mechanisms of AD pathogenesis. 30207230: Lipids participate in Amyloid Precursor Protein (APP) trafficking and processing - important factors in the initiation of Alzheimer's disease (AD) pathogenesis and influence the formation of neurotoxic beta-amyloid (Abeta) peptides. The Role of Lipids and Membranes in the Pathogenesis of Alzheimer's Disease: A Comprehensive View. 31062326: The Roles of Apolipoprotein E, Lipids, and Glucose in the Pathogenesis of Alzheimer's Disease. In this chapter, we discuss the roles of ApoE, lipids, and glucose in the pathogenesis of AD by considering their potential interactions. 33550528: A recent surge in research on lipid handling and metabolism in glia and neurons has established defective lipid clearance from endolysosomes as a central driver of AD pathogenesis. 34483892: Introduction: Prior evidence suggested Apolipoprotein E (APOE) , lipids, and glucose metabolism may act through the same pathways on the pathogenesis of Alzheimer's disease (AD). 36165619: Upstream lipid and metabolic systems are potential causes of Alzheimer's disease, Parkinson's disease and dementias. Using microglia as an example, we review data that suggest increased lipid concentrations cause dysfunctional inflammatory responses to immune challenges, leading to Alzheimer's disease, Parkinson's disease and dementia. 36570536: In this cross-sectional study, we attempted to elucidate the associations of these bioactive lipids with the pathogenesis/pathology of AD through postmortem studies of human brains. 37398438: Our study of circulating lipids and central AD biomarkers enabled identification of lipids that play potential roles in the cascade of AD pathogenesis. 38203341: Several studies in recent years have shown that lipid metabolic dysregulation and neuroinflammation are associated with the pathogenesis of AD. 16675600: In vivo, infusion with AngII but not with norepinephrine into rats for 7 d also enhanced glomerular NF-kappaB activation after systemic application of LPS, suggesting that the effects are independent of concomitantly induced hypertension. 24764457: In a previous study, we discovered that prenatal exposure to inflammatory stimulants, such as lipopolysaccharides (LPS), could lead to hypertension in adult rat offspring. 25025169: BACKGROUND: Prenatal exposure to Lipopolysaccharide (LPS) produces hypertension in adult offspring rats. 26689453: We reported earlier that angiotensin-converting enzyme (ACE) inhibition attenuated the increased vulnerability to neurodegeneration in hypertension and prevented lipopolysaccharide (LPS)-induced memory impairment in normotensive wistar rats (NWRs) and spontaneously hypertensive rats (SHRs). 27995995: Prenatal exposure to lipopolysaccharide (LPS) leads to hypertension in a rat offspring. 30774143: When present in pharmaceutical products, a Gram-negative bacterial cell wall component endotoxin (often also called lipopolysaccharide) can cause inflammation, fever, hypo- or hypertension, and, in extreme cases, can lead to tissue and organ damage that may become fatal. 31334867: The results showed that MET improved LPS-induced hypertension, proteinuria, fetal growth restriction (FGR) and stillbirth, alleviated placental injury and decreased maternal serum marker alpha-fetoprotein (MS-AFP) level; MET suppressed LPS-induced TNF-alpha and IL-6 productions, reduced oxidative/nitrative stress as evidenced by increased superoxide dismutase (SOD) activity, decreased inducible nitric oxide synthase (iNOS) activity, and decreased levels of malondialdehyde (MDA) and nitric oxide (NO); MET inhibited LPS-induced NF-kappaB activation in placentas. 31961431: Finally, we evaluated the effects of oral butyrate on LPS-induced hypertension in pregnant rats. 32247003: RESULTS: Cys-peptide ameliorated LPS-induced hypertension, proteinuria and FGR and other PE symptoms in preeclampia-like rat models. 33236147: Additionally, PDCC4 alleviated hypertension, histopathological changes of placenta and kidney and the expression levels of endothelial injury markers and inflammatory cytokines induced by LPS in rats. 34014393: It is presumed that the intestinal microbiota, and especially its metabolites (LPS and trimethylamine N-oxide (TMAO)), may play an important role in the pathogenesis of arterial hypertension, atherosclerosis, and heart failure. 36425944: One possibility is that the initial drop in LPS-induced arterial hypertension is mediated by a central mechanism. 22211682: For instance, lipopolysaccharides in PD and amyloid beta in AD trigger microglia and astrocytes to release reactive oxygen species (ROS) and proinflammatory cytokines. 25454121: RESULTS: Systemic LPS induced AD, as shown by cognitive impairment; increased levels of Abeta and concomitant increase in the brain NO concentrations. 29447949: RESULTS: It was found that successive intragastric administration of AOF (360 mg/kg) extracts for 14 days showed different degrees of improvement on LPS-induced AD model as measured by Y-maze test, Morris water maze test, and Histopathological examination. 31073286: Design: We explored to investigate the effects of GA on neuroinflammation and memory impairment in an LPS-induced Alzheimer's mouse model. 31463498: Our data showed that SEO improved the cognitive ability of mice with Abeta1-42 or lipopolysaccharides (LPS)-induced Alzheimer's disease (AD) and suppressed the production of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta) in the hippocampus. 32045690: Nasal timosaponin BII dually sensitive in situ hydrogels for the prevention of Alzheimer's disease induced by lipopolysaccharides. 32925065: Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis Induces Bone Loss-Correlated Alzheimer's Disease-Like Pathologies in Middle-Aged Mice.BACKGROUND: Alzheimer's disease (AD) and bone loss are clinically exacerbated. Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis Induces Bone Loss-Correlated Alzheimer's Disease-Like Pathologies in Middle-Aged Mice. 33191624: Here, we identified a non-equilibrium state of interaction between supramolecular lipopolysaccharide (LPS) and Abeta42, an aggregate-prone protein that causes Alzheimer's disease (AD). 33481268: Hydrogen sulfide and mesenchymal stem cells-extracted microvesicles attenuate LPS-induced Alzheimer's disease. Thirty female Wistar albino rats aged 6 months to 1 year were equally divided into five groups; control group, LPS-induced AD group, LPS + MVs group, LPS + NaHS group, and LPS + MVs and NaHS group. The current study was conducted to evaluate the role of miR-155 in a rat model of lipopolysaccharide (LPS)-induced AD and to investigate the effect of using MVs and H 2 S that were given either separately or combined in regulating pro-inflammatory signaling. In conclusion, downregulation of TNF-alpha, miR-155, and pAkt and increased SHIP-1 could improve the neuro-inflammatory state and cognitive function of LPS-induced Alzheimer's disease. 33816329: In recent years, as the infectious theory and endotoxin hypothesis of AD has gained substantial attention, several studies have proposed that Porphyromonas gingivalis ( P. gingivalis ), one of the main pathogenic bacteria of chronic periodontitis, and the lipopolysaccharide (LPS) of P. gingivalis may lead to AD-like pathological changes and cognition impairment. 34091099: These results underline the significance of microbial/ inflammatory involvement in dementia and offer novel perspectives on the roles of LPSs and COX in pathogenesis of AD. 34971183: The role of lycopene on the hippocampus of rat model of lipopolysaccharide-induced Alzheimer's disease. This study was designed to investigate the role of lycopene on hippocampus in lipopolysaccharide- induced Alzheimer's disease. 35273209: Subsequently, we used the CBN and transcriptomic data to identify key molecular pathways driving the astrocyte phenotype in four CNS pathologies: samples from mouse models of lipopolysaccharide-induced endotoxemia, Alzheimer's disease, and amyotrophic lateral sclerosis; and samples from multiple sclerosis patients. 35429976: Further, a transcriptomic meta-analysis revealed that IL-6 and IFN-alpha both contribute to the formation of a core microglia response in animal models of neurodegenerative and neuroinflammatory disorders, such as Alzheimer's disease, tauopathy, multiple sclerosis and lipopolysaccharide-induced endotoxemia. 35890426: DC against Lipopolysaccharide Induced Alzheimer's Disease in Mice. 36499428: Furthermore, systemic treatment of Porphyromonas gingivalis ( Pg ) lipopolysaccharide (LPS) induced Alzheimer's disease-like neuropathological changes in middle-aged mice. 36642360: In conclusion, the study provides evidence that the treatment with Bacterial protease can improve the memory and learning impairments of LPS-induced AD and may be used as a promising therapeutic agent to manage AD since it has anti-inflammatory and antioxidant effect. 37895841: Dapagliflozin/Hesperidin Combination Mitigates Lipopolysaccharide-Induced Alzheimer's Disease in Rats. The aim of this study was to elucidate the potential ameliorative effects of dapagliflozin and/or hesperidin on Alzheimer's disease (AD) induced by lipopolysaccharide (LPS) injection in rats. 38051653: In-depth analyses of lncRNA and circRNA expression in the hippocampus of LPS-induced AD mice by Byu d Mar 25. 38533683: In the present study, the neuroprotective effects of four Morus extracts were assessed in LPS-induced AD in mice. 11198596: Achieving dry weight is critical since chronic fluid overload can result in hypertension and left ventricular hypertrophy. 15167950: The use of a diuretic will often be helpful in patients who already have renal insufficiency, since fluid overload is an important cause of hypertension and may also enhance the effectiveness of drugs that interfere with the RAAS. 16797424: Because fluid overload may cause hypertension, we compared the patients' intraoperative hemodynamic profiles (including the incidence of hypertension) during TURP vs TURT, both performed during spinal anesthesia, by using the bioimpedance method. 20739164: Albino rats weighing 150-200 g were fed with 10% fructose in fluid for 3 weeks for induction of hypertension and subsequently administered FGH (125 and 250 mg/kg, p.o.) or SACS (0.111 and 0.222 mg/kg/day, p.o.) for the next 3 weeks in their respective groups. 20821270: Three weeks of high fructose (10% w/v) in fluid to albino rats resulted in hypertension. 21096059: An inadequate removed volume may lead to chronic fluid overload which can lead to hypertension, left ventricular hypertrophy and heart failure. 22652734: Fluid overload may produce hypertension, reduced arterial distensibility, left ventricular hypertrophy. 23548813: Despite meticulous clinical assessment, fluid overload is common, leading to hypertension and left ventricular hypertrophy (LVH). 27478611: The pathogenesis is unclear, but it has been suggested that IDH may be due to subclinical fluid overload. 28197229: A colonic re-absorptive error is established with excessive fluid and salt retention in the body that would definitely lead to hypertension which is supposed to remain inadequately controlled without correction of the underlying etiologic pathological error. 29723894: An important element is alpha-adrenergic vasoconstriction, which increases viscosity due to leakage of intravascular fluid into the interstitium, and also causes hypertension, favoring plaque rupture. 3635662: In this study it could be demonstrated with the help of computer simulations, that the hypertension was caused by excess fluid being retained by the kidneys, whereas, the elevated hematocrit could only be attributed to primary increase in the resistance to blood flow. 6151422: Beta-blocking drugs can lead to hypertension by causing fluid retention, reversal of catecholamine vasodilatation, or a direct pressor effect. 7865185: The role of fluid overload in the pathogenesis of hypertension in hemodialysis patients is not clear. 8467232: These aggregates, and the intramural entrapment of fluid and cellular debris, occlude progressively the hepatic venous outflow and generate a postsinusoidal intrahepatic hypertension. 15615644: Whether Abeta or tau filaments cause AD is still an open question, as a wide variety of proteins and pathways have been implicated in the initiation and advancement of the disease--processes such as apoptosis, oxidative stress, and protein degradation. 16262633: Abnormal hyperphosphorylation of tau is believed to lead to neurofibrillary degeneration in Alzheimer's disease (AD) and other tauopathies. 16953147: Hence, the abnormal hyperphosphorylation of tau appears to be critical to the pathogenesis of AD. 17044033: The degradation of aberrantly phosphorylated tau in neurons plays an important role in the pathogenesis of Alzheimer's disease (AD). 17077307: These studies describe a novel mechanism for MPTP neurotoxicity, namely a MPTP-inducible, strictly alpha-Syn-dependent, increased formation of PHF-1-reactive Tau, suggesting convergent overlapping pathways in the genesis of clinically divergent diseases such as AD and PD. 17360920: These findings, in combination with evidence for cell cycle regulation of amyloid precursor protein and tau, has led to the hypothesis that reentry into the cell cycle underlies AD pathogenesis. 17361031: The positive correlation trend in MCI and the robust correlation in AD between Pin1 activity and phosphorylated tau implies that increasing phosphorylated tau during AD pathogenesis may induce the compensatory activation/up-regulation of Pin1, while the inverse correlation between Pin1 activity and phosphorylated tau in NCI group implies that decreased Pin1 may play a role in the initial accumulation of phosphorylated tau in AD pathogenesis. 17562708: A combination of casein kinase 1delta and glycogen synthase kinase-3beta activities could account for over three-quarters of the serine/threonine phosphorylation sites identified in PHF-tau, indicating that casein kinase 1delta may have a role, together with glycogen synthase kinase-3beta, in the pathogenesis of Alzheimer disease. 18583940: An altered tau produces cytoskeleton pathology resulting in neurodegenerative diseases such as Alzheimer's disease and tauopathies. 18690834: Mechanism of tau-induced neurodegeneration in Alzheimer disease and related tauopathies. 18855662: Furthermore, several therapeutic strategies for treating AD on the basis of the important role of tau hyperphosphorylation in the pathogenesis of the disease are described. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. 19742193: The mismetabolism of APP and the defective clearance of beta amyloid generate a cascade of events including hyperphosphorylated tau (tau) mediated breakdown of microtubular assembly and resultant synaptic failure which results in AD. 20422200: Hallmark cellular pathology of Alzheimer's disease induced by mutant human tau expression in cultured Aplysia neurons. 20683187: Dementia mimicking Alzheimer's disease Owing to a tau mutation: CSF and PET findings. 20730022: Studies in mice expressing both human amyloid precursor protein and human tau have provided clear evidence that amyloid-beta and tau interact in the pathogenesis of AD. A defined effort must be made to develop therapies that directly address the impact of tau dysfunction in the pathogenesis of AD. 20926667: Our results strongly support a convergent role for PS and tau in axonal transport and neuronal survival and function and implicate their misregulation as a contributor to AD pathogenesis. 21348938: However, given the increasing evidence that pathological forms of tau can compromise neuronal function and that tau is likely an important mediator of Abeta toxicity, there is a growing awareness that tau is a central player in AD pathogenesis. 22401494: The misfolding and aggregation of the intrinsically disordered, microtubule-associated tau protein into neurofibrillary tangles is implicated in the pathogenesis of Alzheimer's disease. 22922102: Tau, a microtubule-associated protein and substrate for GSK3beta, has been implicated in the pathogenesis of tauopathies such as Alzheimer's disease. 23052602: The cerebrospinal fluid (CSF) biomarker profile in Alzheimer's disease (AD) is characterized by decreased beta amyloid (Abeta(1-42)), increased total and hyperphosphorylated tau (t-tau and p-tau, respectively), which is a useful diagnostic tool and gives insight in the pathogenesis of AD. 23517246: Both pro-aggregant Tau variants cause Alzheimer-like features, including synapse loss, mis-localization of Tau into the somatodendritic compartment, conformational changes and hyperphosphorylation. 23659495: In addition to amyloid-beta (Abeta) peptide and phosphorylated tau, lipid dysregulation is suggested to participate in AD pathogenesis. 23828739: Therefore, a disorder primarily affecting structures in medial temporal lobe, with accumulation of amyloid beta and abnormal tau, neuritic plaques and tangles, progressive loss of memory and/or other cognitive deficits, ultimately resulting in dementia should be classified as AD. Alzheimer's disease (AD), the most prevalent disorder causing dementia, is considered a neurodegenerative disease. 23904623: Tau, a microtubule-associated protein, is implicated in the pathogenesis of Alzheimer's Disease (AD) in regard to both neurofibrillary tangle formation and neuronal network hyperexcitability. 24027553: Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease. 24076336: A role for tau at the synapse in Alzheimer's disease pathogenesis. Understanding the role of tau in both normal and degenerating synapses is crucial for the development of therapeutic strategies designed to ameliorate synapse loss and prevent AD pathogenesis. 24493463: Therefore, Abeta is upstream of tau in AD pathogenesis and triggers the conversion of tau from a normal to a toxic state, but there is also evidence that toxic tau enhances Abeta toxicity via a feedback loop. Amyloid-beta and tau: the trigger and bullet in Alzheimer disease pathogenesis. 24785461: Heat shock protein 90 (Hsp90alpha) is a molecular chaperone which was found to regulate the function of number of client proteins including tau that is involved in the cause of the AD. 24936619: Changes in spatial learning ability and memory and induction of AD-like pathogenesis were not detected by in vivo brain imaging for amyloid-beta peptide accumulation and by immunohistochemical staining of amyloid precursor protein, amyloid-beta protein, tau, and phosphorylated tau protein. 25169677: Activated human microglia stimulate neuroblastoma cells to upregulate production of beta amyloid protein and tau: implications for Alzheimer's disease pathogenesis. 25442111: The interaction of amyloid-beta (Abeta) and tau in the pathogenesis of Alzheimer's disease is a subject of intense inquiry, with the bulk of evidence indicating that changes in tau are downstream of Abeta. 26563932: Accumulation of beta-amyloid (Abeta) and phosphorylated tau in the brain are central events underlying Alzheimer's disease (AD) pathogenesis. 26943044: Our findings reveal a novel mechanism underlying the htau-induced neuronal toxicities in AD and other tauopathies. 27034421: According to published research, the inverted tau concentration gradient may be one of the reasons leading to AD. 27079722: This is a reasonable assumption because amyloid-beta peptide (Abeta) accumulation and tau hyperphosphorylation are the defining histological features in AD, and because AbetaPP and tau mutations can cause AD in humans or AD-like features in animal models. Alzheimer's disease (AD) has long been viewed as a pathology that must be caused either by aberrant amyloid-beta protein precursor (AbetaPP) processing, dysfunctional tau protein processing, or a combination of these two factors. 27152883: Tau is a microtubule-associated protein implicated in the pathogenesis of Alzheimer's disease and other related tauopathies. 27651066: Tau is a microtubule-associated protein that plays an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease. 28186985: Hyperphosphorylation of Tau forming neurofibrillary tangles has been considered as a crucial event in the pathogenesis of Alzheimer's disease (AD). 28420695: Cyclin-dependent kinase 5 (Cdk5), which binds to and is activated by p35, phosphorylates multiple substrates and plays an essential role in the development and function of the CNS; however, proteolytic production of p25 from p35 under stress conditions leads to the inappropriate activation of Cdk5 and contributes to hyperphosphorylation of tau and other substrates that are related to the pathogenesis of Alzheimer's disease. 28580182: There is growing evidence that in addition to Abeta deposition, accumulation of hyperphosphorylated oligomeric tau contributes significantly to AD etiology. 28655349: BACKGROUND: Finding ways to reverse or prevent the consequences of pathogenic tau in the brain is of considerable importance for treatment of Alzheimer's disease and other tauopathies. 29237931: OBJECTIVE: To review recent research advances on tau, a major player in Alzheimer's disease (AD) pathogenesis, a biomarker for AD onset, and potential target for AD therapy. 29278891: We investigated the CSF levels of Abeta and tau, another pathological hallmark in the AD pathogenesis. 29554190: Conclusions and Relevance: Alzheimer disease CSF core biomarkers can be used with high specificity for the in vivo identification of patients with pure FTLD-TDP and FTLD-tau when accounting for comorbid AD and genetic status. 29782836: Structural studies show interaction modes of Hsp90 with the intrinsically disordered Alzheimer's disease-causing protein Tau, the kinase Cdk4 in a partially unfolded state and the folded ligand-binding domain of a steroid receptor. 29954063: However, the roles of Aβ and Tau in AD pathology are being questioned and other causes of AD are postulated. 30278184: These findings have implications for further studies of tau under the conditions of protein phosphatase downregulation, aiming to explain mechanisms involved in early events leading to AD. 30382187: Here we show that the fragments of delta-secretase-cleavage, APP (586-695) and Tau(1-368), additively drive AD pathogenesis and cognitive dysfunctions. 30744518: Given that accumulation of hyperphosphorylated MAPT contributes to the pathogenesis of Alzheimer disease and other tauopathies, decreasing endogenous MAPT levels has been shown to be beneficial to neuronal health in models of these diseases. 30864847: Recent studies imply that sleep-wake cycles affect brain tau more significantly than Abeta levels, leading to accelerated AD progression and cognitive decline. 31016584: As the HIV-infected population is aging, it is becoming increasingly important to understand how HIV-Tat may interact with proteins such as amyloid beta and Tau which accumulate in the aging brain and eventually result in Alzheimer's disease. 31308793: Mitochondrial dysfunction is also a prominent feature in AD, and the extracellular Abeta and phosphorylated tau result in the impaired mitochondrial dynamics. 31524157: This finding provides further evidence for a mechanistic connection between Abeta and tau at seminal stages of AD pathogenesis. 31796124: These findings shed light on early PTM changes of tau during AD pathogenesis in human brains. 7532213: Several PDPKs can phosphorylate tau in vitro and induce Alzheimer-like epitopes to many phosphorylation-dependent antibodies. 7533559: These results suggest that abnormal phosphorylation at Ser-202 of PHF-tau in DNs represents one of the earliest neuropathological changes within the neurites of vulnerable neurons and may have a pivotal role in the initial pathogenesis of AD. 7566354: It is unclear whether levels of nuclear tau can be correlated to pathologic events in AD, but its insoluble nature along with reports of intranuclear PHFs warrant further studies of nuclear tau as a molecular candidate in the genesis of AD. 7822152: PURPOSE: Increased immunoreactivity (IR) of beta-amyloid and the amyloid-associated proteins tau and amyloid precursor protein (APP) in the brain have been linked to the pathogenesis of neurodegenerative disorders such as Alzheimer's disease. 7891887: Isoform-specific interactions of apoE with the microtubule-associated proteins MAP2c and tau might affect intracellular maintenance of microtubules and could contribute to a time-dependent pathogenesis of Alzheimer's disease. 8764598: The ability of GSK-3beta to phosphorylate APPcyt and tau provides a putative link between the two lesions and indicates a critical role of GSK-3beta in the pathogenesis of Alzheimer's disease. 31941827: Here, we reveal a previously unappreciated direct role of norepinephrine signaling in connecting beta-amyloid (Abeta) and tau, two key pathological components of AD pathogenesis. 31961372: Elevation of CSF P-tau appears to precede flortaucipir-PET positivity in the progression of AD pathogenesis and related cognitive decline. 31997800: In this review, we emphasize the recent studies about the toxic and shape-shifting nature of tau in the pathogenesis of Alzheimer's disease. 32226410: Given the importance of tau to AD pathogenesis and therapies, it is important to understand non-classic physiological functions for this protein inside and outside the central nervous system (CNS). 32404183: Under the synergistic effects of T807, T807/RPCNP can not only effectively penetrate the blood-brain barrier (BBB), but they also possess high binding affinity to hyperphosphorylated tau in nerve cells where they inhibit multiple key pathways in tau-associated AD pathogenesis. 32572101: Cellular polyamines condense hyperphosphorylated Tau, triggering Alzheimer's disease. 32649026: Alzheimer's Disease risk modifier genes do not affect tau aggregate uptake, seeding or maintenance in cell models.Alzheimer's disease (AD) afflicts millions of people worldwide and is caused by accumulated amyloid beta and tau pathology. 32780352: Hyperphosphorylation Renders Tau Prone to Aggregate and to Cause Cell Death.Alzheimer's disease (AD) is a neurodegenerative disorder without a cure or prevention to date. 32784025: This review will divulge the importance of tau in AD pathogenesis, the interplay of Abeta and tau, the pathological functions of tau, and potential therapeutic strategies for an effective management of neuronal disorders. 32827351: DISCUSSION: Refining the molecular mechanisms connecting tau, Abeta, and apoE with cerebrovascular pathologies is critical for greater understanding of AD pathogenesis and establishing effective therapeutic interventions for the disease. 32967303: The present review will focus on the mechanisms that lead to cytosolic and especially mitochondrial Ca 2+ disturbances occurring in AD and tau-induced FTD, and propose possible therapeutic interventions for these disorders. 32972344: However, much attention has been given to the link between tau and beta-amyloid hypothesis in AD pathogenesis/prognosis. 33013321: Overexpression of GSK-3beta in Adult Tet-OFF GSK-3beta Transgenic Mice, and Not During Embryonic or Postnatal Development, Induces Tau Phosphorylation, Neurodegeneration and Learning Deficits.GSK-3beta or tau-kinase I is particularly abundant in the central nervous system (CNS), playing a key role in the pathogenesis of Alzheimer's disease (AD). 33168053: Although tau is recognized to play a central role in pathogenesis of AD, the precise mechanisms by which these abnormal PTMs contribute to the neural toxicity of tau is unclear. 33224974: Particularly, the aggregation of misfolded amyloid- beta and hyperphosphorylated tau and alpha -synuclein are linked to the pathogenesis of AD and PD, respectively. 33328854: Neurofibrillary tangles (NFTs) are pathological hallmarks of AD and due to accumulated phosphorylated Tau. 33386802: Such stress provides the activation energy needed to induce conformational changes of both Abeta and tau within the lower brain and brainstem region, producing unique neurotoxic oligomer molecule conformations that induce AD. 33425704: Glycogen synthase kinase 3 beta (GSK3 beta) plays a key role in pathologic hyper phosphorylation of tau and plays an important role in the pathogenesis of Alzheimer's disease. 33560154: Areas covered : Considering the significance of Abeta and Tau in AD pathogenesis, these proteins have currently been adopted as the core biomarkers of AD, and their quantification has provided precise diagnostic information to develop next-generation AD therapeutic approaches. 33665647: Despite a wealth of experimental and genetic evidence implicating both Abeta and tau in the pathogenesis of AD, the precise molecular links between these two pathological hallmarks have remained surprisingly elusive. Here, we review emerging evidence for a critical nexus among Abeta, tau, and the lysosomal protease cathepsin D (CatD) that we hypothesize may play a pivotal role in the etiology of AD. Future research into these novel mechanistic links among Abeta, tau and CatD promises to expand our understanding of the etiology of AD and could potentially lead to novel therapeutic approaches for combatting this devastating disease of brain and mind. 33809978: The self-assembly of tau into paired helical filaments (PHFs) in neurofibrillary tangles (NFTs) is a significant event in Alzheimer's disease (AD) pathogenesis. 34015458: Excessive accumulation of amyloid beta-protein (Abeta) is one of the primary mechanisms that leads to neuronal death with phosphorylated tau in the pathogenesis of Alzheimer's disease (AD). 34283221: On the other hand, ELISAs combining antibodies against the later-middle to C-terminal regions of tau produced substantially increased signals from AD samples, compared to those from non-AD controls. 34738809: This study not only provides a further insight into the involvement of subchronic Cd 2+ exposure in the tau etiology of AD but also offers more comprehensive and effective information about the asymptomatic stage of AD upon environmental risk, which has potential applications in the early diagnosis and therapy. 34751792: The hyperphosphorylation of tau is a central mechanism in the pathogenesis of Alzheimer's disease (AD). 35443153: Amyloid-beta and tau are key molecules in the pathogenesis of Alzheimer's disease, but it remains unclear how these proteins interact to promote disease. 35786817: CONCLUSION: The tau deletion mutation significantly improved the synaptic damage caused by Abeta, and tau protein played an indispensable role in the synaptic dysfunction caused by Abeta, suggesting that Abeta and tau have close interactions in the pathogenesis of AD. 35864434: It boosts the antioxidant enzyme activities, prevents Tau-induced oxidative stress, ameliorates eye degeneration, and inhibits cholinesterase activities in Tau-induced AD model. 35928283: However, it is still not clear to what extent DYRK1A overexpression by itself leads to AD-like phenotypes and how these compare to Tau and Amyloid-beta mediated pathology. 36066633: Amyloid-beta 42 (Abeta42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 36399096: Modulation of the effect of the epsilon4 alleles by TOMM40 and APOC1 variants indicates the potential genetic mechanism of differential roles of Abeta and tau in AD pathogenesis. 36634842: Misfolded hyperphosphorylated tau (p-tau) is considered a pivotal point in the pathogenesis of AD and other tauopathies. 36967088: Extracellular tau has been highlighted in the pathogenesis of Alzheimer disease (AD), which is the most common neurodegenerative disease. 37239068: Emerging evidence over the past few decades supports the critical role of Abeta and tau in AD pathogenesis and the participation of glial cells in different molecular and cellular pathways. 37332018: Therefore, in this review, we will discuss for the first time the importance of truncated tau by caspases activation in the pathogenesis of AD and how its negative actions could impact neuronal function. 37333306: A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. 37371067: Herein, we investigated the effects of TREM2 deficiency on tau spreading using a mouse model in which endogenous tau is seeded to produce AD-like tau features. 37503224: A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. 37777806: Accumulating evidence suggests that TDP-43 and p-tau interact and exhibit pathological synergy during AD pathogenesis. 38110916: The neuronal aggregated tau observed in AD cells suggests that the protein folding problem is a major cause of AD. 38178136: And the relation between the peripheral blood Abeta and tau tangles of brain, another crucial pathologic factor contributing to the pathogenesis of AD, is also ambiguous. In the present review, we summarize recent studies on the roles of peripheral blood Abeta and the peripheral innate immune cells in the pathogenesis of AD. More recently, the anti-Abeta monoclonal antibodies are approved for treatment of AD patients through declining the peripheral blood Abeta mechanism of action to enhance plasma and central nervous system (CNS) Abeta clearance, leading to a decrease Abeta burden in brain and improving cognitive function, which clearly indicates that the levels of the peripheral blood Abeta impacted on the Abeta burden in brain and involved in the pathogenesis of AD. 38238309: A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. 38281031: CONCLUSIONS: This work establishes a tau-induced AD-like NHP model with many key pathological and behavioural features of AD. 38434588: This observation, along with the failure of previous clinical trials targeting Abeta or Tau and the modest success of recent trials using Abeta monoclonal antibodies, has led to a reappraisal of the view that Abeta accumulation is the sole factor in the pathogenesis of AD. 12056828: An abnormal handling of renal magnesium has been suggested to cause salt-sensitive hypertension. 12537992: For the most part, epidemiological and experimental studies demonstrate an inverse association between magnesium and blood pressure and support a role for magnesium in the pathogenesis of hypertension. 15073408: Abnormal magnesium metabolism in etiology of salt-sensitive hypertension and type 2 diabetes mellitus. 15692166: High iCa(2+) has several vasoconstrictive effects which lead to hypertension, an indirect result of low magnesium status. Hypertension occurs when cellular Na:K ratios become too high, a consequence of a high sodium, low potassium diet or, indirectly, through a magnesium deficient state which causes a pseudo potassium deficit. Several studies on the effect of calcium on blood pressure need these added considerations of magnesium status to fully understand the impact of the Mg:Ca ratio as the primary cause of hypertension and other aspects of Syndrome X. 18192217: However, there is still a paucity of information, and much research is needed to clarify the exact mechanisms of magnesium regulation in the cardiovascular system and the implications of aberrant transmembrane magnesium transport in the pathogenesis of hypertension and other vascular diseases. 2280429: The relatively high magnesium concentration in sun evaporated sea salt may play a protective role in hypertension induction. 25560239: To evaluate the relationship between high BP induced by a high sodium (Na) diet and Mg, and other mineral balances, two experimental rat models of salt-sensitive, induced-hypertension were used: Ang-II infused and Dahl salt-sensitive (SS) rats. Blood pressure, magnesium and other mineral balance in two rat models of salt-sensitive, induced hypertension: effects of a non-peptide angiotensin II receptor type 1 antagonist. 2693847: The roles of sodium, potassium and magnesium in the etiology of high blood pressure are reviewed. 3003794: Water hardness may have some effect in reducing hypertension incidence, and any effectiveness would probably result from calcium and magnesium in the drinking water. 30446179: Alterations in metabolic pathways associated with the sensitivity of sodium, potassium, magnesium and calcium may lead to obesity, hypertension, and insulin resistance. 3696313: We conclude that hypercalcemic hypertension is due in part to altered serum magnesium and is prevented if serum magnesium is sustained. 7782801: In conclusion, low serum and dietary Mg may be related to the etiologies of CVD, hypertension, diabetes, and atherosclerosis. 10874605: Such intracellular paradoxical Ca overload as a consequence of nutritional calcium deficiency may give rise to a number of diseases common in old age: hypertension, arteriosclerosis, diabetes mellitus, neurodegenerative diseases, malignancy, and degenerative joint disease. 12147319: Prenatal malnutrition-induced hypertension in young rats is prevented by neonatal capsaicin treatment. 12237175: RESULTS: Intrauterine undernutrition induced hypertension in both male and female offspring, but hypertension was more severe in male rats. CONCLUSION: Our data show that intrauterine undernutrition: (1) induces hypertension both in the male and female offspring, hypertension being more severe in male than in female rats; (2) alters endothelium-dependent responses in aortas from the resulting offspring. 12352311: Intrauterine undernutrition induced hypertension, decreased vasodilation to acetylcholine and bradykinin but did not alter the responses to sodium nitroprusside. 12715270: The evidence thus suggests that prenatal undernutrition may programme renal structure in later life, but that renal programming is not one of the primary mechanisms leading to hypertension. 12883324: Intrauterine undernutrition induced hypertension, and vitamins C or E treatments reduced the blood pressure levels. 14748946: Exposure to undernutrition during fetal life has been proposed as an underlying cause of adult hypertension. 16054555: OBJECTIVES: Pre-natal malnutrition induces hypertension and insulin resistance, pathologies commonly linked to atherosclerotic disease. 16930446: Paraventricular-coerulear interactions: role in hypertension induced by prenatal undernutrition in the rat. 17161436: Intrauterine undernutrition induced hypertension and increased response of mesenteric arterioles to Ang II and decreased vasodilation to Bk and Ach. 17464781: Coerulear activation by crh and its role in hypertension induced by prenatal malnutrition in the rat. 19453078: CONCLUSION: These results indicate that glomerular ultrastructure is not affected by maternal undernutrition and suggest that altered glomerular ultrastructure is not a contributory factor to the pathogenesis of hypertension following maternal undernutrition. 19893499: BACKGROUND: Dietary omega-3 fatty acid deficiency can lead to hypertension in later life; however, hypertension is affected by numerous other dietary factors. 20674672: Prenatal undernutrition induces hypertension later in life, possibly by disturbing the hypothalamo-pituitary-adrenal axis through programming decreased expression of hypothalamic glucocorticoid receptors. A putative role for hypothalamic glucocorticoid receptors in hypertension induced by prenatal undernutrition in the rat. 24227755: This review will address the role of these potential renal mechanisms in the fetal programming of hypertension in experimental models induced by maternal undernutrition, fetal exposure to glucocorticoids, placental insufficiency, and maternal sodium overload in the rat. 25287449: BACKGROUND AND AIMS: Maternal undernutrition induces development of the arterial hypertension. 26635631: This review will address the new insights on the maternal diet induced-hypertension that include the potential role of the phenotypic plasticity, specifically the perinatal protein malnutrition, and sympathetic-respiratory overactivity. New Insights on the Maternal Diet Induced-Hypertension: Potential Role of the Phenotypic Plasticity and Sympathetic-Respiratory Overactivity. Besides, environmental conditions during perinatal development such as maternal malnutrition can program changes in the integration among renal, neural, and endocrine system leading to hypertension. 29277911: Our data argue against an early mechanical cause for the sex differences in hypertension development induced by maternal undernutrition. 31347485: Work in animal models has shown that maternal undernutrition (UN) during pregnancy leads to hypertension in adult offspring, with effects thought to be mediated in part via altered renal function. 37431363: This leads to nutritional deficiencies and insufficient growth environment which results in anemia and hypertensive disorders of pregnancy which are potent risk factors for IUGR. 8086868: OBJECTIVES: To test whether nutrition early in infants' development programmes later blood pressure and whether the reported relation between low birth weight and later high blood pressure is due to poor nutrition or growth before full term. 10730508: The first stage of Alzheimer's disease commonly is marked by anxiety and depression secondary to memory impairment, and delusions. 11966459: Thus far, the clinical utility of muscarinic agonists remains unproven, yet recent studies suggest that muscarinic agonists might be useful in treating not only memory deficits, but also psychiatric disturbances and some of the underlying causes of Alzheimer's disease, such as the deposition of Abeta. 14503018: These preliminary findings may be important in understanding, at least in part, the molecular mechanisms that precede memory impairment during chronic brain ischemia and as such, the pre-clinical stage leading to Alzheimer's disease. 17197420: First, conditional inactivation of PS in the adult mouse brain causes progressive memory loss and neurodegeneration resembling AD, whereas mouse models based on overproduction of Abeta have failed to produce neurodegeneration. Based on these and other observations, we propose that partial loss of PS function may underlie memory impairment and neurodegeneration in the pathogenesis of AD. 21535936: Since Abeta and glucocorticoids increase with aging, DEX potentiating Abeta-induced learning and memory impairment may be one of the etiology of Alzheimer's disease. 22886562: This article systematically delineates the steps in the complex cascade leading to AD, focusing on pathology caused by chronic intermittent hypoxia, hypertension, brain hypoperfusion, glucose dysmetabolism, and endothelial dysfunction. Owing to the pathological impact of hypoxia, hypertension, hypoperfusion and impaired glucose metabolism, the adverse cardiovascular, neurocirculatory and metabolic consequences upregulate amyloid beta generation and tau phosphorylation, and lead to memory/cognitive impairment-culminating in AD. 25788560: Paradoxically, we found an attenuated stimulus-response function, compared to controls, suggesting that AD dementia interferes with pain ratings over time, most likely due to memory impairment. 26724580: These pathological changes have complex internal relations with one other, causing memory impairment and participating in the pathogenesis of Alzheimer's disease (AD). 28159908: Amyloid-beta (Abeta) peptides play a key role in synaptic damage and memory deficits in the early pathogenesis of Alzheimer's disease (AD). 32198621: Hyperglycemia is one of the major risk factors responsible for memory impairment in diabetes which may lead to Alzheimer's disease (AD) at a later stage. 34102642: These may be explained whereby awareness of/fear of falling increases with AD due to a preserved emotional awareness, whereas awareness of cognitive impairment is impaired due to memory deficits. 36116555: In addition, MT exerted a superior effect on ameliorating the learning ability of senescence-related and metabolic AD models, and corrected the memory deficit of the toxin-induced AD model. 36915078: Alzheimer's disease (AD) is the most prevalent cause of dementia and is primarily associated with memory impairment and cognitive decline, but the etiology of AD has not been elucidated. 37627238: Since A 2A R overfunction is sufficient to trigger memory deficits, we tested if A 2A R were upregulated in hippocampal synapses before the onset of memory deficits to support the hypothesis that A 2A R overfunction could be a trigger of AD. 37685895: SAMP8 mice have been proposed as a model for studying late-onset AD, since they show age-related learning and memory deficits as well as several features of AD pathogenesis. 38532080: In the context of Alzheimer's disease, this is particularly relevant for patients who seek medical advice due to memory problems. 32982937: As AD results in a complex disease process for cognitive decline, various theories have been suggested as the cause of AD. 36195639: Associations of higher brain copper levels with slower cognitive decline and with less AD pathology support a role for copper dyshomeostasis in AD pathogenesis and suggest that lower brain copper may exacerbate or indicate disease severity. 36336928: OBJECTIVE: Investigating brain topologies would help to mine the neuromechanisms of SCD and provide new insights into the pathogenesis of AD. 36915078: Alzheimer's disease (AD) is the most prevalent cause of dementia and is primarily associated with memory impairment and cognitive decline, but the etiology of AD has not been elucidated. 37074955: Exposure to traffic-related air pollution consisting of particulate matter (PM) is associated with cognitive decline leading to Alzheimer's disease (AD). 37310581: Thus, this study showed that the decline in renal function was correlated with abnormal AD biomarkers and cognitive decline, which provides human evidence that renal function may be involved in the pathogenesis of AD. 37349795: Increasing the number of participants with harmonized cognitive domain scores will enhance the discovery of additional genetic factors of cognitive decline leading to AD and related dementias. 38139415: It appears that the dynamics of AbetaPP-derived i Abeta accumulation is the determining factor that either drives Aging-Associated Cognitive Decline (AACD) and triggers AD or confers the resistance to both. 38334675: Cathepsin B (CatB) is thought to be essential for the induction of Porphyromonas gingivalis lipopolysaccharide ( Pg LPS)-induced Alzheimer's disease-like pathologies in mice, including interleukin-1beta (IL-1beta) production and cognitive decline. 38460555: Alzheimer's disease (AD) poses a complex challenge, with abnormal protein accumulation in the brain causing memory loss and cognitive decline. 38593020: Index Terms- Cognitive impairment, longitudinal data, multimodal data, encoder-decoder LSTM, progression prediction Clinical relevance The proposed approach has the potential to improve understanding of Alzheimer's disease progression in diagnostics, facilitating early identification of various stages of cognitive decline leading to AD by considering its clinical variability. 38639833: CMHs are closely associated with accelerated cognitive decline and are increasingly recognized as key contributors to the pathogenesis of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). 17593691: Hypertension is caused by metabolic syndrome. 17934392: Dysregulation of these adipokines contributes to the pathogenesis of the obesity-associated metabolic syndrome, resulting in insulin resistance, type 2 diabetes, hypertension, hyperlipidemia, and vascular disease. 18282589: The established synergy between obesity and low nephron number on induction of high blood pressure and further decline of renal function identifies subjects with obesity, metabolic syndrome and diabetes mellitus II as particularly susceptible groups. 18800141: Our study shows that in human hypertension, structural and functional cardiac changes induced by MS are not limited to the LV but also involve the right one. 18854744: As fructose-rich diets increase uric acid levels, hyperuricemia may also play a role in the metabolic syndrome, triggering insulin resistance and hypertension.A number of studies on rats rendered hyperuricemic by administration of uricase inhibitors have recently confirmed induction of arterial hypertension and microvascular injury, particularly in the remnant kidney or in cyclosporine-induced renal fibrosis. 19462174: Obese females are at higher risk for metabolic syndrome due to severe hyperandrogenemia, which also leads to high blood pressure. 19702117: Dysregulation of adipocytokines secreted by adipose tissue may play an important role in the development of the obesity-associated metabolic syndrome, resulting in insulin resistance, type 2 diabetes, hypertension, hyperlipidemia, and vascular disease. 22538946: This clinical and social problem is mainly related to the ongoing epidemic of obesity and metabolic syndrome resulting in hypertension and diabetes mellitus. 24162600: Metabolic syndrome caused by abdominal fat accumulation induces diabetes mellitus, dyslipidemia, and hypertension, resulting in an increase in cardiovascular diseases. 24798707: Metabolic syndrome induces hypertension and commonly results in renal damage. 29062182: We conclude, Diabetes and Hypertension are indeed prevailing in Sikkim and that the presence of either an increased waist circumference or an elevated blood pressure mandates a check for the remaining four risk factors for MetS, rendering worthwhile to keep an account of MetS risk types by stratification to comprehend the influence of socio-cultural and ethno-geographical factors in causing MetS. 29127233: Sympathetic hyperactivation, a common feature of obesity and metabolic syndrome, is a key trigger of hypertension. 29731021: Finally, obesity and the metabolic syndrome, through their effects on various hormones and inflammation, might also contribute to the pathogenesis of hypertension and diabetes. The renin-angiotensin-aldosterone system may be upregulated in diabetes, leading to hypertension through a direct effect mediated by angiotensin II, as well as indirectly through upregulation of sympathetic activity. 7995275: Candidate mechanisms whereby this metabolic syndrome might lead to hypertension include renal sodium retention, vascular hyperresponsiveness, arteriolar smooth muscle cell proliferation, altered cellular electrolyte transport and composition, stimulation of sympatho-adrenergic activity and growth promoting effects. 15105262: The emergence of redox-active metals as key players in AD pathogenesis strongly argues that amyloid-specific metal-complexing agents and antioxidants be investigated as possible disease-modifying agents for treating this horrible disease. 16672274: The conformational change and associated aggregation of beta amyloid (Abeta) with or without metals is the main cause of Alzheimer's disease (AD). 17522444: The role of metals in the etiology of Alzheimer's disease. 17612380: OBJECTIVE: Aluminium has lately been implicated as one of the possible causal factors contributing to Alzheimer's disease and other neurodegenerative disorders due to this metal is conducive to oxidative stress in the brain. 18228200: Aluminium exposure induces Alzheimer's disease-like histopathological alterations in mouse brain. Aluminium (Al) is a neurotoxic metal and Al exposure may be a factor in the aetiology of various neurodegenerative diseases such as Alzheimer's disease (AD). 18376063: Recent studies also point to redox active metals such as iron, copper and zinc in mediating oxidative stress in AD pathogenesis. 20308778: Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia, and several studies have also identified metals such as Pb, Fe, Al, Cu, and Zn in AD pathogenesis. 21303349: Despite the crucial role of redox active metals like copper and iron in central biological reactions, their elevated levels are involved in the pathogenesis of Alzheimer's Disease (AD). Iron, copper, and zinc are some of the metals, which intensify this process and contribute for the pathogenesis of AD. 22342404: Exposure to environmental neurotoxic metals, pesticides and other chemicals is increasingly recognized as a key risk factor in the pathogenesis of chronic neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. 22370090: The key points of this review are that metals are implicated in the etiology or pathogenesis of Alzheimer's disease and other protein folding disorders, metals induce the expression GRP78, often associated with oxidative stress, some metals bind to GRP78, and lead (Pb) impairs GRP78 function when it binds to GRP78. 24682942: This metal progressively accumulates in the pathogenesis of Alzheimer's (AD) and Parkinson's (PD) diseases. 25894020: The present studies utilized synchrotron radiation X-ray fluorescence (SRXRF) and focused primarily on zinc and iron, two abundant metals in neurons that have been implicated in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. 30598025: Moreover, it is already established that metals (particularly copper, zinc and iron) have a key role in the pathogenesis of AD. 34502369: The existing data also demonstrate that AGE toxicity seems to mediate the involvement of copper (Cu) and potentially other metals in AD pathogenesis. 35727933: Disruption of the homeostasis of redox-active metals, iron and copper, is an integral part of the pathogenesis of Alzheimer's disease and Parkinson's disease. 36613911: To further assess the involvement of heavy and essential metals in AD pathogenesis, we compared cerebrospinal fluid (CSF) AD biomarkers to macro- and microelements measured in CSF and plasma. 7866588: Substantial evidence has accumulated implicating metals and free radicals in the pathogenesis of the major neurodegenerative disorders (Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis). 22042811: Renin, CD36, and other mRNAs, as well as miRNAs and associated pathways identified in the present study, provide novel insights into hypertension etiology. 22052337: The elucidation of these processes regulated by microRNAs and the identification of novel microRNA targets in the pathogenesis of hypertension is a highly valuable and exciting strategy that may eventually led to the development of novel treatment approaches for hypertension. 24946537: The elucidation of these processes regulated by miRNAs and the identification of novel miRNA targets in the pathogenesis of hypertension is a highly valuable and exciting strategy that may eventually led to the development of novel treatment approaches for hypertension. 25228951: Elucidation of the relationship between exercise training and miRNAs in the pathogenesis of hypertension is fundamental in order to understand how exercise modulates the cardiovascular system at genetic level. 25828869: This review highlights recent updates on the significance of non-coding RNAs such as micro RNAs and long non-coding RNAs (lncRNAs) on the pathogenesis of hypertension, also providing an introduction to basic biology of noncoding RNAs. 26004493: A growing body of recent research indicates that miRNAs are important in the pathogenesis of arterial hypertension. 28287884: OBJECTIVES: The role of microRNAs (miRs,miRNAs) in the pathogenesis of cardiovascular diseases such as hypertension, as well as their diagnostic potential, has recently attracted much attention. 29434681: Previous studies have indicated that microRNAs (miRNAs/miRs) may participate in the pathogenesis of hypertension. 30298350: Recent research progress of microRNAs in hypertension pathogenesis, with a focus on the roles of miRNAs in pulmonary arterial hypertension. 31919615: Differential miRNA expression analysis of extracellular vesicles from brain microvascular pericytes in spontaneous hypertensive rats.OBJECTIVE: This study is to explore the exact roles of extracellular vesicle (EVs) miRNAs from brain microvascular pericytes in the pathogenesis of hypertension. 34944415: In hypertension, microRNAs act on the renin-angiotensin-aldosterone system, sympathetic nervous system and left ventricular hypertrophy, however the signaling pathways that interact in these processes and are regulated by microRNAs inducing hypertension and the worsening of the disease still need to be elucidated. 34988135: Conclusions: Our results demonstrated for the first time that circRNAs are expressed aberrantly in aortic vascular tissues of hypertensive rats and may serve as a sponge linking with relevant miRNAs participating in pathogenesis of hypertension and related ischemic heart diseases via the circRNA-miRNA-mRNA ceRNAnetwork mechanism. 36200021: And these three miRNAs may serve as biomarkers to provide clues to the potential pathogenesis of H-type hypertension. 18525125: We used experimental validation in addition to literature to reveal how the deregulated brain microRNAs are biomarkers for known and novel pathways in AD pathogenesis related to amyloid processing, neurogenesis, insulin resistance, and innate immunity. 21945006: Aberrant expression and dysfunction of brain-enriched miRNAs induce development of neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD). This review is conducted to summarize accumulating studies focused on aberrant miRNA expression in AD brains, and to propose the systems biological view that abnormal regulation of cell cycle progression as a result of deregulation of miRNA target networks plays a central role in the pathogenesis of AD. 22985563: OBJECTIVE: To observe the changes of miRNA expression profiles in APPswe/PSdeltaE9 transgenic mice and explore the possible roles of miRNA in the pathogenesis of Alzheimer's disease. 23443129: These results demonstrated that oxidative stress alters the miRNA expression profile of hippocampal neurons, and the deregulated miRNAs might play a potential role in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD). 23450482: Research on microRNA will facilitate in depth understanding of the pathogenesis of Alzheimer's disease. 23922807: Pathway analysis, taking into account enriched target mRNAs for these signature miRNAs was also carried out, suggesting that the disturbance of multiple enzymatic pathways including lipid metabolism could play a role in AD etiology. 23962497: In conclusion, the abnormal expression of several miRNAs in hippocampus of intermediate- and late-stage AD patients suggests their involvement in AD pathogenesis, and low levels of miR-146a in CSF were associated with AD. 24027266: MicroRNA (miRNA) functions in the pathogenesis of major neurodegenerative diseases such as Alzheimer's disease (AD) are only beginning to emerge. 24423585: Oxidative stress plays a critical role in the etiology and pathogenesis of Alzheimer's disease (AD), and the molecular mechanisms that control the neuron response to oxidative stress have been extensively studied. These results suggested that oxidative stress alters the miRNA expression profile of hippocampal neurons, and the deregulated miRNAs might play potential roles in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD). 26345540: Recent efforts have revealed the microRNA (miRNA) pathways in the pathogenesis of Alzheimer's disease (AD). 26402112: Dysregulation of specific miRNAs leads to impaired synaptic plasticity resulting in Alzheimer's disease (AD). 26708942: This article also highlights Drp1 and its relationships to glycogen synthase kinase 3, cyclin-dependent kinase 5, p53, and microRNAs in AD pathogenesis. 26856603: miR-603, a novel primate-specific miRNA and an intronic miRNA of a human brain highly expressed gene KIAA1217, is implicated in the risk and pathogenesis of AD. 27213057: Our data implicate dysregulation of miRNA methylation as contributor to the pathogenesis of AD. 27396304: Recently, an increasing number of studies revealed that the dysregulation of microRNAs (miRNAs) may be involved in the etiology of cognitive disorders as Alzheimer, Parkinson, and Huntington's diseases, Schizophrenia and Autism spectrum disorders. 27964992: This review briefly describes the studies on changes in the expressions of microRNAs in the pathogenesis of AD. 30881384: AD is a multifactorial disorder, and accumulating evidence shows that microRNAs play a critical role in the pathogenesis of AD. 30887246: Recently, non-coding RNAs such as microRNAs (miRNAs) and circular RNAs (circRNAs) have been reported to contribute to the pathogenesis of AD. 30890906: There is also emerging evidence that miRNAs play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD) or Parkinson's disease (PD). 31685236: The role of microRNAs (miRNAs) in the pathogenesis of Alzheimer's disease (AD) is currently extensively investigated. 31965936: We found that 3, 11, or 8 neuronal development related miRNAs from the brain tissue, 13, 16 or 14 miRNAs from the blood of patient with AD, depression and schizophrenia respectively were also involved in radiation-induced brain pathological changes, suggesting a possibly specific involvement of these miRNAs in radiation-induced development of AD, depression and schizophrenia respectively. 33220166: BACKGROUND: Numerous microRNAs (miRNAs) have been identified as functional molecules in Alzheimer's disease (AD) pathogenesis. 33307856: OBJECTIVE: It is believed that microRNAs (miRNAs) participate in the pathogenesis of Alzheimer's disease (AD), but the specified function of miR-10b-5p in the disease has not been thoroughly understood. 33529652: Non-coding microRNAs (miRNAs or miRs) have been linked to the pathogenesis of AD. 33548978: Many studies have shown that microRNAs (miRNAs) are implicated in the pathogenesis of AD, and alterations of their levels in blood make them potential biomarkers for AD. 33672031: Cx/Panx HCs are also expressed by astrocytes and are likely involved in the release of critical toxic amounts of soluble factors-such as glutamate, adenosine triphosphate (ATP), complement component 3 derivate C3a, tumor necrosis factor (TNFalpha), apoliprotein E (ApoE), and certain miRNAs-known to play a role in the pathogenesis of AD, ALS, and other neurodegenerative disorders. 33771994: Aberrant regulation of microRNAs (miRNAs) has been implicated in the pathogenesis of Alzheimer's disease (AD), but most abnormally expressed miRNAs found in AD are not regulated by synaptic activity. 33790780: The Eminent Role of microRNAs in the Pathogenesis of Alzheimer's Disease. 35273693: In order to further understand the potential roles of miRNAs in the pathogenesis of AD, we analyzed Down syndrome (DS), a special model of AD, by using a TaqMan microRNA array and found that miRNA let-7c was up-regulated in both DS and AD. 35532940: BACKGROUND: Roles for extracellular vesicles (EVs) enriched with micro-RNAs (miRNAs) have been proposed in Alzheimer's disease (AD) pathogenesis, leading to the discovery of blood miRNAs as AD biomarkers. 35615589: Deciphering the Link Between ER UPR Signaling and MicroRNA in Pathogenesis of Alzheimer's Disease. 35783137: To identify the AD-specific differentially expressed miRNAs and mRNAs, we used bioinformatics analysis to study candidate miRNA-mRNA pairs involved in the pathogenesis of AD. 35993941: MicroRNAs are reported to correlate with synaptic plasticity and exert functions in Alzheimer's disease (AD) pathogenesis. 36110561: Several lncRNAs and miRNAs play crucial roles in both these hallmarks of the AD pathogenesis and other AD-related pathological procedures such as neuronal and synaptic plasticity, neuroinflammation, neuronal differentiation and neuronal apoptosis. 36453506: Finally, we constructed lncRNA-miRNA-mRNA and lncRNA-mRNA co-expression networks to reveal the potential regulator roles in AD pathogenesis. 36902178: The aim of this review was to describe the molecular interactions between miRNAs and MAPKs during AD pathogenesis by selecting evidence from experimental AD models. 38501059: Mounting evidence has revealed critical roles of microRNAs (miRNAs) in AD pathogenesis; however, the miRNAs directly targeting presenilin1 ( PSEN1 ), which encodes the catalytic core subunit of gamma-secretase that limits the production of Abeta from amyloid precursor protein (APP), are extremely understudied. 38516808: RESULTS: Molecules involving in OLs' differentiation or maturation, including various transcriptional factors, cholesterol homeostasis regulators, and microRNAs could also participate in the pathogenesis of AD. 38558361: The interconnectedness between membrane transporters (SLCs) and microRNAs (miRNAs) in AD pathogenesis has gained increasing attention. 10074485: Deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. 10489390: Failure to convert cortisol to cortisone in mineralocorticoid-sensitive tissues permits cortisol to bind to and activate mineralocorticoid receptors, causing hypervolemic hypertension. 10884226: We describe a mutation in the mineralocorticoid receptor (MR), S810L, that causes early-onset hypertension that is markedly exacerbated in pregnancy. 11857927: The amino acid substitution of the ligand-binding domain(S810L) of the MR resulted in the early-onset hypertension exacerbated by pregnancy. 1474763: (1) Decreased 11 beta-OHSD activity permits binding of cortisol to the Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid excess (AME). 15242344: An activating mutation in the MR gene causing early-onset, periodic hypertension was reported recently. 15478032: Decreased activity of this isozyme in the kidney, either congenitally in Apparent Mineralocorticoid Excess syndrome or acquired following licorice consumption, allows cortisol access to the MRs, resulting in hypokalemic hypertension. 15718388: In this disorder, cortisol is not inactivated by 11betaHSD2, occupies mineralocorticoid receptors (MRs), and causes excessive sodium retention and hypertension. 15908963: The S810L mutation within the human mineralocorticoid receptor (MR S810L) induces severe hypertension and switches progesterone from antagonist to agonist. 16419642: A gain-of-function mutation resulting in the S810L amino acid substitution in the hormone-binding domain of the mineralocorticoid receptor (MR, locus symbol NR3C2) is responsible for early-onset hypertension that is exacerbated in pregnancy. 16980198: Lack of adrenal steroids in Addison's disease causes life-threatening hypotension, whereas glucocorticoid excess in Cushing's syndrome invariably results in high blood pressure. Mutations in the 11beta-HSD2 gene cause a rare form of inherited hypertension, the syndrome of apparent mineralocorticoid excess (AME), in which cortisol activates the MR resulting in severe hypertension and hypokalemia. 18495825: These data suggest that in Wistar rats, an increase in CSF [Na+] may increase the biosynthesis of corticosterone and aldosterone in the hypothalamus, and mainly aldosterone activates MR in the CNS leading to sympathetic hyperactivity and hypertension. 21207253: In a subgroup of individuals with metabolic syndrome, adipocyte-derived aldosterone-releasing factors cause inappropriate secretion of aldosterone in the adrenal glands during salt loading, resulting in the development of salt-induced hypertension and cardiac and renal damage. Such a local control system for MR can also be relevant to the pathogenesis of salt-sensitive hypertension, and future studies will clarify the detailed mechanism for the intricate regulation of the aldosterone/MR cascade. 22752520: Among them, we have identified that rac1, a small GTPase, activates mineralocorticoid receptor in aldosterone-independent fashion and induces salt-sensitive hypertension in several rodent model. 22843494: However, inappropriate activation of MR within these tissues, and especially in the brain, causes hypertension and pathological vascular, cardiac, and renal remodeling. 23665601: Mutations in this gene affect the enzymatic activity resulting to an excess of cortisol, which causes its inappropriate access to mineralocorticoid receptor leading to inherited hypertension. 24111570: In this rat strain, activation of MR in the distal nephron causes salt-induced hypertension. 27760997: Notably, salt loading increases renal Rac1 activity in several models of salt-sensitive hypertension, which, in the presence of aldosterone, synergistically activates MR signaling, causing hypertension and kidney injury. This crosstalk pathway promotes glomerular podocyte injury, and is also involved in the pathogenesis of hypertension. 37059378: Blockade of MR prevented ethanol-induced hypertension and hypercontractility of endothelium-intact and -denuded aortic rings. 7670488: Human hypertension caused by mutations in the kidney isozyme of 11 beta-hydroxysteroid dehydrogenase. They thus permit cortisol to occupy the renal mineralocorticoid receptor and thereby cause sodium retention and hypertension. 9370341: Mutations of the gene encoding 11beta-HSD-2 are responsible for the syndrome of apparent mineralocorticoid excess, in which cortisol illicitly occupies mineralocorticoid receptors, causing hypertension and hypokalaemia. 1014711: Since patients with low renin and high rectal P.D. responded favourably to spironolactone therapy it is suggested that mineralocorticoids other than aldosterone may contribute to the pathogenesis of the hypertension in these cases. 11353575: The evolution of selective aldosterone receptor antagonists will help us understand the role that mineralocorticoids play in the pathogenesis of hypertension, heart failure, and atherosclerosis. 12092066: Inhibition of the enzyme allows cortisol to act as the major endogenous mineralocorticoid producing a marked elevation in mineralocorticoid activity, resulting in hypertension, hypokalaemia and metabolic alkalosis. 1237495: In order to study the metabolism of 18-OH-11-deoxycorticosterone, the mineralocorticoid hormone responsible for hypertension in rats and humans, we have synthesized the following dihydrogenated and tetrahydrogenated reference derivatives: 18,21-dihydroxy-5alpha-pregnane-3,20-dione, 18,21-dihydroxy-5beta-pregnane-3,20-dione, 3alpha,18,21-trihydroxy-5alpha-pregnan-20-one (I), 3beta,18,21-trihydroxy-5alpha-pregnan-20-one (II), 3alpha,18,21-trihydroxy-5beta-pregnan-20-one (III) and 3beta,18,21-trihydroxy-5beta-pregnan-20-one (IV). 1312541: These results cannot be explained by receptor down-regulation due to higher levels of mineralocorticoids in PIH; a hitherto unknown mineralocorticoid may, thus, be responsible for the hypertension and altered MR status. 1524765: Results indicate a high probability that certain mineralocorticoids, which are inactive by themselves, might play a role in the etiology of hypertension when acting together under physiological conditions. 1531344: We examined changes in the expression of fibronectin during the induction of cardiac hypertrophy by L-triiodothyronine administration and by mineralocorticoid- and salt-induced experimental hypertension. 15666838: In conclusion, a possible direct link exists between fat tissue metabolism and adrenal mineralocorticoid secretion that may be responsible for obesity-related hypertension. 16990342: The pathophysiological consequences of excess mineralocorticoid for salt status include hypertension, vascular inflammation, and cardiac fibrosis. 18697839: Thus, reduced GR density balanced by HPA activation leaves glucocorticoid functions unaffected but mineralocorticoid functions increased, causing hypertension. 20197673: An increased production of mineralocorticoids often leads to hypertension and hypokalemia in both sexes. 21045727: Here, we tested whether hypertension in this model is due to increased renal mineralocorticoid activity. 23318820: CONCLUSION: The dissociation of the antihypertensive response to the blockades of Ang II receptors and mineralocorticoid indicates the involvement of Ang II in the pathogenesis of hypertension associated with obesity. 23378101: The combination of the aforementioned observations underscores the importance of the mineralocorticoid pathway in the pathogenesis of hypertension. 23698003: We propose that a similar clinical trial is warranted in order to definitively clarify the role of inappropriate mineralocorticoid activity in the etiology of human obesity-associated hypertension. 3019053: Glucocorticoid, unlike mineralocorticoid, induced hypertension is not affected by a reduction in renal mass or increased sodium intake. 3078732: The data implicate the involvement of the renin-angiotensin-aldosterone system, the direct effects of mineralocorticoids, and the adrenergic nervous system in the etiology of high blood pressure under OC use. 31358067: Inhibition of 17alpha-hydroxylase causes low levels of cortisol and high levels of adrenocorticotropic hormone in the blood as well as excessive levels of mineralocorticoids that lead to hypertension and hypokalemia. 3170609: Hypertension induced by mineralocorticoids or infusion of angiotensin II caused a marked suppression of kidney FABP expression, whereas amounts of heart FABP in kidney were unchanged. 3284355: The data acquired in these studies agree with the notion that excess mineralocorticoid production causes hypertension by mechanisms that influence the neurohormonal control of blood pressure by the central nervous system. In this article we summarize studies of the hemodynamic and endocrine effects of desoxycorticosterone (DOC)-induced hypertension in dogs and also review new data of the action of this steroid on baroreceptors. 3415809: There is a high probability that certain mineralocorticoids, which are inactive by themselves, are of importance in the etiology of hypertension under physiological conditions. 3553488: We hypothesize the SHR have a genetically determined, generalized membrane defect of increased Na+ permeability, not unlike that which is inducible by excessive exogenous mineralocorticoid and which accompanies the hypertension induced by mineralocorticoids. 3610293: Resistance to mineralocorticoid-induced hypertensive vascular disease. 3762307: Previously, altered aldosterone binding to corticoid receptor I was found in aortic smooth muscle cells cultured from Fischer 344 rats which are extremely resistant to steroid and salt induced hypertension. Rat models of genetic hypertension include spontaneous hypertension and resistance or sensitivity to mineralocorticoid and salt induced hypertension. 3826386: The downregulation observed would be expected to diminish the ability of ANG II to influence glomerular hemodynamics in models such as mineralocorticoid and glucocorticoid-induced hypertension. 3952474: Recent progress in the diagnostic work-up of secondary forms of arterial hypertension caused by mineralocorticoids or catecholamines excess is briefly reviewed. 4556934: Adrenal mineralocorticoids causing hypertension. 533676: Cortisol at 20 mg/hr produced hypertension (MAP + 25 mm Hg on day 5, p less than 0.01) but also produced the 'mineralocorticoid' effect of severe hypokalaemia. These results supported the contention that ACTH induced hypertension in sheep represents a mechanism different from a simple 'mineralocorticoid' or 'glucocorticoid' action. 6206354: Changes in ion transport across the cell membranes have been demonstrated even before the development of hypertension, especially the forms caused by mineralocorticoids or genetic factors. 6369502: The authors hypothesize that AH in the remaining 30% of the hypercorticism cases in this study is due to other mineralocorticoids in excess and suggest that the treatment should be pathogenic and strictly individualized. 6480807: 18-Oxocortisol excretion is increased markedly in the urine of patients with GSA: what role this relatively weak mineralocorticoid plays in the pathogenesis of their hypertension is unknown. 6625419: The same mineralocorticoids are responsible for the hypertension in congenital 11-beta-hydroxylase defects (where virilism is present) and congenital 17-alpha-hydroxylase defects (where impuberism is present). 8386933: Perhaps deoxycorticosterone or a hitherto unknown mineralocorticoid is responsible for the hypertension and altered MR-status. 8538347: Thus, in patients with congenital deficiency of 11 beta-HSD (the syndrome of apparent mineralocorticoid excess, AME), cortisol and not aldosterone acts as a mineralocorticoid, resulting in hypertension and hypokalaemia with suppression of the renin-angiotensin-aldosterone axis. 8903626: CONCLUSION: These results demonstrate that hypertension due to excess mineralocorticoids is characterized by an increase in the gain of the baroreceptor-heart rate reflex. However, the nature of the baroreceptor-heart rate reflex in hypertension due to excess mineralocorticoid has never been fully explored. 9221270: When 11 beta-OHSD activity is impaired, cortisol acts as a potent mineralocorticoid and causes hypertension and hypokalemia with a suppression of the renin-angiotensin-aldosterone system. 10880397: Endocytosis is critical to the function and fate of molecules important to Alzheimer's disease (AD) etiology, including the beta protein precursor (betaPP), amyloid beta (Abeta) peptide, and apolipoprotein E (ApoE). 11785012: INTRODUCTION: With their discovery in 1995, presenilins were put forward as molecules of unknown function but central to the aetiology of Alzheimer s disease. 12826739: It has been suggested that a number of molecules associated with inflammation are involved in the pathogenesis of Alzheimer's disease (AD). 15004329: AIDA-1 proteins are expressed at high levels in the brain; thus, studying their involvement in AbetaPP processing and AID function might give new insights regarding a possible role for these molecules in normal brain development and in the pathogenesis of AD. 17644432: The beta-amyloid peptide (A beta) is widely considered to be the molecule that causes Alzheimer's disease (AD). 21380836: In this regard, recent studies have shown that molecules involved in the pathogenesis of Alzheimer's disease (AD) in fact have a synaptic location. 22675504: We also demonstrate a slower turnover rate for CSF ApoE than that for amyloid beta, another molecule critically important in AD pathogenesis. 24130920: Amyloid-beta peptide (Abeta) is still best known as a molecule to cause Alzheimer's disease (AD) through accumulation and deposition within the frontal cortex and hippocampus in the brain. A series of studies on Abeta clearance mechanism provide new insight into the pathogenesis of AD at the molecular level and suggest a new target for the development of novel therapeutics. 2507928: The regulation of extracellular proteolysis by PN-II and the deposition of at least parts of the molecule in senile plaques is consistent with previous reports that implicate altered proteolysis in the pathogenesis of Alzheimer's disease. 25675299: Given the dual behavior of this molecule, there is some controversy regarding its contribution to the pathogenesis of AD. 26934981: Our recent work has shown that the intracellular domain of the amyloid precursor protein (APP), a molecule central to the aetiology of Alzheimer's disease binds to VAC14 and enhances PIKfyve function. 29729150: These molecules can mediate neuron-microglia interactions in a contact-dependent manner and contribute to the pathogenesis of AD. 30770921: Because the blood-brain barrier tightly regulates the exchange of molecules between brain and blood and maintains brain homeostasis, its impairment is increasingly recognized as a critical factor contributing to Alzheimer's disease pathogenesis. 32123823: As the number of stored light chains in the above protein bank has reached the hundreds, in this study, we screened them against amyloid-beta (Abeta), which is well-known as one of the molecules causing Alzheimer's disease. 35791032: Specifically, we delineate how various aspects of the brain immune microenvironment, including immune gateways, immune cells, and molecules, and the interplay between immune cells and neural cells, accelerate AD pathogenesis during aging. 36140198: Despite these possibilities, improved knowledge of the relative contribution of the different innate immune cells and molecules comprising the chronically inflamed brain network to AD pathogenesis, and elucidation of the network hierarchy, are needed for planning potent preventive and/or therapeutic interventions. 37569296: In this review, we focus on the role of cells (microglia, astrocytes, and oligodendrocytes) and molecules (TREM2, tau, and beta-amyloid) of the innate immune system in the pathogenesis of Alzheimer's disease and their possible exploitation as disease biomarkers and targets of therapeutical approaches. 9015824: The main objective of the manuscript is to review the current progress in understanding the functions of apoE in the nervous system and how malfunctioning of this molecule might result in neurodegenerative disorders such as Alzheimer's disease. 9206974: A number of molecules have been implicated in the pathogenesis of Alzheimer's disease. 9298769: Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology of Alzheimer's disease, served as a model to investigate the developmental and protective effects of SNV. 10097182: The role of ENaC in Na+ homeostasis and in the control of blood pressure has been demonstrated recently by the identification of mutations in ENaC beta and gamma subunits causing hypertension. 10736609: Studies in familial and experimental hypertension reveal that elevated blood pressure is due to mutations in genes implicated in the function of the renin-angiotensin-aldosterone system. 10760060: Mutations in genes encoding ENaC subunits are causative for two human inherited diseases: Liddle's syndrome, a severe form of hypertension associated with ENaC hyperfunction, and pseudohypoaldosteronism (PHA-1), a salt-wasting syndrome caused by decreased ENaC function. 10988280: This is the first report showing direct evidence that hypertension is triggered by a mutation in the adducin gene family. 11228173: Liddle's syndrome is a rare form of hereditary hypertension caused by mutations of the epithelial sodium (Na(+)) channel (ENaC). 11284421: Mutations of mineralocorticoid receptor may cause hypertension in pregnancy and progesterone receptors have several isoforms. 11408395: Recently, mendelian forms of hypertension have demonstrated that mutations that increase renal salt balance lead to higher blood pressure, suggesting that mutations that decrease the net salt balance might have the converse effect. 11496062: In this review, the mechanism by which the mutation causes hypertension, and the implications these findings have for improved understanding of cardiovascular physiology and mineralocorticoid receptor biology, are discussed. 11498583: Human hypertension caused by mutations in WNK kinases. 12166403: Human hypertension caused by mutations in WNK kinases. 12180079: If this is reflected in larger studies, and the link with hypertension is maintained in the Ghanaian population, this mutation could be a significant cause of hypertension in Ghana. 12473849: A new twist on hypertension-causing mutations in the epithelial Na+ channel. 12473861: BACKGROUND: Liddle syndrome is an autosomal dominant form of salt-sensitive hypertension caused by mutations in the epithelial sodium channel expressed in the distal nephron playing an essential role in Na absorption. 12626479: We are using a phenotype-driven approach to identify mutations leading to atherosclerosis, hypertension, obesity, blood disorders, lung dysfunction, thrombosis, and disordered sleep. 12684839: hNedd4 associates with the epithelial sodium channel and mutations disrupting this interaction lead to Liddle's syndrome, a heritable hypertension. 12759227: Liddle's syndrome is a monogenic form of hypertension caused by mutations in the PY motif of the COOH terminus of beta- and gamma-epithelial Na+ channel (ENaC) subunits. 12764146: Mutations in ENaC cause severe hypertension or salt wasting in humans; and consequently, ENaC activity is tightly controlled. 12937297: The Liddle syndrome is a dominant form of salt-sensitive hypertension resulting from mutations in the beta or gamma subunit of ENaC. 14732482: Reduced activity due to inhibition or mutations of 11 beta-HSD2 leads to hypertension and hypokalemia resulting in the Apparent Mineralocorticoid Excess Syndrome (AMES). 15696009: A rare form of monogenic hypertension is familial hyperkalemia and hypertension, which is caused by mutations in the kinases WNK1 or WNK4 and other unknown molecular defects. 15980941: Moreover, excessive formation of aldosterone in glucocorticoid-remediable hypertension leads to severe hypertension. Several monogenic hypertensive disorders are caused by genetic mutations leading to the deranged function and/or regulation of renal tubular NaCl transport, such as mutations of the renal epithelial Na+ channel (ENaC) in Liddle syndrome, of the kinase WNK1 (with no K) in Gordon syndrome, and of the mineralocorticoid receptor, or of 11beta-hydroxysteroid dehydrogenase. 16477034: Liddle's syndrome, an inherited form of hypertension, is caused by mutations that delete or disrupt a C-terminal PY motif in the epithelial Na+ channel (ENaC). 16722436: [Hypertension due to mutation of mineralocorticoid receptors]. 17634077: OBJECTIVE: Liddle syndrome is a rare autosomal-dominant monogenic form of hypertension caused by mutations in the C-termini of the epithelial sodium channel beta- or gamma-subunit encoded by SCNN1B and SCNN1G, respectively, and often presenting with a familial history of hypertension. 17951312: BACKGROUND: Familial hyperkalaemia and hypertension (FHH), also termed pseudohypoaldosteronism type II, is a rare monogenic form of hypertension caused by mutations in the WNK1 or WNK4 kinases. 17961084: Mutations in the serine-threonine kinases WNK1 and WNK4 cause a Mendelian disease featuring hypertension and hyperkalemia. 18316027: Some mutations in PPARgamma (PPARG) cause type II diabetes and severe hypertension. 1846121: Mean allele sharing at APNH is not greater than expected from random assortment in hypertensive siblings (0.92 versus 1.0, p greater than 0.80), and the upper 95% confidence limit of this value (1.04) indicates that mutations at APNH rarely if ever contribute to the pathogenesis of hypertension in this population. 18695394: Mutations of WNK1 and WNK4 in humans cause hypertension and hyperkalemia at least partly by altering renal sodium and potassium transport. 19007435: Liddle syndrome is a hereditary form of early onset hypertension caused by mutations in the epithelial Na+ channel (ENaC). 20675381: Mutation of ENaC PY motifs, responsible for inherited hypertension (Liddle syndrome), decreased Hrs binding to ENaC. 20956807: BACKGROUND: The rare autosomal dominant genetic disorder familial hyperkalemia and hypertension which is caused by mutations in WNK4 kinase, is characterized by childhood hyperkalemia and hypercalciuria, and appearance of hypertension in the third to fourth decade. 22087567: BACKGROUND: 17alpha-hydroxylase deficiency is a rare autosomal recessive disorder characterized by sexual infantilism, amenorrhea, hypertension and hypokalemia, which is caused by mutations in the CYP17A1 gene. 22114204: Mutations in two members of this family (WNK1 and WNK4) cause pseudohypoaldosteronism type II featuring hypertension, hyperkalemia, and metabolic acidosis. 22550170: Pseudohypoaldosteronism type II is a salt-sensitive form of hypertension with hyperkalemia in humans caused by mutations in the with-no-lysine kinase 4 (WNK4). 23348731: Liddle syndrome is monogenic hypertension caused by mutations in the epithelial Na+ channel (ENaC) that interfere with its ubiquitylation by Nedd4-2. 23657971: Mutation of the protein kinase I alpha leucine zipper domain produces hypertension and progressive left ventricular hypertrophy: a novel mouse model of age-dependent hypertensive heart disease. 23914427: Mutation at MTHFR gene (C677T) has been implicated in the pathogenesis of common complex diseases such as thrombosis, hypertension, stroke, myocardial infarction, and recurrent pregnancy loss across world populations. 24266877: FHHt (familial hyperkalaemic hypertension; also known as Gordon's syndrome) is a salt-dependent form of hypertension caused by mutations in the regulators of the thiazide-sensitive Na+-Cl- co-transporter NCC [also known as SLC12A3 (solute carrier family 12 member 3)] and is effectively treated by thiazide diuretics and/or dietary salt restriction. 24463189: Whether hypertension in ADPKD is a primary vasculopathy secondary to mutations in the polycystin genes or secondary to activation of the renin-angiotensin-aldosterone system by cyst expansion and intrarenal ischemia is unclear. 24641320: The present study provides further insights into how Kelch-like adaptor proteins recognize their substrates and provides a structural basis for how mutations in WNK4 and KLHL3 lead to hypertension. 25539907: CONCLUSIONS: This study showed that mutations in mtDNA may contribute to the pathogenesis of hypertension in these Chinese Han families. 26100637: Hypertension-causing Mutations in Cullin3 Protein Impair RhoA Protein Ubiquitination and Augment the Association with Substrate Adaptors. 26167459: Mutations in ENaC subunit genes result in hypertension or hypotension, depending on the nature of the mutations. 26345810: However, the genetic mutations leading to hypertension might differ among various populations, as they have different origins and are subjected to different environmental pressures. 27293068: CONCLUSIONS: These findings expand on the clinical spectrum of phenotypes associated with KCNJ5 mutations and implicate these mutations in the pathogenesis of hypertension associated with increased aldosterone response to ACTH stimulation. 27378813: Familial hyperkalemic hypertension (FHHt) is a rare inherited form of salt-dependent hypertension caused by mutations in proteins that regulate the renal Na(+)-Cl(-) cotransporter NCC Mutations in four genes have been reported to cause FHHt including CUL3 (Cullin3) that encodes a component of a RING E3 ligase. 27638882: Mitochondrial transfer RNA (tRNA) mutation with high-salt stimulation can cause high blood pressure. 27942049: Mutations in KLHL3 cause constitutively increased renal salt reabsorption and impaired K+ secretion, resulting in hypertension and hyperkalemia. 28507170: Hypertension-Causing Mutation in Peroxisome Proliferator-Activated Receptor gamma Impairs Nuclear Export of Nuclear Factor-kappaB p65 in Vascular Smooth Muscle. 28710092: Liddle syndrome is an autosomal dominant form of hypokalemic hypertension due to mutations in the beta- or gamma-subunit of the epithelial sodium channel (ENaC). 29211511: Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. 30143066: Mutations in these genes are responsible for Mendelian hypertension, increased sodium chloride cotransporter activity, metabolic acidosis, and hyperkalemia. 30783460: Molecular analysis revealed that patients carrying the 5587T>C and 12280A>G mutations had a lower copy number of mtDNA compared with a control with hypertension, but without the mutations, suggesting that these mutations may cause mitochondrial dysfunctions that are responsible for hypertension. 30967423: CONCLUSIONS: Mutations in Cul3 cause severe hypertension by affecting both renal and vascular function, the latter being associated with activation of RhoA. 31296661: Mutations and overexpression of P450 11B2 (also known as aldosterone synthase) can lead to hypertension, congestive heart failure, and diabetic nephropathy. 31382627: We also found that WNK4 (its mutations lead to hypertension) expression, but not WNK1, was significantly increased in CLDN7-/- CD cell lines as well as in primary CLDN7-/- CD cells, suggesting that the expression of WNK4 was modulated by CLDN7. 31813255: Hypertension-causing cullin 3 mutations disrupt COP9 signalosome binding. The discovery of new genetic mutations that cause hypertension has illuminated previously unrecognized physiological pathways. 33048843: A mutation in its encoding gene causes hypertension in humans, which is associated with abnormal ion homeostasis. 33167351: Characterized by increased blood pressure due to excessive sodium retention and plasma volume, it is caused by a mutation in the HSD11B2 gene encoding the oxydoreductase enzyme 11beta-hydroxysteroide dehydrogenase type 2. 34064609: Monogenic hypertension is rare and caused by genetic mutations, but whether factors associated with mutations are disease-specific remains uncertain. 34223773: PURPOSE: Liddle syndrome is a hereditary form of arterial hypertension caused by mutations in the genes coding of the epithelial sodium channel - SCNN1A, SCNN1B and SCNN1G. CONDENSED ABSTRACT: Liddle syndrome is a hereditary form of arterial hypertension caused by mutations in the genes encoding the epithelial sodium channel's alpha-, beta- and gamma-subunit. 35179207: Fluorescence polarisation and structural modelling experiments revealed that its phosphorylation would abrogate the KLHL3 interaction similarly to hypertension-causing mutations. 35774371: Background: Liddle syndrome is a form of monogenic hypertension caused by mutations in the three homologous subunits of the epithelial sodium channels (ENaCs), alpha, beta, and gamma. 35946480: Pseudohypoaldosteronism associated with hypertrophic cardiomyopathy, hypertension and thrombocytosis due to mutation in the ELAC2 gene: a case report. 36140271: The with-no-lysine (WNK) kinase family, comprising four serine-threonine protein kinases (WNK1-4), were first linked to hypertension due to their mutations in association with pseudohypoaldosteronism type II (PHAII). 38099339: Liddle syndrome is an autosomal dominant form of monogenic hypertension that is caused by mutations in SCNN1A , SCNN1B or SCNN1G , which respectively encode the alpha, beta and gamma subunits of the epithelial sodium channel. 7567973: To date, mutations in three genes have been implicated in the pathogenesis of human hypertension: mutations resulting in ectopic expression of aldosterone synthase enzymatic activity cause a mendelian form of hypertension known as glucocorticoid-remediable aldosteronism; mutations in the beta subunit of the amiloride-sensitive epithelial sodium channel cause constitutive activation of this channel and the mendelian form of hypertension known as Liddle syndrome; finally, common variants at the angiotensinogen locus have been implicated in the pathogenesis of essential hypertension in Caucasian subjects, although the nature of the functional variants and their mechanism of action remain uncertain. 7670488: Human hypertension caused by mutations in the kidney isozyme of 11 beta-hydroxysteroid dehydrogenase. They thus permit cortisol to occupy the renal mineralocorticoid receptor and thereby cause sodium retention and hypertension. 7780735: The basis of one type of inherited hypertension has been discovered-it is caused by mutations in the gene for the beta subunit of a renal sodium channel. 7954808: Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel. 8177268: Precisely how mutations in this region may result in hypertension remains to be determined. 8521520: Liddle's syndrome is an inherited form of hypertension caused by mutations that truncate the C-terminus of human epithelial Na+ channel (hENaC) subunits. 8665845: Liddle syndrome is an autosomal dominant form of hypertension, resulting from mutations in the cytoplasmic C-terminus of either the beta or gamma subunits of the amiloride-sensitive epithelial Na channel (ENaC) which lead to constitutively increased channel activity. 8952579: This autosomal recessive form of severe hypertension results from mutations in the HSD11K (HSD11B2) gene. 8984121: OBJECTIVE: To investigate whether mutations in the beta subunit of the epithelial sodium channel (Scnn1b) contribute to the pathogenesis of hypertension in the spontaneously hypertensive rat (SHR) and the Dahl salt-sensitive rat. If disordered activity of the epithelial cell sodium channel contributes to the pathogenesis of hypertension in the SHR or Dahl models, it must stem from genetic lesions in sequences that regulate Scnn1b function or in sequences important to the structure or function of the other sodium channel subunits. 9100575: Liddle's syndrome is an autosomal dominant form of hypertension that resembles primary hyperaldosteronism, is characterized by the early onset of hypertension with hypokalemia and suppression of both PRA and aldosterone, and is caused by mutations in the carboxyl-terminus of the beta- or gamma-subunits of the renal epithelial sodium channel. 9120678: Human hypertension caused by mutations in the 11 beta-hydroxysteroid dehydrogenase gene: a molecular analysis of apparent mineralocorticoid excess. AME AS A CAUSE OF HYPERTENSION: The mutations in the 11 beta-HSD2 gene, together with those currently being sought by us for other kindreds with AME, establishes AME as a monogenic cause of human hypertension and will provide insight into the structure-function relationships of this important enzyme. 9221280: Liddle's syndrome: heritable human hypertension caused by mutations in the Beta subunit of the epithelial sodium channel. 9325269: Liddle's syndrome, an inherited form of hypertension, is caused by mutations that delete or alter PY domains in the carboxyl termini of beta or gamma ENaC subunits, leading to increased channel activity. 9535415: The mutation of NOS2 and the role of this enzyme in the pathogenesis of salt-sensitive hypertension in the Dahl/Rapp rat require further investigation. 9626162: Liddle's syndrome is an autosomal dominant form of salt sensitive hypertension caused by mutations in the beta or gamma subunit of the epithelial sodium channel. 10025714: Many cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the presenilin 1 (PS1) and PS2 genes. 10051671: Mutations in the human presenilin genes PS1 and PS2 cause early-onset Alzheimer's disease. 10193509: First, the three genes in which mutations are known to result in early onset autosomal dominant familial Alzheimer's disease will be discussed. 10439444: Mutation in the presenilin-1 (PS-1) gene at chromosome 14q24.3 is the most common cause of autosomal dominant early-onset Alzheimer's disease. 10549825: Autosomal dominant early-onset Alzheimer's disease results mainly from mutations of the presenilin 1 (PSEN1) gene, which codes for an integral membrane protein of 467 amino acids. 10594046: Mutations in presenilin (PS) genes cause early onset familial Alzheimer's disease (FAD) by increasing production of the amyloidogenic form of amyloid beta peptides ending at residue 42 (Abeta42). 10854108: Mutations in the presenilin-1 (PS-1) gene have been shown to cause early onset Alzheimer's disease (EOAD) in an autosomal dominant manner. 10963361: Mutations in the amyloid precursor protein (APP) gene cause one form of early onset familial Alzheimer's disease (AD). 11122949: Mutations in the amyloid precursor protein and presenilin 1 (PS1) genes are fully penetrant and cause early-onset AD. 11124892: APP is a transmembrane precursor of beta-amyloid, and its mutations cause early-onset familial Alzheimer's disease. 11126202: BACKGROUND: Mutations in the presenilin proteins cause early-onset, familial Alzheimer's disease (FAD). 11161700: Most cases of familial early-onset Alzheimer's disease are caused by mutations in the presenilin 1 (PS1) gene. 11432849: Mutations in presenilin (PS) genes cause early-onset familial Alzheimer's disease by increasing production of the amyloidogenic form of amyloid beta peptides ending at residue 42 (Abeta42). 11444983: Mutations in the presenilin genes PS1 and PS2 cause early-onset Alzheimer's disease by altering gamma-secretase cleavage of the amyloid precursor protein, the last step in the generation of Abeta peptide. 11489281: Most familial early-onset Alzheimer's disease (FAD) is caused by mutations in the presenilin-1 (PS1) gene. 11710891: This genetic change may be a prevalent cause of early-onset familial AD in the Caribbean Hispanic population. A founder mutation in presenilin 1 causing early-onset Alzheimer disease in unrelated Caribbean Hispanic families. 11816789: Amyloid plaques, primarily composed of Abeta, progressively develop in the brains of AD patients, and mutations in three genes (APP, PS1, and PS2) cause early onset familial AD (FAD) by directly increasing synthesis of the toxic, plaque-promoting Abeta42 peptide. 11817902: Mutations in the presenilin genes PS1 and PS2 are a major cause of early onset familial Alzheimer's disease (AD). 11898555: To date, mutations in three genes (APP, PSEN1, PSEN2) have been described to cause familial early-onset AD. 11992262: Nicastrin regulates gamma-secretase cleavage of the amyloid precursor protein by forming complexes with presenilins, in which most mutations causing familial early-onset Alzheimer disease (EOAD) have been found. 12052536: The E693G (Arctic) mutation of the amyloid precursor protein was recently found to lead to early-onset Alzheimer's disease in a Swedish family. 12059037: Mutations in the amyloid precursor protein (APP) gene are known as causative factors in the pathogenesis of early-onset familial Alzheimer's disease (FAD). 12139484: A significant proportion of early onset Alzheimer's disease (AD) is caused by mutations in human genes for amyloid precursor protein (APP), presenilins 1 and 2 (PSEN1,2). 12154011: We report the identification of a novel rat cDNA encoding a peptide homologous to Humanin, a secreted peptide that specifically protects against neuronal cell death induced by beta-amyloid peptide (Ab) or by mutations causing early-onset familial Alzheimer's disease. 12223532: The autosomal-dominant inherited forms of early-onset Alzheimer's disease are caused by mutations in the genes encoding APP, presenilin-1 (chromosome 14), and presenilin-2 (chromosome 1). This review covers the trafficking and processing of APP, amyloid cascade hypothesis in AD pathogenesis, physiological and pathological roles of presenilins, molecular characteristics of alpha-synuclein, their interactions, and therapeutic strategies for AD. 12355988: First, the three genes in which mutations are known to result in early onset autosomal dominant familial AD (presenilins 1 and 2, and amyloid beta protein precursor [APP]): well characterized but that account for only a small proportion of AD cases. Many of these are controversial and studies have shown conflicting results, but apoE polymorphism seems to be only one of the possible genetic factors suggested to play a role in the multifactoral pathogenesis of AD. 12390529: Mutations in the presenilin-1 (PS1) gene cause early onset familial Alzheimer's disease (FAD) by a mechanism believed to involve perturbed endoplasmic reticulum (ER) function and altered proteolytic processing of the amyloid precursor protein. 12540060: The identification of the neurotoxic effects of beta-amyloid and the discovery of mutations responsible for early-onset Alzheimer's disease (EOAD) and their linkage to beta-amyloid overproduction, has made the amyloid hypothesis of AD the predominant influence for therapeutic targets. 12558063: AD appears to have a heterogeneous etiology with a large percentage termed sporadic AD arising from unknown causes and a smaller fraction of early onset familial AD (FAD) caused by mutations in one of several genes, such as the beta-amyloid precursor protein (APP) and presenilins (PS1, PS2). 12605888: Mutations in the presenilin (PS) genes, PS1 and PS2, are a major cause of early-onset familial Alzheimer's disease (FAD). 12629906: Mutations in the amyloid precursor protein gene (APP) and the presenilin genes (PSEN1 en PSEN2) cause early onset Alzheimer's disease. Research in the field of Alzheimer's disease has shown that genetic factors play an important role in the aetiology of the disease. 1303172: These data suggest that mutations in APP are a rare cause of familial early onset AD (3/21 families tested) and that within APP most, possibly all, mutations which cause AD are in exon 17. 14610118: BACKGROUND: Plasma amyloid [beta]-peptide (A[beta]) 40 and A[beta]42 levels are increased in persons with mutations causing early-onset familial Alzheimer's disease (AD). 14643748: Most familial early-onset Alzheimer's disease (FAD) is caused by mutations in the presenilin-1 (PS1) gene. 14769392: Mutations in three causative genes have been identified in patients with an autosomal-dominant form of early-onset Alzheimer's disease (EOAD). 15038915: Familial early onset AD is a heterogeneous disorder that can be caused by mutations in at least three different genes. 15126696: Data that have accumulated for well over a decade have implicated the beta-amyloid (Abeta) peptide as a central player in the pathogenesis of Alzheimer's disease (AD). Amyloid plaques, composed primarily of Abeta progressively form in the brains of AD patients, and mutations in three genes (amyloid precursor protein [APP] and presenilin 1 and 2 [PS1 and PS2]) cause early-onset familial AD (FAD) by directly increasing production of the toxic, plaque-promoting Abeta42 peptide. 15249849: Early-onset AD can be due to mutations in several autosomal dominant genes. 15337637: Mutations in the presenilin-1 (PS-1) gene are the main cause of autosomal-dominant early onset Alzheimer's disease (EOAD) and show a high penetrance of symptoms. Genotype-phenotype analysis in early-onset Alzheimer's disease due to presenilin-1 mutations at codon 139. 15534188: BACKGROUND: Early-onset familial Alzheimer disease is caused by mutations in the amyloid precursor protein (APP), presenilin-1 (PSEN1), or presenilin-2 (PSEN2) genes. 15544501: These studies together with findings that A beta is neurotoxic in vitro, provide evidence that some aggregates of this peptide are the key to the pathogenesis of AD. A small fraction of early onset familial AD (FAD) is caused by mutations in genes, such as the beta-amyloid precursor protein (APP) and presenilins that increase the load of A beta in the brain. 15663477: In support of our hypothesis, the four verified PS2 FAD mutations cause substantial changes in the Abeta 42/40 ratio, comparable with PS1 mutations that cause very-early-onset FAD. 15950763: Mutations of presenilin 1 (PS1) gene are the causative gene for early onset familial AD (FAD) due to the overproduction and deposition of pathogenic Abeta1-42 peptides. The pathogenesis of Alzheimer's disease (AD) is now thought to be tightly linked to Abeta deposition and oxidative stress, but it is still unknown how these factors result in neuronal dysfunction and cell death. 16857570: Plasma concentrations of Abeta(1-40) and Abeta(1-42) rise with age and are increased in people with mutations that cause early-onset Alzheimer's disease. 16897084: In the current letter, we expand this observation by describing an additional 15 independent families with the Ala431Glu substitution in the PSEN1 gene and conclude that this mutation is not an uncommon cause of early-onset autosomal dominant AD in persons of Mexican origin. 17131822: Most cases of familial early-onset Alzheimer's disease are caused by mutations in the presenilin 1 (PS1) gene. 17169464: Mutations in the presenilin 1 gene cause most early onset familial Alzheimer's disease (FAD). 17645236: Over 100 mutations in the presenilin-1 gene (PSEN1) have been shown to result in familial early onset Alzheimer disease (EOAD), but only a relatively few give rise to plaques with an appearance like cotton wool (CWP) and/or spastic paraparesis (SP). A single point mutation, p.L420R (g.1508T > G) that gives rise to a missense mutation in the eighth transmembrane (TM8) domain of PS1 was identified in two affected members of the family. p.L420R (g.1508T > G) is the mutation responsible for EOAD, seizures and CWP without SP in this family. 17728018: Mutations in presenilin (PS) genes cause majority of early onset Alzheimer's disease (AD), an age related neurodegenerative disorder. 17920016: Mutations in the amyloid precursor protein (APP) cause early-onset Alzheimer's disease (AD), but the only genetic risk factor for late-onset AD is the varepsilon4 allele of apolipoprotein E (apoE), a major cholesterol carrier. 17927985: Mutations in presenilin which result in early-onset Alzheimer disease (AD) cause both increased calcium release from intracellular stores, primarily endoplasmic reticulum (ER), and changes in NF-kappaB activation. 18367332: Presenilin (PS1 and PS2) mutations cause early-onset familial Alzheimer's disease (AD). 18403054: Mutations in amyloid precursor protein (APP) and presenilin (PSEN) genes are known to cause familial early-onset Alzheimer's disease (AD), which account for around 5% of AD cases. 18437002: Although mutations in three genes, amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2), have been identified as genetic causes of early-onset Alzheimer s disease (EOAD), there has been a single report on a PSEN1 mutation in Koreans. 18580586: CONCLUSIONS: This is the first description of neuropathologic findings in EOFAD owing to N135S PSEN1 mutation. OBJECTIVE: Early onset familial Alzheimer disease (EOFAD) can be caused by mutations in genes for amyloid precursor protein, presenilin 1 (PSEN1), or presenilin 2 (PSEN2). 18973685: ZAbeta3 coexpression moreover permits the recombinant production of Abeta(1-42) carrying the Arctic (E22G) mutation, which causes early onset familial AD. 19076441: CMRglc reductions were observed on FDG-PET before the onset of disease in several groups of at-risk individuals, including patients with mild cognitive impairment (MCI), often a prodrome to AD; presymptomatic individuals carrying mutations responsible for early-onset familial AD; cognitively normal elderly individuals followed for several years until they declined to MCI and eventually to AD; normal, middle-aged individuals who expressed subjective memory complaints and were carriers of the apolipoprotein E epsilon-4 allele, a strong genetic risk factor for late-onset AD. 19196715: Mutations of the presenilin 1 (PS1) gene are the most common cause of early onset familial Alzheimer disease (FAD). 19363265: Mutations in the amyloid-beta protein precursor (AbetaPP) gene can cause autosomal dominant early-onset Alzheimer's disease, or Alzheimer's disease (AD) associated with cerebral amyloid angiopathy (CAA), cerebral hemorrhage, or both. 1944558: Early-onset Alzheimer's disease caused by mutations at codon 717 of the beta-amyloid precursor protein gene. 19524115: Mutations in presenilin (PS) and amyloid precursor protein (APP) genes are a predominant cause for early-onset familial Alzheimer disease (AD). 19659892: To date, three genes have been identified in which mutations cause early-onset autosomal dominant inherited AD: APP, PSEN1, and PSEN2. 19716367: Studies of mutations that cause early onset AD and promote Abeta accumulation in the brain strongly support the notion that inhibiting Abeta aggregation will prevent AD. 19853579: Presenilin is the catalytic member of the gamma-secretase proteolytic complex and mutations in presenilins are the major cause of early-onset familial Alzheimer's disease. 20076796: This review will give an overview of FDG-PET results in individuals at risk for developing dementia, including: presymptomatic individuals carrying mutations responsible for early-onset familial AD; patients with Mild Cognitive Impairment (MCI), often a prodrome to late-onset sporadic AD; non-demented carriers of the Apolipoprotein E (ApoE) epsilon4 allele, a strong genetic risk factor for late-onset AD; cognitively normal subjects with a family history of AD; subjects with subjective memory complaints; and normal elderly followed longitudinally until they expressed the clinical symptoms and received post-mortem confirmation of AD. 20119496: MAIN METHODS: Here, we have explored the anti-amyloid properties of these SMAbetaBA's in mice doubly transgenic for human prensenilin-1 (PS1) and APP gene mutations that cause early-onset AD. AIMS: One promising approach for treatment of Alzheimer's disease (AD) is use of anti-amyloid therapies, based on the hypothesis that increases in amyloid-beta (Abeta) deposits in brain are a major cause of AD. 20129170: Mutations in the presenilin genes cause early-onset familial Alzheimer's disease, but mutation carriers have substantial phenotypic heterogeneity. 20213228: Mutations in the presenilin 1 (PSEN1) gene are more commonly identified as genetic causes of early-onset familial Alzheimer's disease than mutations in the amyloid precursor protein (APP) and the presenilin 2 (PSEN2) genes. 20541250: PS1 mutations causing early-onset AD produce a similar lysosomal/autophagy phenotype in fibroblasts from AD patients. 20559464: By contrast, mutations in the presenilin genes responsible for early onset familial AD cause rapid disease progression and accentuate clinical and pathological features including inflammation. 20586737: Approximately 0.5% of those with Alzheimer's disease have an autosomal dominant inherited early onset Alzheimer's disease, caused by mutations in the APP, PSEN1 or PSEN2 gene. 21130746: Mutations in APP (amyloid-beta precursor protein), which flanks the Abeta sequence, cause early-onset familial AD, and evidence has pointed to the APP-to-Abeta conversion as a possible therapeutic target. 21297272: Studies in carriers of mutations that cause early-onset familial Alzheimer's disease (eoFAD) are of significant interest.We showed previously that regional glucose hypometabolism could be detected many years before disease onset in presenilin 1(PSEN1) mutation carriers. 21524270: Mutations in the presenilin genes cause the majority of early-onset familial Alzheimer's disease. 21544564: Mutations in the presenilin 2 (PSEN2) gene are less commonly identified as genetic causes of early-onset familial Alzheimer's disease than mutations in the amyloid precursor protein (APP) and the presenilin 1 (PSEN1) genes. 21784978: Mutations in presenilins (PS) account for most early-onset familial Alzheimer's disease (FAD). 21785673: Amyloid precursor protein, presenilin 1 and presenilin 2 mutations are known to cause familial early-onset AD, whereas apolipoprotein E (APOE) epsilon4 is a susceptibility gene for late-onset AD. 22033785: Mutations in these genes have been found to cause mainly early-onset AD. 22221884: To date, more than 200 mutations in three genes have been identified as cause of early-onset autosomal dominant inherited AD. 22359955: Although most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin 1 (PS1) gene, the functions of PS1 and its role in synaptic disfunction are not yet completely understood. 22766738: Presenilin 1 (PS1) mutations are the most common cause of early-onset familial Alzheimer's disease (EOFAD). 22815225: Mutations in the PSEN1 gene are the most common genetic cause of early onset Alzheimer's disease, whereas APP and PSEN2 gene mutations are less frequent. 22867970: Mutations in presenilins are the major cause of early onset familial Alzheimer disease. 22872014: Plasma concentrations of Abeta40 and Abeta42 rise with age and are increased in people with mutations that cause early-onset Alzheimer's disease (AD). 23123781: CONCLUSIONS: This novel presenilin-1 sequence variant cosegregated with early onset dementia in the proband and at least one other affected family member, and likely represents a mutation causing familial, early-onset Alzheimer's disease. BACKGROUND: Mutations in the gene for presenilin-1 cause familial, early-onset Alzheimer's disease. 23593396: Mutations in the presenilin 1 gene, affecting the function of gamma-secretase, are the most common genetic cause of familial, early-onset Alzheimer's disease. 23707529: Mutations in presenilins (PS1 and PS2) have been linked to the pathogenesis of early onset familial Alzheimer's disease. 23850332: BACKGROUND: Early-onset familial Alzheimer disease (AD) is an autosomal dominant disorder caused by mutations in the amyloid precursor protein, presenilin 1 (PSEN1), or presenilin 2 gene. 24416243: Presenilin 1 (PSEN1) encodes the catalytic subunit of gamma-secretase, and PSEN1 mutations are the most common cause of early onset familial Alzheimer's disease (FAD). 24599465: Rare, familial, early-onset autosomal dominant forms of familial Alzheimer's disease (FAD) are caused by mutations in genes encoding beta-amyloid (Abeta) precursor protein (APP), presenilin-1 (PS1), and presenilin-2. 24650794: Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 24669286: Mutations in APP, PS1, and PS2 genes are causes for early onset AD. 24773620: U1 small nuclear ribonucleoproteins (snRNPs) aggregate in Alzheimer's disease due to autosomal dominant genetic mutations and trisomy 21. However little is known about snRNP biology in early onset AD due to autosomal dominant genetic mutations or trisomy 21 in Down syndrome. 24838186: The mutations in the presenilin 2 (PSEN2) gene as causes of early-onset familial Alzheimer's disease (AD) have never been reported in Asia. 24844686: Mutations in the gene PSEN2 are a rare cause of early onset Alzheimer's disease (EOAD). 24906965: Clinical presentation of early-onset Alzheimer's disease as a result of mutation in exon 12 of the PSEN-1 gene. INTRODUCTION: Mutations in the gene for presenilin 1 (PSEN-1) cause familial, early-onset Alzheimer's disease (EOAD). 25045597: Early-onset AD (EOAD) is caused by mutations in the genes APP, PSEN1 and PSEN2. 25138979: Mutations in the amyloid precursor protein (APP), presenilin-1 and presenilin-2 genes have been recognized to be the cause of EOAD. 25589721: Presenilin 1 (PS1) mutations are responsible for many early-onset familial AD (FAD) cases. 25720399: While early-onset familial Alzheimer's disease (AD) is caused by a genetic mutation, the vast majority of late-onset AD is likely caused by the combination of genetic and environmental factors. 25933409: Early onset AD (EOAD) is commonly caused by mutations in amyloid precursor protein (APP) or genes involved in the processing of APP including the presenilins (e.g. PSEN1 or PSEN2). 26092625: A large, genetically-isolated community in Antioquia, Colombia, with early-onset familial Alzheimer's disease due to a presenilin-1 mutation is ideally suited for the study of molecular mechanisms of AD, and hence accelerate the discovery of new or alternative treatment approaches. 26268329: Its subunit, presenilin (PS) is the catalytic component, of which mutations are a major cause of early onset familial Alzheimer disease (FAD). 27120160: Using this approach, we generated human induced pluripotent stem cells with heterozygous and homozygous dominant early onset Alzheimer's disease-causing mutations in amyloid precursor protein (APP(Swe)) and presenilin 1 (PSEN1(M146V)) and derived cortical neurons, which displayed genotype-dependent disease-associated phenotypes. 27128372: Mutations in the presenilin 2 gene (PS2) are an extremely rare cause of early-onset autosomal dominant Alzheimer's disease (AD), accounting for only 5% of these families. 28065273: In recent years, we have successfully generated high-affinity, conformation-sensitive anti-gamma-secretase Nanobodies. gamma-Secretase is a multimeric membrane protease involved in processing of the amyloid precursor protein with high clinical relevance as mutations in its catalytic subunit (Presenilin) cause early-onset Alzheimer's disease. 28461250: Presenilin 1 (PSEN1) mutations are the main cause of autosomal dominant Early-onset Alzheimer Disease (EOAD). 28550254: BACKGROUND: Presenilin-1 (PSEN1) mutations are the most common cause of familial early onset Alzheimer's disease (AD). 28623607: Presenilin-1 gene (psen1) mutations are the main cause of early-onset autosomal-dominant Familial Alzheimer Disease. 28764909: A novel PSEN1 (S230N) mutation causing early-onset Alzheimer's Disease associated with prosopagnosia, hoarding, and Parkinsonism. 28781776: Early onset AD is caused by mutations in three genes: Amyloid-beta precursor protein, presenilin 1 (PSEN1) and PSEN2. 29404783: The majority (~ 55%) of early onset familial Alzheimer disease (FAD) is caused by mutations in the presenilin 1 gene (PSEN1). 29740579: Mutations in the APP, PSEN1, and PSEN2 genes cause early onset Alzheimer's disease (EOAD) that follows a Mendelian inheritance pattern. 31153663: Mutations in PSEN1 are the most common cause of early-onset Alzheimer's disease (AD). 31182772: Alzheimer's disease (AD) is the most common type of neurodegenerative dementia, but the cause of AD remained poorly understood. Many mutations in the amyloid precursor protein (APP) and presenilin 1 and 2 (PSEN1 and PSEN2) have been reported as the pathogenic causes of early-onset AD (EOAD), which accounts for up to 5% of all AD cases. 32354700: Mutations in the PS genes are a major cause of familial early-onset Alzheimer disease and affect the cleavage of the amyloid precursor protein, thereby altering the production of the amyloid beta-peptide. 32767553: Gene mutations associated with early onset familial Alzheimer's disease in China: An overview and current status.BACKGROUND: Mutations of three causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 32957903: AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically whereas early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). 33274538: Mutations in three genes (APP, PSEN1, and PSEN2) are the main cause of the autosomal dominant early-onset Alzheimer's disease (AD-EOAD). 34189411: One consistent observation for all PRESENILIN gene mutations causing EOfAD is that a transcript is produced with a reading frame terminated by the normal stop codon-the \reading frame preservation rule\. Background: Mutations in PRESENILIN 2 ( PSEN2 ) cause early onset familial Alzheimer's disease (EOfAD) but their mode of action remains elusive. 35203497: We also know that mutations in certain proteins generate early-onset Alzheimer's disease (EOAD), and many other genes modulate the disease in its sporadic form. 35354048: Here, we examine synaptic and sleep homeostasis in a Drosophila model by overexpressing human amyloid precursor protein (APP), whose duplication and mutations cause familial early-onset AD. 35366787: The etiology of AD is complex with a substantial portion of sporadic AD emerging from unknown reasons and a lesser proportion of early-onset familial AD (FAD) caused by mutation in several genes, such as the amyloid precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) genes. 36361714: AD occurs in two forms, early onset familial and late-onset sporadic; genetic mutations in PS1, PS2, and APP genes cause early onset familial AD, and a combination of lifestyle, environment and genetic factors causes the late-onset sporadic form of the disease. 36555791: Mutations in the PS1 gene ( PSEN1 ) are the most common cause of early onset familial Alzheimer's disease (FAD). 37108607: The etiology of early-onset Alzheimer's disease (EOAD) is associated with alterations in the production of amyloid beta (Abeta) species caused by mutations in the APP , PSEN1 , and PSEN2 genes. 38396302: We review here the structure, function, and pathobiology of gamma-secretases, with a focus on how mutations in presenilin genes result in early-onset AD. The GSAS represent, in theory, a precision medicine approach to the prevention of amyloid deposition, as they specifically target a discrete aspect in a complex cell biological signalling mechanism that initiates the pathological processes leading to Alzheimer's disease. 38607732: Early-onset AD is a rare (~1%), autosomal dominant, caused by mutations in presenilin-1, presenilin-2, and amyloid precursor protein genes and the other is a late-onset, prevalent and is evolved due to age-associated complex interactions between environmental and genetic factors, in addition to apolipoprotein E4 polymorphism. 7567974: Mutations in the amyloid precursor protein gene (APP) can cause early-onset autosomal dominant AD. 8357039: Mutations in the amyloid precursor protein (APP) gene on chromosome (CHR) 21 have been shown to cause early-onset AD in a small number of pedigrees. 8410047: On the other hand, our data suggest that this mutation is not a common cause of Japanese early-onset FAD. 8574969: Mutations in two recently identified genes appear to cause the majority of early-onset familial Alzheimer's disease (FAD). 8766720: The majority of cases of early-onset familial Alzheimer disease are caused by mutations in the recently identified presenilin 1 (PS1) gene, located on chromosome 14. 8799182: Mutations in the recently identified presenilin 1 gene on chromosome 14 cause early onset familial Alzheimer disease (FAD). 8858181: Early data suggest that mutations found within the two genes cause early onset Alzheimer's disease by influencing the proteolytic processing of amyloid beta-peptide in a pathological manner. 8881379: This review reports the different genetic factors that have been identified either as risk factor for Alzheimer's disease (AD) or directly causing the disease. The second part describes the mutations responsible for early-onset autosomal dominant AD found in three different genes. 8972483: Mutations in the recently cloned Presenilin genes (PS-1 and PS-2) are by far the most common cause of early onset familial AD. 8986743: Our data demonstrate that the presenilin mutations cause a dominant gain of function and may induce AD by enhancing A beta 42 production, thus promoting cerebral beta-amyloidosis. The mechanism by which mutations in the presenilin (PS) genes cause the most aggressive form of early-onset Alzheimer's disease (AD) is unknown, but fibroblasts from mutation carriers secrete increased levels of the amyloidogenic A beta 42 peptide, the main component of AD plaques. 9129725: Mutations in the Presenilin 1 (PS1) gene on chromosome 14 cause most early-onset familial Alzheimer's disease (AD). 9151738: Most autosomal dominant inherited forms of early onset Alzheimer's disease (AD) are caused by mutations in the presenilin-1 (PS-1) gene on chromosome 14. 9169406: Most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin genes. 9185547: Mutations in the presenilin-1 (PS1) gene is a cause of early- onset familial Alzheimer's disease (AD). 9219695: Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 (PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease. 9371838: Mutations in the amyloid precursor protein (APP) gene cause early-onset familial Alzheimer disease (AD) by affecting the formation of the amyloid beta (A beta) peptide, the major constituent of AD plaques. 9422341: Many cases of autosomal dominant inherited forms of early-onset Alzheimer's disease are caused by mutations in the genes encoding presenilin-1 (PS-1; chromosome 14) and presenilin-2 (PS-2; chromosome 1). 9485068: Mutations in the presenilin 1 (PS1) gene on chromosome 14 are a major cause of autosomal dominant, early-onset Alzheimer's disease. 9500965: Mutations in the presenilin-1 gene (PS-1) on chromosome 14 are causative for early-onset familial Alzheimer's disease (AD). 9521423: Mutations in the presenilin genes (PS-1 and PS-2) cause early onset autosomal dominant Alzheimer's disease (AD). 9535737: Mutations in presenilin 1 (PS1) gene are the major cause of early-onset familial Alzheimer's disease. 9546349: Mutations of the newly discovered PS1 gene are responsible for early-onset familial Alzheimer disease (AD), and PS1 is abnormally accumulated in sporadic and familial AD brain. 9652956: The majority of cases of early-onset familial Alzheimer disease are caused by mutations in the recently identified presenilin 1 (PS 1) gene, located on chromosome 14. 9728730: Early-onset Alzheimer's disease due to mutations of the presenilin-1 gene on chromosome 14: a 7-year follow-up of a patient with a mutation at codon 139. Mutations in the presenilin-1 gene (PS-1 gene) on chromosome 14 have recently been identified as a cause of familial early-onset Alzheimer's disease (EOAD). 9751187: Mutations in the presenilin genes PS1 and PS2 cause the most common form of early-onset familial Alzheimer's disease. 9790190: Mutations of the presenilin-1 gene are a major cause of familial early-onset Alzheimer's disease. 10564706: Long-term administration of NG-nitro-L-arginine methyl ester (L-NAME) induces development of hypertension and hypertrophy of the left ventricle in rats. 10696524: NG-Nitro-L-arginine methyl ester-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites NO2- and NO3- and was aggravated when rats drank 0.9% NaCl in place of tap water. These results suggest that long-term inhibition of NO synthesis produces a sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension. 10744360: L-NAME treatment induced arterial hypertension, in vitro aortic hyperresponsiveness to phenylephrine, impaired vasodilatory response to acetylcholine and no significant change in response to sodium nitroprusside. 10993766: A high-calcium diet attenuated the development of hypertension induced by L-NAME and abrogated the associated impairments of endothelium-independent mesenteric arterial relaxations to nitroprusside, isoproterenol, and cromakalim. 11399644: Recent studies have suggested that subtle microvascular and tubulointerstitial injury in the kidney can cause salt-sensitive hypertension. To test this hypothesis, we determined whether the mild renal disease induced by transient blockade of nitric oxide (NO) synthesis would result in salt-sensitive hypertension and whether prevention of the renal injury by coadministration of the immunosuppressive agent mycophenolate mofetil (MMF) would block the development of salt sensitivity. Mycophenolate mofetil prevents salt-sensitive hypertension resulting from nitric oxide synthesis inhibition. L-NAME treatment resulted in acute hypertension and the development of mild renal injury. 11522044: Six weeks' lasting inhibition of NO synthase by NG-nitro-L-arginine methyl ester (L-NAME) induced stabilized hypertension. 11564976: CONCLUSIONS: Chronic inhibition of NO synthesis per se promotes structural intimal remodeling of the rat aorta, which is potentiated by L-NAME-induced hypertension. 11741518: Blood pressure variability is increased in genetic hypertension and L-NAME -induced hypertension. Time course of L-NAME-induced hypertension was measured by the tail-cuff method. 11791005: Treatment with L-NAME induced marked arterial hypertension and cardiomyocyte hypertrophy, both of which were significantly reduced by propranolol and atenolol. The effects of propranolol and atenolol were investigated on arterial hypertension, cardiomyocyte hypertrophy, and ventricular ischaemic lesions induced by an 8-week treatment with the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 20 mg/rat per day) in Wistar rats. Our study demonstrates that propranolol and atenolol reduce arterial hypertension, cardiomyocyte hypertrophy and myocardial fibrosis induced by L-NAME, suggesting that beta-blockers are of beneficial value in treatment of vascular and cardiac alterations caused by chronic nitric oxide deficiency. 11936844: Because of its key role in proteosynthesis, the total content of elongation factor-2 (EF-2) and the distribution of six main EF-2 variants were investigated after Pseudomonas Exotoxin A catalyzed [37P]ADP-ribosylation using 1D-PAGE and isoelectric focusing (IEF) in a rat model of hemodynamic overload with variable degrees of cardiac hypertrophy: Chronic NO-synthase inhibition by L-NAME (N-omega-nitro-L-arginine-methyl-ester; 0.75 mg/ml drinking water) induced arterial hypertension without hypertrophy but myocardial apoptosis; additional treatment with IGF-1 (osmotic micropumps) did not modify hypertension but reduced apoptosis allowing moderate hypertrophy of the left ventricles. 12070623: In rat, exercise reduces the elevated blood pressure in L-NAME-induced hypertension via increasing nitric oxide synthase activity. 12084390: The aim of this study was to investigate the effects of Angiotensin II (ANG II) receptor antagonist losartan on the blood-brain barrier (BBB) permeability in L-NAME-induced hypertension and/or in ANG II-induced acute hypertension in normotensive and hypertensive rats. Acute hypertension was induced by ANG II (60 microg/kg). 12198334: N(G)-nitro-L-arginine methyl ester-induced hypertension and natriuretic peptide gene expression: inhibition by angiotensin II type 1 receptor antagonism. Results suggest that >l-NAME-induced hypertension and the associated activation of ventricular ANP and BNP gene expression are, at least in part, mediated by angiotensin II, whereas the resistance vessel hypertrophy following nitric oxide synthase inhibition is angiotensin II independent. 12424422: The aim of this study was to investigate oxidant-antioxidant systems of renal tissue in rats with hypertension induced by L-NAME. Renal antioxidant status in rats with hypertension induced by N sup omega nitro-L-arginine methyl ester. 12663263: The oral administration of L-NAME for 2 wk induced a serious hypertension, and the HbNO concentration was reduced (change in [HbNO] = 5.7 microM). 12794274: Animals were given the inhibitor of nitric oxide synthase, L-NAME (Nomega-nitro-L-arginine methyl ester), for 4 wk to induce chronic hypertension. 12861333: The L-NAME-induced high BP and cardiac hypertrophy were attenuated in rats expressing AT(1)R-AS. 14561528: Our previous publication has stressed the benefits of losartan, an angiotensin II receptor blocker, on the permeability of blood-brain barrier (BBB) and blood pressure during L-NAME-induced hypertension. Epinephrine-induced acute hypertension in diabetic hypertensive rats increased the content of EB dye dramatically in cerebellum and diencephalon (p < 0.01) and slightly in both cerebral cortex (p < 0.05). 14623032: Results suggested that products from cyclooxygenase pathway are involved in the genesis or maintenance of LN-induced hypertension, playing a role in the increased vascular reactivity, in the reduction of the endothelium-dependent relaxation and in the inhibition of the functional activity of the Na+, K+-ATPase. L-NAME (LN) induces hypertension by blocking nitric oxide (NO) synthesis. The aim of this work was to investigate whether products of the cyclooxygenase pathway are involved in alterations of vascular reactivity and Na+-pump activity in the tail artery from LN-induced hypertension rats. 14697405: Effect of simvastatin on remodeling of the left ventricle and aorta in L-NAME-induced hypertension. 15036467: A pharmacological inhibition of nitric oxide synthase (NOS) in rats produces renal vasoconstriction, renal dysfunction, and hypertension. Taken together, these results suggest that BFWE prevents the increase of SBP in the L-NAME-induced hypertension that may have been caused by enhanced generation of vascular NO and amelioration of renal functions. 15123544: Three experiments were performed to investigate: (i) the influence of sex on the development of L-NAME-induced hypertension; (ii) the effects of gonadectomy on the dimorphism of L-NAME-induced hypertension; and (iii) the effects of testosterone in ovariectomized female and of 17beta-oestradiol in orchidectomized male rats. In this study we have evaluated the influence of sex, gonadectomy and sex hormones on the development of L-NAME-induced hypertension in the rat, focusing our investigation on blood pressure (BP), plasma renin activity (PRA), cardiac hypertrophy and proteinuria. 15475829: L-NAME-induced hypertension has been shown to produce concentric (eutrophic) remodeling of the heart despite an enhanced afterload. 15943756: L-NAME-induced hypertension is characterized by chronic inhibition of nitric oxide synthesis. The superoxide dismutase mimetic, tempol, reduces the bioavailability of nitric oxide and does not alter L-NAME-induced hypertension in rats. 15976509: METHODS: Renal damage (UPV, UAV, and FGS) was assessed in ACI, ACI.FHH-(D1Rat324-D1Rat156)(Rf-1B), and ACI.FHH-(D17Rat117-D17Arb5)(D17Rat180-D17Rat51) (Rf-5) congenic rats in the two-kidney (2K) control situation, and following L-NAME-induced hypertension, unilateral nephrectomy (UNX), and UNX combined with L-NAME. 16197366: In conclusion, the combined treatment of zofenopril or enalapril with hydrochlorothiazide completely prevented the development of arterial hypertension induced by L-NAME. 16223511: RESULTS: The hypotensive effect of L-arg and hypertension induced by L-NAME were not modified by haloperidol. 16837819: METHODS: Renal damage susceptibility was assessed in Rf-1B, Rf-1B+5, Rf-1B+4 congenics and ACI control rats in four situations: two-kidney control (2K), unilateral nephrectomy (UNX), L-NAME-induced hypertension (2K+L-NAME) and UNX+L-NAME. 16914418: Rats received L-NAME for 15 days to produce hypertension and melatonin the last 5 days before I/R studies. 16988888: In this study, we aimed to investigate whether lisinopril treatment has any biochemical and/or histopathological effect on rat liver tissue in a L-NAME-induced hypertension model. Although the beneficial effects in L-NAME-induced hypertension treatment, lisinopril can lead to some unexpected results like hepatocyte degeneration, serum enzyme level elevation, and slight mononuclear cell infiltration. 17177624: The time-dependent effect of Provinols on brain NO synthase activity in L-NAME-induced hypertension. The aim of this study was to analyze a time course of Provinols effects on brain NO synthase activity and oxidative damage in L-NAME-induced hypertension. 17223729: Ultrastructure observation revealed enhanced neoformation of side-to-side type while internalization of end-to-end type (intercalated disc-related) of gap junctions prevailed in the myocardium of rats suffering from either spontaneous or L-NAME-induced hypertension. 17334538: We evaluated the hemodynamic pattern and the contribution of the sympathetic nervous system in conscious and anesthetized (1.4 g/kg urethane, iv) Wistar rats with L-NAME-induced hypertension (20 mg/kg daily). Sympathetic activation in rats with L-NAME-induced hypertension. 1750517: At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect. 17824807: Simvastatin decreased coenzyme Q in the left ventricle and skeletal muscle but not in the brain and liver in L-NAME-induced hypertension. 17898543: Small artery remodeling and erythrocyte deformability in L-NAME-induced hypertension: role of transglutaminases. 18373397: The present study was focused on regulatory role of nitric oxide on functional properties of the cardiac Na, K-ATPase in three various animal models of hypertension: spontaneously hypertensive male rats (SHR) with increased activity of nitric oxide synthase (NOS) by 60 % (Sh1), SHR with decreased activity of NOS by 40 % (Sh2) and rats with hypertension induced by L-NAME (40 mg/kg/day) with depressed activity of NOS by 72 % (LN). 18479899: Soy protein hydrolysate ameliorates cardiovascular remodeling in rats with L-NAME-induced hypertension. In the present study, we investigated the effects of soy protein hydrolysate with angiotensin-converting enzyme (ACE) inhibitory potential on the blood pressure and cardiovascular remodeling in rats with N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension. 18712676: L-NAME caused arterial hypertension and cardiomyocyte hypertrophy. 18927469: ADU (100 microg/mL in drinking water) lowered blood pressure in angiotensin II-infused hypertension, but not in L-NAME-induced hypertension. 19049674: The extract showed good prophylactic as well as curative effect against L-NAME-induced hypertension, whereby its content of chlorogenic acids may play a minor role. Solanum indicum ssp. distichum extract is effective against L-NAME-induced hypertension in rats. Giving the extract (100 and 300 mg/kg) orally once daily during the 1 week hypertension induction period with L-NAME prevented the development of hypertension. 19262491: Effect of L-NAME-induced hypertension on melatonin receptors and melatonin levels in the pineal gland and the peripheral organs of rats. 19439171: AIM: The present work evaluates acute toxicity and effects of oral administration of AEST in chronic arterial hypertension induced by L-NAME. 19961262: The aim of the present study was to evaluate the role of inhibitory G (G(i)) proteins, which are involved in tonic sympathetic vasoconstriction, in the pathogenesis of NO-deficient hypertension. Influence of pertussis toxin pretreatment on the development of L-NAME-induced hypertension. 20005970: Nitric oxide (NO) has numerous important functions in the kidney, and long-term blockage of nitric oxide synthases in rats by L-NAME results in severe hypertension and progressive kidney damage. 20823716: CONCLUSION: Decreased NOS activity along with increased oxidative load may be responsible for decreased NO bio-availability and further BP increase after NF-kappaB inhibition in L-NAME-induced hypertension. Effect of nuclear factor kappa B inhibition on L-NAME-induced hypertension and cardiovascular remodelling. 21479940: In this study, we aimed to investigate whether lisinopril treatment has any biochemical alterations on renal tissue in L-NAME (Nepsilon-nitro-L-arginine methyl ester) induced hypertension model. 21899859: Carotid body remodelling in l-NAME-induced hypertension in the rat. The aim of this study was to evaluate the morphological changes of the CB and carotid glomus in the rat model of l-NAME-induced hypertension. Immunohistochemistry showed increased expression of nuclear factor kB, substance P, vascular endothelial growth factor and neuronal nitric oxide synthase in the LN group, while expression of the protein gene product 9.5 was decreased. l-NAME alters cell morphology and the expression of extracellular matrix molecules in the CB and carotid glomus in rats with l-NAME-induced hypertension. 21907795: These results indicate that BA decreased blood pressure and improved ACh-induced endothelium-dependent vasorelaxation in L-NAME-induced hypertension rats, which may be mediated by reducing oxidative stress and retaining the bioavailability of NO in the cardiovascular system. 21995907: The effect of indapamide on development of myocardial hypertrophy and fibrosis in L-NAME-induced hypertension in rat. 22051897: Taken together, these results demonstrated that the sap of Acer okamotoanum ameliorated high BP induced by L-NAME treatment in a rat model. 22052053: Tamoxifen was renoprotective despite having no effect on the sustained, severe hypertension induced by L-NAME. 22128421: Our results demonstrate that AT1 receptor stimulation is related to renal vasculature hypersensitivity in L-NAME-induced hypertension. 22128423: Our results suggest that Ang II hypersensitivity in L-NAME-induced hypertension can be due to increased AT1 receptor expression or sensitivity changes. In this work, we determined the Ang II type 1 (AT1) receptor role in L-NAME-induced hypertension in pithed rats. 22258332: Furthermore, female rats showed blunted BP response and elevated plasma adiponectin in the salt-induced and L-NAME-induced hypertension models. 22578103: Individual and concomitant effects of cardioprotective programs on cardiac apelinergic system and oxidative state in L-NAME-induced hypertension. 22819707: Novel diallyldisulfide analogs ameliorate cardiovascular remodeling in rats with L-NAME-induced hypertension. 2282451: In separate groups of animals spontaneous oral ingestion of NG-monomethyl-L-arginine (L-NMMA; 1 mg ml-1) or NG-nitro-L-arginine methyl ester (L-NAME; 0.1 mg ml-1) caused marked hypertension but no significant bradycardia. 22943192: Effects of lisinopril on NMDA receptor subunits 2A and 2B levels in the hippocampus of rats with L-NAME-induced hypertension. 22961602: The present study investigated the effects of a 6-week swimming training on blood pressure, nitric oxide (NO) levels and oxidative stress parameters such as protein and lipid oxidation, antioxidant enzyme activity and endogenous non-enzymatic antioxidant content in kidney and circulating fluids, as well as on serum biochemical parameters (cholesterol, triglycerides, urea and creatinine) from Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension treated rats. Physical training prevents oxidative stress in L-NAME-induced hypertension rats. 23072319: Hypertension was induced by l-NAME (10 mg/kg) for 8 weeks and six sessions a week. 23079793: Syringic acid ameliorates (L)-NAME-induced hypertension by reducing oxidative stress. 23545992: Resistance training controls arterial blood pressure in rats with L-NAME- induced hypertension. 23756396: The aim of our study was to evaluate the relationship of selected biomarkers in L-NAME-induced hypertension to the left ventricular remodeling in the two different periods of hypertension development. Although the systolic blood pressure increases about 50% in L-NAME-induced hypertension in rat, both hypertrophy and fibrosis were expressed only slightly in this experiment. 23883679: L-NAME-induced hypertension increased renal T cell infiltration and indices of renal injury in both sexes, yet female SHR exhibited greater increases in Th17 cells and greater decreases in regulatory T cells than males. 23946694: These findings suggest that lutein affords significant antihypertensive and antioxidant effects against L-NAME-induced hypertension in rats. 24302630: METHODS AND RESULTS: NG-nitro-l-arginine methyl ester (l-NAME)-induced hypertension was blunted in TLR4(-/-) when compared with wild-type mice. Damage-associated molecular pattern activated Toll-like receptor 4 signalling modulates blood pressure in L-NAME-induced hypertension. 24658348: We found that a single pharmacological dose of sodium nitrite exerts antihypertensive effects in L-NAME-induced hypertension. Here, we evaluated the antihypertensive effects of a daily dose of sodium nitrite for 4 weeks in L-NAME-induced hypertension in rats. 24744878: These results suggest that TRPV4 channels play a minor role in blood pressure regulation in l-NAME- but not Ang II-induced hypertension, but may be importantly involved in Ang II-induced endothelial dysfunction. 24772821: The effect of an aqueous Mentha cordifolia (MC) extract on the haemodynamic status, vascular remodeling, function, and oxidative status in NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension was investigated. Vascular and antioxidant effects of an aqueous Mentha cordifolia extract in experimental N(G)-nitro-L-arginine methyl ester-induced hypertension. 24878382: We examined whether sodium nitrite (15 mg/kg; or vehicle; by gavage): (I) attenuates the pressor responses to angiotensin I at doses of 0.03, 0.1, 0.3, 1, 3, and 10 MUg/kg intravenously; (II) attenuates the acute hypertension induced by L-NAME (100 mg/kg; or vehicle; by gavage); (III) attenuates the chronic hypertension induced by L-NAME (1 g/L in drinking water; or vehicle) administered for 6 weeks; (IV) attenuates the hypertension in the 2 kidney-1 clip (2K1C) chronic hypertension model. 24942010: Changes in adrenoceptors and G-protein-coupled receptor kinase 2 in L-NAME-induced hypertension compared to spontaneous hypertension in rats. This work compares the expression of adrenoceptors (ARs) and G-protein-coupled receptor kinase (GRK) 2 (RT-PCR and immunoblotting) and functional responses in conductance (aorta) and resistance vessels (mesenteric resistance arteries; MRA) in two different models of rat hypertension: hypertension induced by chronic treatment with L-NAME (N(G)-nitro-L-arginine methyl-ester) (L-NAME-treated rats; LNHR), and genetically induced hypertension (spontaneously hypertensive rats; SHR). 25418643: CONCLUSIONS: The macerated garlic given for an 18-week period effectively produced a hypotensive effect in rats with hypertension induced by L-NAME. 25517031: L-NAME exposure induced hypertension in the 12-week-old offspring, which CIT therapy prevented. We examined whether maternal CIT supplementation can prevent N(G)-nitro-L-arginine-methyl ester (L-NAME, NO synthase inhibitor)-induced programmed hypertension and examined their effects on the renal transcriptome in male offspring using next generation RNA sequencing (RNA-Seq) technology. 25986148: The plasma level of OPN and its expression in aortic tissue were increased in various animal models of hypertension including spontaneous hypertensive rats and hypertensive mice induced by angiotensin II or L-NAME. 26133972: Ellagic Acid Prevents L-NAME-Induced Hypertension via Restoration of eNOS and p47phox Expression in Rats. L-NAME induced high systolic blood pressure (SBP) and increased heart rate (HR), hindlimb vascular resistance (HVR) and oxidative stress. The effect of ellagic acid on oxidative stress and hypertension induced by Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME) was investigated. 26234646: Asiatic acid alleviates cardiovascular remodelling in rats with L-NAME-induced hypertension. Male Sprague-Dawley rats were treated with L-NAME (40 mg/kg per day) for 3 weeks in order to induce hypertension. 26949504: Hypertension was induced by NG-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg/day) administration in drinking water, and BP was measured weekly. 27457113: RESULTS: NG-nitro-L-arginine-methyl ester exposure during pregnancy induced programmed hypertension in adult male offspring, which was prevented by maternal melatonin or N-acetylcysteine therapy. Next, we aimed to identify potential gatekeeper pathways that contribute to NG-nitro-L-arginine-methyl ester -induced programmed hypertension using the next generation RNA sequencing technology. Among them, genes belong to the renin-angiotensin system, and arachidonic acid metabolism pathways were potentially involved in the NG-nitro-L-arginine-methyl ester-induced programmed hypertension. Nitric oxide deficiency during pregnancy causes hypertension in adult offspring. Protective effects of melatonin and N-acetylcysteine against NG-nitro-L-arginine-methyl ester-induced programmed hypertension were associated with an increase in hydrogen sulfide-generating enzymes and hydrogen sulfide synthesis in the kidneys. 27720848: MATERIALS AND METHODS: SHR, DOCA-salt- and L-NAME-induced hypertension models were used. 28234674: Gallic acid attenuates hypertension, cardiac remodeling, and fibrosis in mice with NG-nitro-L-arginine methyl ester-induced hypertension via regulation of histone deacetylase 1 or histone deacetylase 2. 28757582: In addition, the lactacystin-model was compared with NG-nitro-l-arginine-methyl ester (L-NAME)- and continuous light-induced hypertension. LV weight and the cross-sectional area of the aorta were increased only in L-NAME-induced hypertension. 28842425: C57Bl/6 mice were treated with the NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME) from gestational day (GD) 11 to GD18 to induce hypertension. 29087727: In this study, we investigated the effects of 20-HETE on the vascular responsiveness and BP in an L-NAME-induced hypertension. This study demonstrates an important role of 20-HETE in increasing BP and altering vascular responsiveness in L-NAME-induced hypertension model, which suggests a possible involvement of 20-HETE in essential hypertension development in humans. Although various experimental animal hypertension models demonstrated that 20-HETE contributes to increased vascular resistance and BP, these effects have not been studied in Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension model. 20-HETE inhibition by HET-0016 significantly decreased BP in L-NAME-induced hypertension model. Effect of 20-HETE inhibition on L-NAME-induced hypertension in rats. 29333212: In conclusion, our results showed that active substances of Aronia melanocarpa may have a positive effect on blood pressure, NOS activity, and proinflammatory processes in L-NAME-induced hypertension. 29378249: Contrasting effects of low versus high ascorbate doses on blood pressure responses to oral nitrite in L-NAME-induced hypertension. 29382124: Melatonin exerts its protective effect in l-NAME-induced hypertension without affecting RAAS. Effect of Melatonin on the Renin-Angiotensin-Aldosterone System in l-NAME-Induced Hypertension. Four groups of 3-month-old male Wistar rats (n = 10) were treated as follows for four weeks: untreated controls, rats treated with melatonin (10 mg/kg/day), rats treated with l-NAME (40 mg/kg/day), and rats treated with l-NAME + melatonin. l-NAME administration led to hypertension and left ventricular (LV) fibrosis in terms of enhancement of soluble, insoluble and total collagen concentration and content. 30028078: LC40 prevents gut dysbiosis, alters the Th17/Treg balance in MLN, vascular oxidative stress, and inflammation, slightly improves endothelial dysfuncion but do not inhibit the development of l-NAME-induced hypertension. 30112041: The present study investigated the effects of NGN on left ventricular hypertrophy in rats with NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension, and sought to determine the underlying mechanism of action. 30282928: We conclude that ivabradine improved the LV function of the hypertensive heart in L-NAME-induced hypertension. Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension. This study investigated whether ivabradine is able to protect a hypertensive heart in the model of L-NAME-induced hypertension and to interfere with the RAAS. 30347181: L-NAME-induced hypertension is commonly used to study endothelial dysfunction and related vascular effects. 30590121: Male Sprague-Dawley rats were administrated with L-NAME (40mg/kg/day) for five weeks to induce hypertension. 30706510: Forty adult Sprague-Dawley rats were divided into four groups: control, NaHS (0.037 mg kg day-1 )-treated control, L-NAME-induced hypertension (40 mg kg day-1 ) and NaHS-treated L-NAME-induced hypertension. 30790319: Ivabradine reversed nondipping heart rate in rats with l-NAME-induced hypertension. Sixty-six Wistar rats were divided into non-diseased controls and rats with l-NAME-induced hypertension to compare the haemodynamic effects of daytime-dosed and night-time-dosed ivabradine. l-NAME-induced hypertension inverted the physiological 5.6% night-to-day HR dip to an undesirable HR rise by 11.1%. 31108332: We examined whether postnatal HF diet can aggravate maternal NG-nitro-L-arginine-methyl ester (L-NAME) treatment-induced programmed hypertension and whether resveratrol therapy can prevent it. 31167124: 5-Lipoxagenase deficiency attenuates L-NAME-induced hypertension and vascular remodeling. 31312143: alpha-CGRP acts as a depressor to attenuate the rise in blood pressure in three different models of experimental hypertension: (1) DOC-salt, (2) subtotal nephrectomy-salt, and (3) L-NAME-induced hypertension during pregnancy. 31868952: Effects of Hydrogen Sulfide on Oxidative Stress, Inflammatory Cytokines, and Vascular Remodeling in L-NAME-induced Hypertension. This study was designed to evaluate the protective effects of hydrogen sulfide (H 2 S) against NG-Nitro L-Arginine Methyl Ester (L-NAME)-induced hypertension and its possible effects on the inflammatory process, oxidative stress, and vascular remodeling in rats. 32202168: Antioxidant and vasorelaxant effects of aqueous extract of large cardamom in L-NAME induced hypertensive rats.PURPOSE: The present work aimed to study the effect of aqueous extract of large cardamom (AELC) to prevent vascular remodeling and oxidative stress in N omega -Nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 32507041: Intriguingly, G6PD S188F mutants, as compared with WT rats, developed less large arterial stiffness and hypertension evoked by high-fat diet and nitric oxide synthase inhibition with L-N G -nitroarginine methyl ester. Finally, our results suggested that (1) lower resting membrane potential of smooth muscle caused by increased expression of K + channel proteins and (2) decreased voltage-gated Ca 2+ channel activity in smooth muscle contributed to reduced hypertension and arterial stiffness evoked by L-N G -nitroarginine methyl ester and high-fat diet to G6PD S188F mutants as compared with WT rats. 32754607: Ivabradine Ameliorates Kidney Fibrosis in L-NAME-Induced Hypertension. Thirty-six adult male Wistar rats were divided into non-diseased controls and rats with N G -nitro-L-arginine methyl ester (L-NAME)-induced hypertension to assess ivabradine's site-specific effect on kidney fibrosis. 32810514: Sub-acute exposure to L-NAME and BPA induced hypertension and mediated-neuroinflammation at CA-2 and CA-4 of hippocampus cells. 32950570: MAIN METHODS: L-NAME (N G -Nitro-L-arginine-methyl ester) was used to induce the hypertension. 33014103: Conclusion: Our findings suggest that the extract of A. digitata has antihypertensive and antioxidant effects in L-NAME-induced hypertension rat models. 33557258: Genistein prevented L-NAME-induced hypertension in rats. 33747111: In previous studies, the methanol/methylene chloride stem-bark extract of Vitex cienkowskii (MMVC) showed a preventive activity in L-NAME-induced hypertension and improved blood pressure of spontaneously hypertensive rats. 33826116: CONCLUSION: This study therefore demonstrates that MEADF possesses an in vivo ACE inhibitory activity, hypotensive potential and the ability to avert further degeneration of biochemical and physiological upsets associated with L-NAME induced hypertension. Fruit Pulp on N G -Nitro-L-Arginine Methyl Ester (L-NAME) Induced Hypertension in Rats. AIM: This study investigated the effect of methanol extract of Adansonia digitata fruit (MEADF) pulp on N G -nitro-L-arginine methyl ester (L-NAME) induced hypertension in rats. 33846799: Central AT1R is involved in almost all types of hypertension, including spontaneous hypertension, salt-sensitive hypertension, obesity-induced hypertension, renovascular hypertension, diabetic hypertension, L-NAME-induced hypertension, stress-induced hypertension, angiotensin II-induced hypertension and aldosterone-induced hypertension. Present in more than one billion adults, hypertension is the most significant modifiable risk factor for mortality resulting from cardiovascular disease. 34133045: Nevertheless, chronic NO-synthase inhibition with L-NAME induced a greater hypertension in Opa1 +/- than in WT mice without compensatory arterial wall hypertrophy. 34144158: Clitoria ternatea L. extract prevents kidney damage by suppressing the Ang II/Nox4/oxidative stress cascade in L-NAME-induced hypertension model of rats. 34335852: In this study, we evaluated the effect of a traditional herbal formula, Ma Huang Tang (MHT), on blood pressure and vasodilation in a rat model of N G -nitro-L-arginine methylester- (L-NAME-) induced hypertension. New Therapeutic Insight into the Effect of Ma Huang Tang on Blood Pressure and Renal Dysfunction in the L-NAME-Induced Hypertension. 34345384: This study evaluated the effect of the saffron petal on hypertension induced by angiotensin II (AII) and NG-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor). Effects of hydroalcoholic extract of saffron petal on blood pressure and heart rate in hypertension induced by angiotensin II and L-NAME in anesthetized rats. 34403364: Moreover, FG-4592 treatment was hypotensive in L-NAME-induced hypertension. 34774683: AIM: The current research evaluates the antihypertensive potential of aqueous methanolic extract of Z. oxyphylla (AMEZO) in NG-nitro-L-arginine methyl ester (LNAME) induced hypertension in rats. 34904852: METHODS: N-nitro-L-arginine methyl ester (L-NAME)-induced HT model was performed on nondiabetic male rats. 35000635: Daily consumption of wild olive (acebuche) oil reduces blood pressure and ameliorates endothelial dysfunction and vascular remodelling in rats with L-NAME-induced hypertension. The aim of this study was to analyse the possible beneficial effects of an extra virgin ACE oil on vascular function in a rodent model of arterial hypertension induced by L-NAME (NG-nitro-L-arginine methyl ester). 35554529: The present study investigated the novel antihypertensive action of Naringenin on N Upsilon -Nitro-L-arginine Methyl Ester (L-NAME)-induced hypertension together with possible molecular mechanism of action. 35555985: Ameliorative Effect of Morinda Lucida on L-nitro Arginine Methyl Ester (L-name) Induced Hypertension in Male Wistar Rats. 35812238: The current study characterized a rat model of transient hypertension with an extended period of normotensive recovery: F344 rats were treated with L-NG-Nitroarginine methyl ester (L-NAME) for 1 month to induce hypertension then allowed up to 4 months of recovery. 35897759: Here, we investigated the effect of esomeprazole in a mouse model of L-NAME-induced hypertension (decreased eNOS activity). 35973627: CONCLUSIONS: It can be concluded that either the increment in blood pressure (systolic, diastolic, and median) or cardiorenal remodeling effects in male and female rats submitted to L-NAME-induced hypertensive condition, were prevented and well-preserved without a significant variation during a period of 6-week of pretreatment with CESs and saponins pretreatments. AIM OF THE STUDY: This study aimed to determine the influence of chronic oral administration of the crude root extract and saponins obtained from S. sisymbriifolium Lam., on the blood pressure of male and female rats with hypertension induced by L-NAME, and its consequences on diuresis, the body weight, blood glucose, and level of serum parameters of liver and kidney functionality. RESULTS: A protective effect of CESs (100.0 mg/kg/day), and saponins (1.0, and 10.0 mg/kg/day) against hypertension induced by L-NAME was verified in the systolic, diastolic, and mean blood pressure values, which were significantly lower than the positive L-NAME-hypertensive control group (male and female) at the end of the 6-week treatment. The antihypertensive and diuretic effect of crude root extract and saponins from Solanum sisymbriifolium Lam., in L-NAME-induced hypertension in rats. 36140333: Treatment with L-arginine via oral gavage or infusion into the cistern magna (i.c.), but not i.c. tempol or mitoQ 10 , significantly offset the l-NAME-induced hypertension in young rats. 36503395: RESULTS: The results showed that ALAE reduced blood pressure parameters (systolic, mean, and diastolic blood pressure) in L-NAME-induced hypertension rats after repeated oral treatment over seven days without affecting normotensive rats. 37088236: RESULTS: ADED exhibited significant antihypertensive effects in L-NAME-induced hypertension models and phenylephrine-induced vasoconstriction. 37380045: 1,8-Cineole ameliorates endothelial injury and hypertension induced by L-NAME through regulation of autophagy via PI3K/mTOR signaling pathway. 38134595: Here, the roles of TWIST1 in macrophage activation during N w -nitro-l-arginine-methyl ester (L-NAME; NO-synthase (NOS) inhibitor)-induced hypertension were investigated in ApoE -/- mice fed a high-fat diet (HFD) and RAW264.7 cells treated with oxidized low-density lipoprotein(ox-LDL). 38136662: L-NAME-induced hypertension and proteinuria were mitigated when SERPINA5 expression was suppressed. 38358640: This study evaluated the vascular relaxation of hydroalcoholic extracts from seeds of three varieties of P. dactylifera; Sukkari seed (SS), Ajwa seed (AS), and Mabroom seed (MS) on L-NAME-induced hypertension and spontaneously hypertensive rats (SHR). 38388918: Angiotensin II in combination with L-NAME-induced hypertension was used to elicit CMH. 38616386: This review provides compelling evidence for the antihypertensive potential of flavonoids against L-NAME-induced hypertension. Flavonoids have been extensively studied in cell cultures, animal models, and, to lesser extent, in human trials to evaluate their effectiveness against L-NAME-induced hypertension. This comprehensive review summarizes the antihypertensive activity of specific flavonoids, including quercetin, luteolin, rutin, troxerutin, apigenin, and chrysin, in L-NAME-induced hypertension models. 7532833: Methoxamine (0.1 mg/kg i.v.) was used to mimic the marked hypertension caused by L-NAME. 7558232: We also found that L-NAME-induced hypertension, once developed, is completely reversed by acute ganglionic blockade. Pharmacological inhibition of nitric oxide synthase causes sustained hypertension in many animal species. 7653592: The impact of chronic NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (20 mg.kg-1.day-1 po, for 25 days) on pressure responsiveness was assessed in vessels ranging from arcuate arteries (ArcA) to juxtaglomerular afferent arterioles (JAA), using videomicroscopy and blood-perfused juxtamedullary nephron (JMN) preparations. 7721413: In normal Sprague-Dawley rats, selective reduction of medullary flow with medullary interstitial or intravenous infusion of small amounts of NG-nitro-L-arginine methyl ester resulted in hypertension. 7955145: In baroreceptor-denervated cats, reversible suppression of peripheral SNA produced by cooling of the ventral surface of the rostral ventrolateral medulla oblongata (RVLM) caused significant hypotension (61.1 +/- 2.6 mm Hg) and almost completely reversed the hypertension caused by L-NAME (76.0 +/- 3.7 mm Hg). In contrast, hypertension induced by angiotensin II could not be reversed by RVLM cooling. 7963507: Decreased cardiac baroreflex sensitivity is not due to cardiac hypertrophy in NG-nitro-L-arginine methyl ester-induced hypertension. 7990975: Pretreatment with L-NAME caused marked hypertension and bradycardia, associated with reduction in CBF (-34 +/- 16%) and LCX diameter (-9.5 +/- 0.8%). 8190263: Cerebrovascular autoregulation in response to hypertension induced by NG-nitro-L-arginine methyl ester. 8205483: Sympathetic denervation and the cerebrovascular response to hypertension induced by NG-nitro-L-arginine methyl ester. Unilateral sympathectomy at the superior cervical ganglion had no effect, suggesting that the autoregulatory response to L-NAME-induced hypertension is independent of sympathetic activity. 8258672: OBJECTIVE: To determine whether induction of arterial hypertension in young normotensive Wistar rats by chronic inhibition of nitric oxide production with NG-nitro-L-arginine methyl ester (L-NAME) produced a form of self-sustained hypertension, and to investigate the role of the renin-angiotensin system and vascular hypertrophy in the hypertensive process. 8557958: Vascular structure in NG-nitro-L-arginine methyl ester-induced hypertension: methodological considerations for studies of small arteries in hypertension. 8586814: Vascular structure in hypertension induced by NG-nitro-L-arginine methyl ester: methodological considerations for studies of small arteries in hypertension--reply. 8794817: Alterations in vascular reactivity in this model have not been extensively studied and could potentially be involved in the pathogenesis of L-NAME-induced hypertension. In vitro alteration of aortic vascular reactivity in hypertension induced by chronic NG-nitro-L-arginine methyl ester. 8967473: Oral administration of NG-nitro-L-arginine methyl ester (L-NAME) for 4 wk caused hypertension and a significant reduction in urinary NO2- and NO3- excretion. 8997619: NO synthase inhibition, as obtained by N omega-nitro-L-arginine methyl ester (L-NAME; 0.63 mg/kg i.v. + 20 mg/kg/h), induced sustained systemic hypertension (mean maximal increase, delta, in mean systemic arterial pressure = 38 +/- 6 mmHg; P < 0.05 vs. vehicle) associated with slight bradycardia (delta heart rate = -42 +/- 8 beats/min; P < 0.05 vs. vehicle) and delayed- (> 30 min) onset pulmonary hypertension (delta mean pulmonary arterial pressure = 10 +/- 3.4 mmHg; P < 0.05 vs. vehicle). 9039110: Calcitonin gene-related peptide is a depressor in NG-nitro-L-arginine methyl ester-induced hypertension during pregnancy. 9396239: Although the inhibition of nitric oxide (NO) synthesis is known to induce systemic hypertension, the underlying mechanisms mediating this type of hypertension are incompletely understood. L-NAME-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites, NO2- and NO3-, and was aggravated when rats drank 0.9% saline in place of tap water. These results suggest that the inhibition of chronic NO synthesis produces sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension. 9458851: L-NAME treatment induced hypertension that was associated with increased plasma renin activity. 9496441: The aim of the present study was to investigate the role of bradykinin in the inhibitory action of captopril in hypertension induced by L-NAME in anesthetized rats. Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats. 9533419: Sympathetic functions in NG-nitro-L-arginine-methyl-ester-induced hypertension: modulation by the renin-angiotensin system. 9813931: We examined the effect of CGRP to ameliorate L-NAME-induced hypertension during pregnancy, and the efficacy of CGRP and progesterone in combination to inhibit L-NAME-induced hypertension during the post-partum period. 9933759: L-NAME-induced hypertension was associated with cardiac hypertrophy and this was prevented by captopril. 10435012: OBJECTIVE: Both disruption of the endothelial nitric oxide synthase (eNOS) gene and pharmacological inhibition of the NOS produce modest hypertension. 16804287: BACKGROUND: Obstructive sleep apnea syndrome (OSAS) influences endothelial function and causes hypertension. 17081226: The findings oppose the theory of generalized vasoconstriction and impaired endothelial function in the pathogenesis of hypertension after transplantation. 17620955: CONCLUSIONS: Our findings suggest an additive adverse effect of hypoalphalipoproteinemia and hyperhomocysteinemia on endothelial function to generate clinical hypertension and cardiac muscle hypertrophy mediated by dysregulation in nitric oxide metabolism. 17673017: [Role of sympathetic nerve activity and arterial endothelial function in pathogenesis of hypertension in patients with obstructive sleep apnea-hypopnea syndrome]. 18075809: The genetic deletion of eNOS seems to lead to higher SBP and DBP, but the circadian blood pressure pattern is still preserved with higher values during the night (active phase) and lower values during the daytime (rest phase). 19342603: Impaired insulin signaling via phosphatidylinositol 3-kinase/Akt to endothelial nitric oxide synthase (eNOS) in the vasculature has been postulated to lead to arterial dysfunction and hypertension in obesity and other insulin resistant states. 20186125: NOLA exacerbated dexamethasone-induced hypertension. BACKGROUND: Glucocorticoid-induced hypertension is associated with imbalance between nitric oxide (NO) and superoxide. Effects of sepiapterin supplementation and NOS inhibition on glucocorticoid-induced hypertension. In the present study, adrenocorticotrophic hormone (ACTH)- and dexamethasone-treated rats were further treated with sepiapterin, a precursor of tetrahydrobiopterin, or N-nitro-L-arginine (NOLA), an inhibitor of NOS, to investigate the role of eNOS uncoupling in glucocorticoid-induced hypertension. Sepiapterin did not prevent ACTH- (129 +/- 4 mm Hg, NS) or dexamethasone-induced hypertension (135 +/- 3 mm Hg, NS), although plasma total biopterin concentrations were increased. These data suggest that eNOS uncoupling does not play a major role in the genesis of glucocorticoid-induced hypertension in the rat. CONCLUSION: Sepiapterin did not prevent ACTH- or dexamethasone-induced hypertension. 2151671: Tissue systems, endothelial and growth factors as new elements of arterial hypertension pathogenesis may influence the further development of new antihypertensive drugs. 21531372: OBJECTIVE: To determine whether oxidative stress plays a role in the development of hypertension using a mouse model of fetal programming induced by endothelial nitric oxide synthase deficiency. 22458744: These findings raise the possibility that female sex may impart a greater risk of CV events in patients with untreated stage 1 hypertension potentially due to poorer endothelial function. 22829869: Selective endothelial overexpression of arginase II induces endothelial dysfunction and hypertension and enhances atherosclerosis in mice. 24926270: Interestingly, diminished endothelial function, manifested by low angiogenic capacity, leads to hypertension in animal studies. 25034792: Endothelial nitric oxide synthase deficiency (eNOS(-/-)) results in moderate hypertension and the development of nodular glomerulosclerosis and hyaline arteriosclerosis in streptozotocin-induced diabetic C57BL/6J mice. 25185128: As angiotensin II-infused TNF knockout mice had exaggerated endothelial nitric oxide synthase expression in the kidney and enhanced nitric oxide bioavailability, we examined the actions of TNF-alpha generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF knockout kidneys into wild-type recipients before the induction of hypertension. 26694820: In addition, nitric oxide (NO), synthesized by nitric oxide synthases (endothelial and inducible), is also associated with IR when both impaired release and reduced bioavailability of all which lead to inflammation and hypertension. 27906746: RECENT FINDINGS: This article presents past and recent findings that focus on the role of 20-HETE in the regulation of the vasculature in health and disease and the implication of its actions on endothelial and vascular smooth muscle cells to the pathogenesis of hypertension and stroke. 28455674: Chronic inflammation and adipocyte dysfunction may alter endothelial function leading to hypertension. 29934052: Taken together, these data suggested that mangiferin has played an important part in alleviating hypertension induced by hyperuricemia via increasing NO secretion and improving endothelial function. In this study, we aimed to evaluate the effect of mangiferin on alleviating hypertension induced by hyperuricemia. 29950683: We previously reported that systemic heterozygous ATP2B1-null (ATP2B1+/-) mice exhibited hypertension due to impaired endothelial nitric oxide synthase (eNOS) activity and decreased nitric oxide (NO) production. 29997131: Nephron-Specific Disruption of Nitric Oxide Synthase 3 Causes Hypertension and Impaired Salt Excretion. 31328772: Secreted Monocyte miR-27a, via Mesenteric Arterial Mas Receptor-eNOS Pathway, Causes Hypertension. 35089811: Together, our data demonstrate that ECV exposure activates NADPH oxidase and uncouples eNOS, causing a vicious cycle of superoxide generation and vascular oxidant stress that triggers VED and hypertension with predisposition to other cardiovascular disease. 35557373: CONCLUSION: Our data demonstrate that ECV exposure activates NADPH oxidase and uncouples eNOS, causing a vicious cycle of superoxide generation and vascular oxidant stress that triggers VED and hypertension with predisposition to other cardiovascular disease. 7812826: To determine if endothelial and ROS-induced changes in hypertension, atherosclerosis, ischemia/reperfusion etc. are the primary cause of specific diseases or merely secondary effects remains to be clarified in several areas from inflammatory processes to cardiovascular diseases. 9728076: The purpose of the current study is to determine if HTN is most likely a cause or result of impaired endothelial function. 11276400: Finally, mutations in cytoskeleton proteins may stimulate renal Na+,K+-ATPase activity by way of protein/protein interaction and lead to salt retention and hypertension. 12861334: Effect of polyphenolic compounds on the renal Na(+),K(+)-ATPase during the restoration of normotension after experimentally induced hypertension in rats. 17976639: These responses seem to be caused by reduced Na(+),K(+)-ATPase activity and increased intracellular calcium, suggesting that inhibition of Na(+),K(+)-ATPase by overexpression of TCTP is involved in the pathogenesis of hypertension. 2579261: They are also compatible with the concept that an endogenous inhibitor of Na-K-ATPase - in the presence of decreased baroreceptor reflex sensitivity due to blood volume expansion - may play a role in the pathogenesis of human arterial hypertension. 26105942: This endogenous mammalian vasoconstrictive compound, is a selective inhibitor of the alpha1 subunit of Na+,K+-ATPase, leading to hypertension and natriuresis. 2824367: Inhibition of the sodium pump in vascular smooth muscle caused by such a circulating factor could increase vascular tone and sensitivity to vasoactive agents, and thereby result in arterial hypertension. 2990771: Thus, vasoconstriction due to inhibition of sodium pump activity of the vascular smooth muscle cell may contribute to the pathogenesis of human arterial hypertension. 6248683: Increased activity of the Na-K-ATPase in red cell-ghosts of patients with Cushing's syndrome: possible significance for the pathogenesis of glucocorticoid-induced hypertension. 7449259: An increase in cellular sodium as a result of altered sodium pump activity may be the cause of hypertension in pre-eclampsia. 8103335: A significant increase (34%) in the apparent affinity constant (KD) but no change in the maximum binding capacity (Bmax) for [3H]ouabain binding to the cerebromicrovascular Na+,K(+)-ATPase occurs after induction of acute hypertension. 1130932: This case should call attention to the renin-secreting tumor as a cause of even mild hypertension. 11928050: Juxtaglomerular cell tumor is an extremely rare neoplasm of the kidney that causes blood hypertension. 11969054: Pheochromocytoma as a catecholamine secreting tumour causing severe hypertension is exceedingly rare in children. 12381537: Pheochromocytoma and paragangliomas are rare tumors of chromaffin tissue that secrete catecholamines either intermittently or continuously, producing hypertension with a constellation of symptoms and signs that can be frightening to the patient and that continue to provide perplexing problems for clinicians. 12381539: Pheochromocytomas are dangerous tumors that, although a rare cause of hypertension, require consideration among large numbers of patients. 12480212: However, there is little reference to tumors causing hypertension by local compression of the vagal nerve or the ventrolateral medulla oblongata. 12566722: Phaeochromocytoma is a tumour of the adrenal medulla, which, although rare, is a major cause of correctable hypertension with a prevalence of 0.1-0.5% in the hypertensive population. 12910061: We report a case of a renin secreting tumor, which is a very rare cause of secondary high blood pressure. 13009500: By recently developed tests, it has been possible to differentiate high blood pressure due to these tumors from hypertension due to other causes. 13073544: [Hypertension caused by tumors of the adrenal cortex]. 14605591: Pheochromocytomas are rare tumours of catecholamine-producing chromaffin cells leading to hypertension and symptoms of catecholamine excess. 15157558: Pheochromocytoma is a lethal tumor of chromaffin cells of the adrenal medulla that produces episodes of hypertension with the symptoms of palpitations, severe headaches, and sweating. 15198238: Manipulation of the tumor induced hypertension. 15400771: [Bronchoalveolar hypertension, osteoarthropathy and gynecomastia syndrome caused by endobronchial neoplasm]. 16429666: Renin-secreting tumour is a rare, benign entity, responsible for hypertension due to secondary hyperaldosteronism. 1647868: The tumor is most likely to cause uncontrolled hypertension, nervousness, diaphoresis, and palpitations, but, at other times, may show no symptoms at all. 16821216: These tumors produce the hypertension which can be cured with surgical excision of the lesion. 17432020: Pheochromocytoma is a catecholamine producing tumour that can cause severe hypertension and other systemic disturbances. 1745805: Pheochromocytoma is a catecholamine secreting tumor which has been traditionally considered as a potentially curable cause of hypertension. 1793381: A crucial role of the tumour in the genesis of hypertension is suggested. 18192852: Reninoma is a tumor of the renal juxtaglomerular cell apparatus that causes hypertension and hypokalemia via hypersecretion of renin. 18463772: CONCLUSIONS: The tumours of cauda equina could cause endocranial hypertension and consequently a papilledema because of hyperproteinorachia. 1942353: Renin-secreting juxtaglomerular tumor causing severe hypertension: diagnosis by computerized tomography-directed needle biopsy. Renin-secreting tumors are a rare cause of severe hypertension accompanied by hypokalemia. 19808327: Although these tumors have long been postulated to induce hypertension and cardiomyopathy through the hypersecretion of catecholamines, catecholamines alone may not fully explain the profound myocardial remodeling induced by these tumors. 20434032: A juxtaglomerular cell tumor (JCT) is a rare, renin-secreting tumor of the kidney and can cause hypertension. 20662291: 0.1-0.2% of all cases of hypertension are caused by pheochromocytomas, or catecholamine-producing tumors derived from chromaffin tissue. 20671982: Rare and novel DOC producing tumors are an important cause of resistant hypertension. Deoxycorticosterone producing tumor as a cause of resistant hypertension. 21556813: Cushing's syndrome is associated with excessive cortisol secretion by the adrenal gland or ectopic tumours and may result in diabetes, hypertension, and life-threatening infections with high mortality rates especially in the case of surgical resection. 2160342: A 17 year old female presented with severe hypertension, hypokalaemia and elevated levels of plasma renin activity due to a renin-secreting tumour. 2234473: It is a catecholamine producing tumor of the sympathochromaffin system that typically cause sustained hypertension or hypertensive crisis. 22385767: This tumor may cause endocranial hypertension, which requires placement of a ventriculoperitoneal shunt after surgical resection. 2260476: A satellite tumor which was attached to the wall of the abdominal aorta induced marked hypertension due to obstruction of the renal arteries. 22644561: The patient was examined with gamma camera imaging and iodine-123 metaiodobenzylguanidine (MIBG), because her hypertension was thought to be due to a suspected adrenomedullary tumor. 22868025: They are catecholamine secreting tumours which cause severe hypertension and other systemic disturbances. 23638251: Ward round--A rare tumor of the kidney resulting in hypertension, renal failure and a cerebrovascular accident in a young female. 2407814: Hypertension resulting from a renin-secreting tumor was first reported in 1967 by Robertson et al. Since the description of these first two cases, it has become clear that renin-secreting tumors of both renal and nonrenal origin can cause surgically curable hypertension. 25276129: Arterial hypertension caused by paediatric adenomas or tumours of the adrenal cortex or medulla has been associated with various hypertension-related neurological manifestations. 2532339: [Arterial hypertension secondary to renin-producing tumor of ovarian origin]. 25339601: Fetal death was attributed to endocrine effects of the tumor causing fetal hypertension, arrhythmia, and/or placental dysfunction. 25928524: Although rare, chronic pyelonephritis and renal tumors as rennin-producing tumors, nephroblastoma, hypernephroma, and renal cell carcinoma might also induce hypertension and should be in the diagnostic list of clinicians. 26162468: The tumor produced excessive amounts of noradrenaline causing hypertension and symptoms of catecholamine excess. 26877959: Reninoma is a tumor of the renal juxtaglomerular cell apparatus that causes hypertension and hypokalemia because of hypersecretion of renin. 274940: Hypertension due to a renin-secreting tumour localised by segmental renal vein sampling. Although the immediate post-operative blood pressure fell to normal, hypertension recurred temporarily and was associated with elevated plasma aldosteron, producing a syndrome similar to primary aldosteronism. 28405904: In this review we consider the phenotype and genetic features of patients with tumor-induced hypertension and focus on their diagnostic work-up. Some tumors are a relatively rare and amendable cause of hypertension, often associated with a higher cardiovascular morbidity and mortality, as compared with that of both general population and patients with essential hypertension. 2942112: Blood flow of human tumors and normal tissue during the full course of induced hypertension with AT-II were measures by means of radionuclide angiography (99mTc-RBC) and laser Doppler velocimetry. 29578356: Pheochromocytoma is a rare catecholamine-secreting neoplasm that is the cause of hypertension in <0.2% of patients with hypertension. 29923996: RATIONALE: Pheochromocytomas are rare catecholamine-secreting tumors arising from adrenomedullary chromaffin cells, usually causing hypertension, palpitation and headache. 3535837: Severe hypertension in a ten-year-old boy secondary to an aldosterone-producing tumour identified by adrenal sonography. 3566299: On the basis of the functional characteristics of microcirculation in tumor tissue, the clinical results of angiotensin II-induced hypertension chemotherapy (IHC) have been reported. These results confirmed that blood flow remarkably increased not only in animal tumors but also in human tumors under the induced hypertension caused by angiotensin II. [Increase of blood flow in human tumor tissue under angiotensin II-induced hypertension]. 4715934: Role of renin and aldosterone in hypertension due to a renin-secreting tumor. 5851923: Curable hypertension due to aldosterone secreting tumors of the adrenal cortex. 5960988: [Arterial hypertension in a child due to a retroperitoneal tumor and renal artery stenosis]. 596587: Manipulation of the tumour provoked hypertension and after excision marked hypotension occurred which responded to the administration of metaraminol and blood. 6262473: Three times as much renin was extracted from tumor tissue as from adjacent renal parenchyma, suggesting that the tumor itself was the primary source of the renin and cause of the hypertension. 6664353: Renin producing tumors, hyperthyroidism and hyperparathyroidism are rare causes of hypertension in children. Inflammatory, traumatic, and tumorous disorders of the central nervous system rarely result in chronic hypertension but may frequently be associated with acute hypertensive crisis. 6986606: Eleven cases of hypertension secondary to a renal tumour secreting renin have been described in the literature between 1967 and 1978. [Hypertension secondary to a \renin tumor\. 6993568: [Another case of hypertension due to a tumour of the juxta-glomerular apparatus (author's transl)]. Eleven cases of hypertension secondary to a renal tumour secreting renin have been described in the literature between 1967 and 1978. 7992949: The authors report a case of pheochromocytoma recognized during surgery, at the manipulation of the tumor resulting in severe arterial hypertension, arrhythmia and a final unresponsive ventricular fibrillation. 8403356: BACKGROUND: Pheochromocytoma is a catecholamine-secreting tumor of chromaffin cells that causes hypertension. 8893935: Phaeochromocytoma as a catecholamine-secreting tumour causing severe hypertension is exceedingly rare in children. We highlight the problems encountered in making the diagnosis in an 11-year-old Chinese girl who presented with sustained hypertension, heart failure and transient renal impairment with two normal 24-hour urinary vanillyl mandelic acid (VMA) results before a third produced the diagnosis. 31984157: The majority of our patients (33 [89.1%]) had a secondary cause of hypertension. 32318499: Hypertension secondary to hydronephrosis is rarely described in clinical studies. Initial evaluation for a secondary cause of hypertension was negative. 33185153: Among secondary causes of paediatric hypertension, endocrine causes are relatively rare but important due to their unique treatment options. 33270939: OBJECTIVE: Primary aldosteronism (PA) is a potentially curable cause of hypertension associated with worse cardiovascular prognosis than blood pressure-matched essential hypertension (EH). Routine biochemical screening for PA remained the most reliable way of detecting this treatable secondary cause of hypertension. 33745915: Renal artery stenosis is the most common secondary cause of hypertension and predominantly caused by atherosclerosis. 34171624: Primary aldosteronism, the most common secondary cause of hypertension is likely to be significantly underdiagnosed in pregnancy and is associated with high rates of adverse maternal and fetal outcomes. 34240276: Renovascular disease is an important secondary cause of hypertension in childhood. 34247751: In patients presenting for the evaluation of resistant hypertension, taking a thoughtful approach to excluding pseudoresistant hypertension or a secondary cause of hypertension is important. 34307254: Regardless of the age of the child, it is recommended to carefully check for a secondary cause of hypertension as in 2/3 of cases it has a renal or cardiac origin. 34843971: Primary aldosteronism (PA) is the most common secondary cause of hypertension. 35068762: And, an accurate diagnosis of secondary cause of hypertension provides the treating clinician with a unique opportunity that renders dramatic response to the patient, either with pharmacologic therapy or surgery. One such secondary cause of hypertension is congenital adrenal hyperplasia due to 11 beta hydroxylase or 17 alpha hydroxylase deficiency. 35569086: CONTEXT: Primary aldosteronism (PA) is a common secondary cause of hypertension. 36027401: We suggest that first line testing only for primary hyperaldosteronism and renovascular hypertension would be sufficient for patients with resistant hypertension without clinical clues suggestive of another particular secondary cause of hypertension. 36103983: There is still inconsistency regarding whether ambulatory blood pressure monitoring should be used routinely both before and after RDN, and whether patients with a secondary cause of hypertension could be treated with RDN if their blood pressure remains uncontrolled after definitive treatment (treatment-resistant secondary hypertension). 36273684: Primary aldosteronism (PA) is a highly prevalent yet underdiagnosed secondary cause of hypertension. 36321804: CONCLUSION: A high proportion of patients are willing to engage in testing for a secondary cause of hypertension. Willingness to be tested for a secondary cause of hypertension: a survey of the Australian general community. RESULTS: Of 520 adult respondents (mean age 50.4 years, SD 27.3 years; 28.8% hypertensive; 56.0% female), the majority of non-hypertensive and hypertensive respondents (82.7% vs 70.0%; P = 0.03) were willing to undergo testing for a secondary cause of hypertension that involved blood and urine tests. 36374634: An identifiable secondary cause of HTN is present in approximately 10% of adult patients with HTN. 36982445: The excess of aldosterone, also known as primary aldosteronism, is the most common secondary cause of hypertension. 37650287: This review highlights PA as a potentially over-looked secondary cause of hypertension in SLE, and offers future directions in research to improve the detection of this highly modifiable cardiovascular risk factor in the SLE population. 37897111: OBJECTIVES: Primary aldosteronism (PA) is a common but underdiagnosed secondary cause of hypertension. 38039843: PE is a clinical syndrome characterized by hypertension secondary to systemic inflammation, endothelial dysfunction, and syncytiotrophoblast stress leading to hypertension and multiorgan dysfunction. 38116667: Primary aldosteronism (PA) is the leading secondary cause of hypertension. 38138198: The Modern Environment: The New Secondary Cause of Hypertension? 38205546: The high prevalence of diabetes and hypertension in patients with CKD increases the risk for secondary consequences such as cardiovascular disease and peripheral neuropathy. 10752521: The remnant kidney model of progressive renal disease is marked by arterial hypertension, especially when produced by nephrectomy and partial infarction. 11074011: Induction of renal failure by five-sixths nephrectomy of Sprague-Dawley rats resulted in hypertension (163 +/- 19 vs. control pressures of 108 +/- 6 mmHg), proteinuria (83 +/- 47 vs. 14 +/- 2 mg/day), and increased renal expression of fibronectin, thrombospondin, collagen I and III, transforming growth factor-beta (TGF-beta), and plasminogen activator inhibitor-1 (PAI-1) mRNA. 11193506: Hypertension was induced by right nephrectomy and surgically induced stenosis of the left renal artery. 11562406: Five/six nephrectomy produced systemic hypertension, a 50% reduction in GFR, and a 67% increase in single-nephron GFR due to elevated glomerular pressure and single-nephron plasma flow as well as proteinuria. 1218518: The authors examined the changes in arterial blood pressure and the content of Noradrenaline in the myocardium, brain and aorta of rats with hypertension due to nephrectomy and treatment with desoxycorticosterone and NaCl, and after a chronic 6-month treatment of hypertension with various antihypertensive means. 1243566: Detailed studies before and after nephrectomy suggested that hyperactivity of the renin-angiotensin-aldosterone system may participate in the pathophysiology of this unusual cause of hypertension in man. 1492978: In Wistar male rats, hypertension was induced by 5/6 nephrectomy (5/6N). 16500513: METHODS: Mice rendered hypertensive by Ang II infused intravenously at 30 ng/min for 6 h or by osmotic minipump at 0.9 mug/h for 7 or 14 days, were compared to saline-infused normotensive controls and to mice with hypertension induced by subtotal nephrectomy and 1% saline as drinking water. 1772650: In Wistar male rats, hypertension was induced by five-sixth nephrectomy (5/6N). 17853043: MATERIAL AND METHODS: The right renal artery was constricted by a silver clip in 63 male Sprague-Dawley rats to induce hypertension, while a sham operation was performed in 17 control rats. Six months after the induction of hypertension, nephrectomy of the clipped kidney was performed. 18698242: The observed increase in diagnosed hypertension may be due to nephrectomy or more blood pressure measurements received by donors in follow-up and requires prospective study. 19219214: AIMS: This work focuses on the morphological and mechanical changes in the wall of the subrenal aorta in rats suffering from arterial hypertension and chronic renal failure induced by subtotal nephrectomy (NX). 20026760: In the present study, we tested the hypothesis that, in rats with 5/6 nephrectomy (5/6Nx)-induced hypertension, Ac-SDKP reduces renal damage, albuminuria, and dysfunction by decreasing inflammatory cell infiltration and renal fibrosis and by increasing nephrin protein. 20940692: METHODS: Six months after induction of hypertension, systolic blood pressure, sodium balance, water intake and urine excretion were measured under normal conditions, after nephrectomy of the clipped kidney, and under conditions of sodium load. 21666123: Vascular reactivity to calcitonin gene-related peptide is enhanced in subtotal nephrectomy-salt induced hypertension. In subtotal nephrectomy (SN)- and salt-induced hypertension, calcitonin gene-related peptide (CGRP) plays a compensatory role to attenuate the blood pressure increase in the absence of an increase in the neuronal synthesis and release of this peptide. 23071874: CONCLUSION: Induction of 5/6 nephrectomy in mice for two weeks leads to systemic arterial hypertension and to functional and morphological damage of the remnant kidney, which are considered the main characteristics of chronic kidney disease. 24244677: SV129 mice were subjected to 5/6-nephrectomy which resulted in arterial hypertension and albuminuria. 2455124: Subtotal nephrectomy led to hypertension, proteinuria, reduced creatinine clearance, and glomerulosclerosis over 6 weeks. 25761478: RESULTS: The groups were matched by age (median 64), gender (male 67%), Heng risk (favorable 25%, intermediate 59%, poor 16%), prior nephrectomy (92%), RCC histology (clear cell 86%), pre-treatment NLR (>3 in 55%, n=27), sunitinib induced hypertension (45%), and sunitinib dose reduction/treatment interruption (41%). 25786223: STNx led to hypertension (P<0.01), kidney hypertrophy (P<0.001) and impaired kidney function (P<0.001) compared to Control rats. 27339045: BACKGROUND: Significant renal mass reduction induced by 5/6 subtotal nephrectomy (Nx) is associated with a chain of events that culminates in hypertension and chronic kidney disease (CKD). 27571511: STNx led to hypertension, diastolic dysfunction, left ventricular hypertrophy, cardiac fibrosis, and increased cardiac ACE, ACE2, Ang II and Ang 1-7 levels. 27721797: 5/6 nephrectomy led to hypertension, which was higher in SAD+CKD animals. 27917928: Rats underwent 5/6 nephrectomy for 8 weeks, which induced CKD and hypertension. Renal Denervation Improves the Baroreflex and GABA System in Chronic Kidney Disease-induced Hypertension. 28081856: Interestingly, 5/6 nephrectomy in ATRAP-knockout mice on the hypertension-resistant C57BL/6 background caused hypertension with increased plasma volume. 28192475: STNx led to hypertension, renal impairment, cardiac hypertrophy and fibrosis, and increased both left ventricular ACE2 activity and ACE binding. 32833922: RESULTS: Exercise training ameliorated the 5/6 nephrectomy-induced hypertension, proteinuria, renal dysfunction, glomerular sclerosis and renal interstitial fibrosis. 5492890: Constriction of one renal artery with contralateral nephrectomy caused sustained hypertension and an increase in aortic sodium in normal and \partial\ immunosympathectomized rats. 8430875: Accordingly, core temperature was monitored in response to PGE1 injections both preoperatively and on days 4, 8, 12, and 18 after either unilateral nephrectomy or the induction of hypertension due to nephrectomy plus renal artery clipping. 8457330: In Wistar male rats, hypertension was induced by 5/6 nephrectomy (5/6N). 10928742: As the previous studies have almost always used the visual modality for presentation, they speculate that auditory presentation, especially of nonverbal material, may be compromised in AD because of neural degeneration in auditory areas in the temporal lobes. 11226152: Our results demonstrate that in vivo overexpression of GSK-3beta results in neurodegeneration and suggest that these mice can be used as an animal model to study the relevance of GSK-3beta deregulation to the pathogenesis of Alzheimer's disease. 15036597: While many studies have addressed the atherogenic or anti-atherogenic potential of this polymorphism, little is known about its effect on neurodegeneration, despite the fact that CETP is expressed in the brain and the disturbance of cholesterol homeostasis appears to be an important factor in the pathogenesis of Alzheimer's disease (AD). 15197750: The most visible and, until very recently, the only hypothesis regarding the involvement of microglial cells in Alzheimer's disease (AD) pathogenesis is centered around the notion that activated microglia are neurotoxin-producing immune effector cells actively involved in causing the neurodegeneration that is the cause for AD dementia. 15704193: To elucidate the involvement of protein citrullination in human neuronal degeneration, we examined whether citrullinated proteins are produced during Alzheimer's disease (AD). 17017913: We will review recent findings in in vitro cell models, in vivo mouse models, and post mortem AD brain tissue in view of the effects of different Abeta peptide species on neurodegeneration during AD pathogenesis. 17197420: First, conditional inactivation of PS in the adult mouse brain causes progressive memory loss and neurodegeneration resembling AD, whereas mouse models based on overproduction of Abeta have failed to produce neurodegeneration. Based on these and other observations, we propose that partial loss of PS function may underlie memory impairment and neurodegeneration in the pathogenesis of AD. 18067990: Elucidation of the events that control the transitions from neuroprotection to neurodegeneration should be a critical point toward elucidation of AD pathogenesis. 18157656: Amyloid beta (Abeta) deposition and neurodegeneration are the two related events in the pathogenesis of Alzheimer's disease. 18645613: The neuroinflammatory response during the course of Alzheimer's disease (AD) is triggered by the neurodegeneration and the deposition of the beta-amyloid peptide in extracellular plaques. 18648646: Analysis of postmortem brain tissue from AD patients can provide information on molecular alterations present at the end of the disease process, but cannot discriminate between changes that are specifically involved in AD versus those that are simply a consequence of neuronal degeneration. 19114068: As one of the earliest pathologic changes, the aberrant re-expression of many cell cycle-related proteins and inappropriate cell cycle control in specific vulnerable neuronal populations in Alzheimer's disease (AD) is emerging as an important component in the pathogenesis leading to AD and other neurodegenerative diseases. Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease. 19264902: Together, these data indicate that UPR activation in AD neurons occurs at an early stage of neurofibrillary degeneration and suggest that the prolonged activation of the UPR is involved in both tau phosphorylation and neurodegeneration in AD pathogenesis. 19373562: Here, we will review reports of host and viral factors associated with HAND and place these studies in the context of the data employed to support current theories regarding the molecular and cellular mechanisms that lead to HIV-induced neurodegeneration with additional focus on mechanisms common to AD pathogenesis. 19683527: Similar type of intraneuronal Abeta accumulation, which precedes senile plaque formation, may link Abeta to tauopathy and neurodegeneration in Alzheimer's disease pathogenesis. 19685437: The most prevalent form of neurodegeneration is Alzheimer's disease(AD) reaching a prevalence of over 30 % above age 80.The question is reviewed whether nutrients may protect or slow down the age associated mental decline due to neuronal degeneration. 19801631: Evidence from both in vitro and in vivo studies indicates that increased GSK3beta activity contributes to neurodegeneration and to the pathogenesis of Alzheimer disease. 19903025: AD usually shows poor prognosis owing to progressive neuronal degeneration, while depression is basically reversible. 20080301: The accumulation of toxic amyloid-beta (Abeta) peptide aggregates in AD brain are thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline, an idea that underlies the 'amyloid hypothesis' of AD etiology in both the familal (FAD) and sporadic forms of the disease. 20594619: AD is caused by severe neurodegeneration in the hippocampus and neocortical regions of the brain but the cause of this neuronal loss is unclear. 21371450: Apoptosis or programmed cell death has been suggested as an important mode of neurodegeneration in Alzheimer's disease pathogenesis. 21547225: Oligomerization, conformational changes, and the consequent neurodegeneration of Alzheimer's beta-amyloid protein (AbetaP) play crucial roles in the pathogenesis of Alzheimer's disease (AD). 21663966: The accumulation of toxic amyloid-beta (Abeta) peptide aggregates in AD brain is thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline, an idea that underlies the 'amyloid hypothesis' of AD etiology in both the familal (FAD) and sporadic forms of the disease. 21786197: The accumulation of toxic amyloid-beta (Abeta) peptide aggregates in AD brain is thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline, an idea that underlies the 'amyloid hypothesis' of AD etiology in both the familal (FAD) and sporadic forms of the disease. Our latest work on studies of ER Ca(2+) leak channel function of presenilins and implications of these findings for understanding AD pathogenesis are discussed in this article. 22232001: With regards to Alzheimer's disease (AD) pathogenesis, it is not yet established whether entangled tau represents a cause or a consequence of neurodegeneration. 22266106: The result that APP proteins and specifically their soluble alpha-cleaved ectodomains can protect against progressive neurodegeneration in vivo provides support for the hypothesis that a disruption of the physiological function of APP could play a role in the pathogenesis of Alzheimer's Disease. 22505366: The lack of differences between AD and controls may result from a relatively advanced neurodegeneration in AD brains. 23151073: Oxidative damage and mitochondrial dysfunction have been also implicated in the pathogenesis of AD, but the question as to whether they are involved in the onset and progression of the pathology or rather represent a consequence of neurodegeneration is still debated. Vascular factors and mitochondrial dysfunction: a central role in the pathogenesis of Alzheimer's disease. 23701948: We argue that the interaction between the APOE-dependent non-pathological vulnerabilities and age-related pathological changes is one mechanism that can trigger neurodegeneration, resulting in AD and other complex phenotypes. However, the biological mechanisms underlying this association are still unclear because of the complexity of the pathological processes that cause AD. 23783773: RATIONALE: Acetylcholinesterase inhibitors (AChEIs) are approved to treat the symptoms of mild to moderate Alzheimer's disease by restoring acetylcholine levels at synapses where the neurotransmitter has been depleted due to neurodegeneration. 24514870: We highlight how structural network damage caused by axonal injury might interact with neuroinflammation and neurodegeneration in the pathogenesis of Alzheimer disease and chronic traumatic encephalopathy, which are late complications of TBI. 25399848: Neurodegeneration is the progressive loss of neuronal structure and function, which ultimately leads to neurological disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis, and Huntington's disease. 25511446: Although pathological hallmarks of AD are senile plaques, neurofibrillary tangles, and neuronal degeneration which are associated with increased oxidative stress, synaptic loss is an early event in the pathogenesis of AD. Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies. 25713139: Brain accumulation of neurotoxic amyloid beta (Abeta) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of synapses and neurodegeneration, is central to the pathogenesis of Alzheimer disease (AD). 26083882: Alzheimer's disease (AD) is a clinical syndrome caused by neurodegeneration and characterized by a progressive deterioration in cognitive ability and capacity for independent living. 26555572: Despite recent advances criticized the direct role in neurodegeneration of cortical neurons, Abeta is considered responsible for synaptopathy and impairment of neurotransmission and therefore remains the major trigger of AD and future pharmacological treatment remain Abeta oriented. 26557086: Here, we review the emerging evidence regarding the roles of lipid and glucose metabolism in the modulation of beta-amyloid, tau, and neurodegeneration during the pathogenesis of AD. 26880859: The anxiety status is changed along with memory impairments in intracerebroventricular colchicine injected rat model of Alzheimer Disease (cAD) due to neurodegeneration, which has been indicated to be mediated by inflammation. 26898910: Thus, pSer26Abeta could represent a critical species in the neurodegeneration during AD pathogenesis. 27111252: OBJECTIVE: Alzheimer's disease (AD) is the result of neurodegeneration, which manifests clinically as deficits in memory, thinking, and behavior. 27776205: Neuroinflammatory mechanisms mediated by activated glial and cytokines (TNF-alpha, IL-1beta) might contribute to neuronal degeneration leading to Alzheimer's (AD) and Parkinson's disease (PD). 27879212: Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease causing neural cell degeneration and brain atrophy and is considered to be the most common form of dementia. 28094792: Our in silico analysis, suggesting a novel function for APOE4 at the DNA level, offers a potential mechanism for the observed tissue specific neurodegeneration and the role of environmental factors in Alzheimer's disease etiology. 28157684: These results were confirmed in an Alzheimer's disease mouse model, which exhibited increased levels and nuclear localization of Foxo3 in hippocampal neurons, which preceded neurodegeneration and Abeta plaque formation, indicating this phenomenon is an early event in Alzheimer's disease pathogenesis. 28861684: Amyloid beta (Abeta) peptide deposition is the primary cause of neurodegeneration in Alzheimer's disease (AD) pathogenesis. 29159058: The relationships between beta-amyloid (Abeta), tau and neurodegeneration within Alzheimer's Disease pathogenesis are not fully understood. 30041064: Seizures have traditionally been related to neuronal loss in the late stages of AD as a consequence of neurodegeneration, however, recent studies indicated that seizures may contribute to the emergence of AD symptoms in early stages of the disease, mainly in familial AD. Mutations in genes encoding presenilin 1 (PSEN1), presenilin 2 (PSEN2) and amyloid precursor protein (APP) are responsible for early-onset familial AD (EOFAD). 30058479: Alzheimer's is an age-related disease with a hallmark of progressive loss of memory formation followed by a damage in the brain function due to the neural degeneration and extracellular beta-amyloid (Abeta) plaques accumulation. 30120962: Symptoms of AD worsen over time due to progressive neurodegeneration, requiring institutional care at the later stage and resulting in a heavy burden on patients, caregivers, and the public-health system. 30595042: Alzheimer's disease (AD) is considered as a potential risk factor for the development of seizure due to neurodegeneration and imbalance between stimulatory and inhibitory circuits in the brain. 31121578: AD results from progressive neurodegeneration leading to dysfunctional synaptic transmission in the brain. 31686097: BACKGROUND: The National Institute on Aging and Alzheimer's Association (NIA-AA) have proposed a new Research Framework: Towards a biological definition of Alzheimer's disease, which uses a three-biomarker construct: Abeta-amyloid, tau and neurodegeneration AT(N), to generate a biomarker based definition of Alzheimer's disease. 31689310: BACKGROUND AND PURPOSE: The loss of retinal ganglion cells observed in Alzheimer's disease (AD) may be attributable to a neurodegeneration of the neuro-retinal structure. 32143546: RECENT ADVANCES: Solid recent evidence clearly suggest that metabolic factors, systemic infections, Microbiota dysbiosis, and oxidative stress are implicated, although at different extent, in the development in brain diseases CRITICAL ISSUE: Here, we reviewed the most solid published evidence supporting the implication of the axis systemic inflammation-neuroinflammation-neurodegeneration in the pathogenesis of AD, VAD, PD and MS, highlighting the possible cause of the putative downstream component of the axis. 32183332: Alzheimer's disease is an age-related disease characterized by the progressive loss of memory and cognitive function, caused by the unstoppable neurodegeneration and brain atrophy. 32651317: Neurodegeneration of Trigeminal Mesencephalic Neurons by the Tooth Loss Triggers the Progression of Alzheimer's Disease in 3*Tg-AD Model Mice. Neurodegeneration of Trigeminal Mesencephalic Neurons by the Tooth Loss Triggers the Progression of Alzheimer's Disease in 3*Tg-AD Model Mice.BACKGROUND: The mesencephalic trigeminal nucleus (Vmes) is not only anatomically adjacent to the locus coeruleus (LC) but is also tightly associated with the function of the LC. 32795415: Dysregulated microglia are intimately involved in neurodegeneration, including Alzheimer's disease (AD) pathogenesis, but the mechanisms controlling pathogenic microglial gene expression remain poorly understood. 32813239: Neurodegeneration leading to Parkinson's disease (PD) and Alzheimer's disease (AD) has become a major health burden globally. 32903806: PARP-1 inhibition may also exert a protective effect against neurodegeneration by its action to diminish neuroinflammation and microglial activation which are also implicated in the pathogenesis of AD. 33180216: Failure of this machinery and any alterations during mitochondrial biogenesis underlies neurodegeneration resulting in Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD) etc. 33290860: In conclusion, we provide clinical trial evidence to confirm that restoration of BMI1 activity through EVOO administration in MCI patients constitutes a potential therapeutic approach against neurodegeneration leading to AD. 33337366: BACKGROUND: Alzheimer's disease (AD) is the most common type of dementia caused by irreversible neurodegeneration, with the onset mechanisms elusive. 33459705: In the subgroup of 19 AD and 19 NC with ATN results, AD-RAI results matched completely with ATN classification. 33495355: Defining the mechanisms underlying molecular neurodegeneration in the EC is crucial to determining its contributions to the pathogenesis of AD. Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease. 33788812: OBJECTIVE: Alzheimer disease is characterized by progressive decline in cognitive function due to neurodegeneration induced by accumulation of Abeta and hyperphosphorylated tau protein. 33977208: Here, we explain how vascular dysfunction mechanistically contributes to thrombosis as well as inflammation and neurodegeneration in AD pathogenesis. 34072862: After a brief summary of the molecular and cell biology of AD and HD this review covers what is known about the role of these three groups of kinases in the brain and in the pathogenesis of the two neurodegenerative disorders. Alzheimer's disease (AD) is a mostly sporadic brain disorder characterized by cognitive decline resulting from selective neurodegeneration in the hippocampus and cerebral cortex whereas Huntington's disease (HD) is a monogenic inherited disorder characterized by motor abnormalities and psychiatric disturbances resulting from selective neurodegeneration in the striatum. 34087544: One of the major causes of neurodegeneration in the pathogenesis of Alzheimer's disease is the accumulation of cytotoxic amyloid species within the intercellular compartments of the brain. 34100423: Therefore, an imbalance caused by mutations in presenilin 1/gamma-secretase might cause aberrant signaling, synaptic dysfunction, memory impairment, and increased Abeta 42 /Abeta 40 ratio, contributing to neurodegeneration during the initial stages of Alzheimer's disease pathogenesis. 34681867: Chronic Rhinosinusitis and Alzheimer's Disease-A Possible Role for the Nasal Microbiome in Causing Neurodegeneration in the Elderly. 35283778: The ischemic injury in the brain starts a cascade of events that lead to neuronal death, inducing neurodegeneration which could lead to Alzheimer's disease (AD). 35346299: BACKGROUND: Increased total tau (t-tau) in cerebrospinal fluid (CSF) is a key characteristic of Alzheimer's disease (AD) and is considered to result from neurodegeneration. 36012707: Neurodegeneration leading to Alzheimer's disease results from a complex interplay of a variety of processes including misfolding and aggregation of amyloid beta and tau proteins, neuroinflammation or oxidative stress. 36091826: Disturbed retinoic acid signaling causes inflammatory responses, mitochondrial impairment, oxidative stress, and neurodegeneration, leading to Alzheimer's disease (AD) progression. We outlined the physiology of retinoids in this review, focusing on their possible neuroprotective actions, which will aid in elucidating the critical function of such receptors in AD pathogenesis. 37190116: While attention has been focused on neurodegeneration in AD pathogenesis, recent decades have provided evidence of the importance of microglia, and resident immune cells in the central nervous system. 37477796: Recent studies have shown that, coupled with other environmental factors, aluminium exposure may lead to neurodegeneration resulting in cognitive impairment resembling Alzheimer's disease. 38020769: Autophagy acts as a proteostasis process to remove protein clumps, although it progressively weakens with aging and AD, thus facilitating the accumulation of toxic proteins and causing neurodegeneration. 38542219: This model, highlighting microglia as a pivotal player in risk factor-mediated neurodegeneration, offers a new point of view on the complex associations of modifiable risk factors and proteinopathy in AD pathogenesis, which may act in parallel to the thoroughly studied amyloid-driven Tau pathology, and strengthens the therapeutic rationale of combining immune modulation with tight control of risk factor-driven insults. 8423065: These results suggest that microglial activation in AD may be secondary to neurodegeneration and that, once activated, microglia may participate in a local inflammatory cascade that promotes tissue damage and contributes to amyloid formation. 8620894: Alzheimer's disease is a senile dementia caused by progressive neurodegeneration of the central nervous system. Here functional implications of these mutations on the processing of the precursor protein and the beta A4 amyloid deposition will be discussed with respect to the pathogenesis of Alzheimer's disease and related disorders. 9223085: The association of astrocytes with plaques is a well-established feature of Alzheimer's disease (AD) and has generally been interpreted as a secondary reaction to amyloid deposition or neuronal degeneration. 9514829: These findings indicate that nNOS expressing neurons are highly susceptible to neurodegeneration and that nNOS might contribute to the pathogenesis of AD. 9700651: Alzheimer's disease entails multiple neuronal systems and results from neuronal cytoskeletal degeneration of only a few types of nerve cells. 12570697: Recently, interest in the therapeutic potential of CDKIs has expanded to include neurodegenerative diseases, where dysregulated CDK activity has been linked to the pathogenesis of Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and stroke. 16955484: Alzheimer's disease (AD) is a neurodegenerative disease of the central nervous system characterized by two major lesions: extracellular senile plaques and intraneuronal neurofibrillary tangles. beta-Amyloid (Abeta) is known to play a major role in the pathogenesis of AD. 18778193: Although clinical management of neurodegenerative diseases usually involves symptomatic treatment, Colostrinin() (CLN), which has efficacy in counteracting neural degradation and in stimulating neural growth, might prove to be a more effective means to deal with the causes of Alzheimer's and other neurodegenerative diseases. 18781980: Nevertheless, the available data indicate that endocannabinoids are likely to play in this disorder a role similar to that suggested in other neurodegenerative diseases, that is, to represent an endogenous adaptive response aimed at counteracting both the neurochemical and inflammatory consequences of beta-amyloid-induced tau protein hyperactivity, possibly the most important underlying cause of AD. 19042040: Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease and is an important cause of chronic disability. 20810758: The 4 most common neurodegenerative disorders that cause dementia-Alzheimer disease, frontotemporal dementia, dementia with Lewy bodies, and dementia in Parkinson disease-have different underlying etiologies and pathogenetic mechanisms. 21210060: In this review, we discuss the role of metals in neurodegenerative diseases with emphasis on the utility of Caenorhabditis elegans (C. elegans) genetic models in deciphering mechanisms associated with the etiology of PD and AD. Many neurodegenerative diseases including Parkinson's disease (PD) and Alzheimer's disease (AD) are the result of neurodegenerative processes. 22647475: In the last 30 years, the elucidation of the molecular pathogenesis of neurodegenerative diseases has undergone remarkable progress, including the discoveries of the causative genes and risk factors of Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. 22870188: BDNF has recently garnered significant attention as a potential therapeutic target for neurodegenerative diseases such as Alzheimer disease (AD), but emerging evidence suggests that BDNF may also be mechanistically involved in the pathogenesis of AD. 23303475: The activity of metabotropic glutamate receptors (mGluRs) is known to be altered as the consequence of neurodegenerative diseases such as Alzheimer, Parkinson, and Huntington disease. 23678459: INTRODUCTION: Alzheimer's disease (AD) is a common neurodegenerative disorder in elderly people with an impairment of cognitive decline and memory loss. beta-amyloid (Abeta) as a potent neurotoxic peptide has a pivotal role in the pathogenesis of AD. 24680827: My findings may provide new directions not only for investigating the role of APP in neuropathology associated with HPRT-deficiency in LNS but also for the research in neurodevelopmental and neurodegenerative disorders by which various APP isoforms involved in the pathogenesis of the diseases such as Alzheimer's disease. 24747741: Although Alzheimer's disease (AD) is the most common neurodegenerative disease, the etiology of AD is not well understood. 25719338: Also, these findings may be of significance for research in neurodevelopmental and neurodegenerative disorders in which the APP gene is involved in the pathogenesis of diseases such as autism, fragile X syndrome (FXS) and AD, with its diversity and complexity, SAD in particular. 25999816: Growing evidence indicates that mitochondrial dysfunction is a common feature of neurodegenerative diseases and is observed at an early stage in the pathogenesis of AD. 26295822: Alzheimer's disease (AD) is a neurodegenerative disease characterized by deposit of amyloid plaques and neurofibrillary tangles and oxidative stress plays an essential role in the pathogenesis of AD. These results indicate that JAT may be the potential target to treat AD induced by oxidative stress and apoptosis. 26398526: My findings accounted for epigenetic mechanism in the regulation of alternative APP pre-mRNA splicing as well as for epigenetic control of genomic rearrangements of APP gene may provide therefore new directions not only for investigating the role of APP in neuropathology associated with HGprt-deficiency in LNS and LNVs patients but also for the research in neurodevelopmental and neurodegenerative disorders by which APP gene involved in the pathogenesis of the diseases such as autism, fragile X syndrome (FXS), and Alzheimer's disease (AD) with its diversity and complexity, especially for sporadic form of AD (SAD). 27166223: Impaired protein degradation has been discussed as a cause or consequence of various neurodegenerative diseases, such as Alzheimer's, Parkinson's and Huntington's disease. 28192196: The method is useful for identifying the defective APP-mRNA isoform in LND patients, and in neurodevelopmental and neurodegenerative disorders in which the APP gene is involved in the pathogenesis of diseases such as autism, fragile X syndrome, amyotrophic lateral sclerosis, and Alzheimer's disease, and may pave the way for new strategies applicable to rational antisense drugs design. 28694424: Alzheimer's disease (AD) is a major and devastating neurodegenerative disease, and the amyloid-beta (Abeta) hypothesis is still the central theory for AD pathogenesis. 29933008: This review summarizes the current knowledge and concepts regarding the connection between long-term consequences of TBI and aging-associated neurodegenerative disorders including Alzheimer's disease (AD), chronic traumatic encephalopathy (CTE), and Parkinsonism, with implications for novel therapy targets. 30083812: PCA is a clinico-radiological syndrome that is often caused by Alzheimer's disease and other neurodegenerative diseases as Lewy body dementia and corticobasal degeneration. 30250265: Animal models of adult-onset neurodegenerative diseases have enhanced the understanding of the molecular pathogenesis of Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. 30605723: Although tau plays important physiological roles in neurons, its involvement in neurodegenerative diseases, and most prominently in the pathogenesis of Alzheimer disease (AD), has directed the majority of tau studies. 30983949: Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. 32275992: Molecular insights into the inhibitory mechanisms of gallate moiety on the Abeta 1-40 amyloid aggregation: A molecular dynamics simulation study.Alzheimer's disease is the most common form of neurodegenerative disease and the formation of Abeta amyloid aggregates has been widely demonstrated to be the principal cause of Alzheimer's disease. 32968718: Both Alzheimer's disease (AD) and HIV-associated neurocognitive disorders (HAND) could progress to dementia, a severe consequence of neurodegenerative diseases. 33204697: Alzheimer's disease (AD) is a chronic progressive neurodegenerative disease that affects the quality of life of elderly individuals, while the pathogenesis of AD is still unclear. 35114208: Alzheimer's disease (AD) is a progressive memory related neurodegenerative disease, for which the current Food and drug administration approved therapeutics are only meant for a symptomatic management rather than targeting the root cause of AD. 35207764: Mild cognitive impairment (MCI), a neurodegenerative disease leading to Alzheimer's disease or dementia, is often associated with physical complaints. 35243650: John Hardy's research identified key mutations linked to prevalent neurodegenerative diseases in humans and contributed to our understanding of the molecular pathogenesis of Alzheimer disease. 35347731: Since Abeta is an important hallmark of Alzheimer's disease (AD), which is a socially significant neurodegenerative disorder of the elderly worldwide, analysis of its endogenous variations is of particular importance for elucidating the pathogenesis of AD, predicting increased risks of the disease onset, and developing effective therapy. 35601340: Neurodegenerative disorders, caused by prone-to-aggregation proteins, such as Alzheimer disease or Huntington disease, share other traits such as disrupted homeostasis of essential metal ions, like copper. 35756499: Thus, in this review, we focus on summarizing the consequences of ROS NDs, while taking the four prevalent NDs as examples, including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD), to illustrate the key signaling pathways and relevant drugs. 37380605: As a neurodegenerative disease that is difficult to prevent and cure, the pathogenesis of AD is complex and there is no effective cure. 10519044: Aluminum is a recognized neurotoxin in dialysis encephalopathy and may also be implicated in the etiology of neurodegenerative disease, particularly Alzheimer's disease. 12853325: This paper explores the effect of MPP(+) and beta-amyloid fragment 25-35, neurotoxins that are known to generate Parkinson's-like syndrome and Alzheimer's disease, on the regulation of the mitochondrial pores. 17202404: beta-Amyloid peptides, tentatively regarded as the principal neurotoxins responsible for Alzheimer's Disease, make up a set of products that varies significantly among different biological systems. 21071869: There have been many reports suggesting that soluble oligomers of amyloid beta (Abeta) are neurotoxins causing Alzheimer's disease (AD). 2680002: A review of published reports on conventional and unconventional viruses, aluminum, neurotoxic metals and trace elements, neurotoxins of biological origin and immune systems, suggest that environmental factors, possibly multiple ones, play a significant role in the etiology of Alzheimer's disease. 28918635: There is a serious dispute on the existence of beta-N-methylamino-l-alanine (BMAA) in water, which is a neurotoxin that may cause amyotrophic lateral sclerosis/Parkinson's disease (ALS/PDC) and Alzheimer' disease. 29889206: Among various aggregates, Abeta oligomer is widely accepted as the leading neurotoxin in the progress of Alzheimer's disease (AD) and is considered to be the crucial event in the pathogenesis of AD. 30551539: D-galactose (D-gal) is a senescence agent, while aluminium is a known neurotoxin linked to pathogenesis of AD. 31363819: Aluminum (Al) is a neurotoxin and is associated with the etiology of neurodegenerative diseases, such as Alzheimer's disease (AD). 32030485: The comparison is based on the selectivity of the neurotoxins which cause experimental PD and AD, towards the cellular membrane and intracellular molecular targets as well as towards the selective neurons/non-neuronal cells, and the particular brain regions. 33687726: Zebrafish as a Promising Tool for Modeling Neurotoxin-Induced Alzheimer's Disease. 3666247: Are Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis caused by neurotoxins? 38473975: An extensive body of genetic evidence suggests soluble aggregates of beta-amyloid (Abeta) as the primary neurotoxin in the pathogenesis of AD. New data suggest that the aggregation of misfolded native proteins initiates and drives the pathogenic cascade that leads to Alzheimer's disease (AD) and other age-related neurodegenerative disorders. Understanding the distinct roles of soluble and insoluble amyloid aggregates on AD pathogenesis has been the key missing piece of the Alzheimer's puzzle. 10428013: Effects of chronic treatment with (+)-nicotine on the stress-induced hypertension and downregulation of central nicotinic receptors in rats: comparative study with (-)-nicotine. 12524664: We have previously reported that smokeless nicotine resulted in hypertension, but not a deterioration in glucose tolerance or insulin action in young adult male rats. 1267535: Smoking of tobacco cigarettes produced increased ventilation and systemic hypertension, which were found to be due to their nicotine content. 1267536: Low doses of nicotine were found to induce reflex hyperventilation and hypertension, mainly due to excitation of carotid body chemoreceptors. 13202335: [Experimental studies on the role of the pituitary in intraocular hypertension produced by nicotine and water]. 13964283: [Effect of 5-hydroxytrptamine and nicotine on hypertension induced by 5-hydroxytryptamine, nicotine, tryptamine and acetaldehyde]. 20050989: These metabolic pathways are important in the development of nicotine-induced atherosclerosis and hypertension. 22254206: Oral administration of taurine also ameliorates impairment of vascular reactivity, intimal thickening, arteriosclerosis, endothelial apoptosis, oxidative stress and inflammation, associated primarily with diabetes and, to a lesser extent with obesity, hypertension and nicotine-induced vascular adverse events. 22557134: An experimental evaluation of the effect of rudraksha (elaeocarpus ganitrus roxb) in adrenaline and nicotine induced hypertension. Elaeocarpus ganitrus (Roxb) reduces adrenaline induced hypertension and also normal blood pressure; but it is not effective in nicotine induced hypertension. 29571021: In this study, interference with this inhibitory pathway was analyzed in a model of olmesartan-induced intestinal hypermotility (OIH) in rats with nicotine-induced hypertension exposed to chronic immobilizing stress. 31172810: Nicotine induced premature hypertension, renal expression of the sodium-potassium chloride cotransporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla. 12446934: Other studies show complex interactions between nAChR, nicotinic agonists, and agents implicated in AD etiology. 17069698: [Effect of beta-amyloid peptides on alpha-7 nicotinic receptor status in astrocytes and neurons, and its relationship to pathogenesis of Alzheimer's disease]. 17493709: The consequences of reducing expression of the alpha7 nicotinic receptor by RNA interference and of stimulating its activity with an alpha7 agonist in SH-SY5Y cells indicate that this receptor plays a neuroprotective role in connection with the pathogenesis of Alzheimer's disease. In order to examine the neuroprotective effects of the alpha7 nicotinic receptor (nAChR) in relationship to the pathogenesis of Alzheimer's disease (AD), neuroblastoma (SH-SY5Y) cells were transfected with small interference RNAs (siRNAs) that targets specifically towards alpha7 nAChR or exposed to 20microM 3-[2,4-dimethoxybenzylidene] anabaseine (DMXB), a selective agonist of this same receptor. These findings indicate that alpha7 nAChR may play a significant neuroprotective role by enhancing cleavage of APP by alpha-secretase, regulating signal transduction, improving antioxidant defenses and inhibiting the toxicity of Abeta, which is connected with the pathogenesis of AD. 17569627: Elevated amyloid-beta peptide (Abeta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). 18509986: OBJECTIVES: To investigate the neuroprotective function of alpha7 nicotinic receptor (nAChR) and its roles in the pathogenesis of Alzheimer's disease (AD). CONCLUSION: The findings indicate that alpha7 nAChR may play a significant neuroprotective role by enhancing cleavage of APP, improving antioxidant defenses and limiting the toxicity of Abeta, which has been implied in the pathogenesis of AD. 18647633: In order to examine the effects of alpha3 nicotinic acetylcholine receptor (nAChR) in connection with the pathogenesis of Alzheimer's disease (AD), neuroblastoma (SH-SY5Y) cells were transfected with small interference RNAs (siRNAs) that target specifically towards alpha3 nAChR. 20205670: Elevated amyloid-beta peptide (Abeta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). 21763291: Aberrant amyloid-beta peptide (Abeta) accumulation along with altered expression and function of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). 27396406: The purpose of this study was to investigate the alterations in the levels of nuclear factor kappaBp65 (NF-kappaBp65), monocyte chemoattractant protein 1 (MCP-1/CCL-2) and macrophage inflammatory protein 1alpha (MIP-1alpha/CCL-3) in relationship to the expression of alpha3 nicotinic acetylcholine receptor (nAChR) during the pathogenesis of Alzheimer's disease (AD). 27498631: Nicotinic acetylcholine receptors of alpha7 subtype (alpha7 nAChRs) attenuate the inflammatory cytokines production by macrophages and are involved in pathogenesis of Alzheimer disease by directly influencing the processing of amyloid-beta (Abeta) precursor protein in the brain. 10067799: OBJECTIVE: Chronic inhibition of nitric oxide synthesis has been shown to cause arterial hypertension and an important blunting of the pressure diuresis and natriuresis response. 10403604: CONCLUSION: These studies support the notion that (i) products of lipid oxidation may reduce NO bioactivity without affecting endothelial NO synthase mass or catalytic activity, (ii) the mechanisms involved in the endothelial dysfunction induced by hypercholesterolaemia and oxidized lipids may differ among vascular beds, and (iii) decreased NO bioavailability does not necessarily result in systemic hypertension, but it may enhance the sensitivity to the hypertensinogenic effect of dietary salt. 10491314: These data support the suggestion that ROS and RNS, including superoxide radicals and nitric oxide, may play an important role in development of stress-induced hypertension in ISIAH rats. Manifestation of oxidative stress in the pathogenesis of arterial hypertension in ISIAH rats. 10523364: The long-term administration of nitric oxide synthesis inhibitors induces arterial hypertension accompanied by left ventricular hypertrophy and myocardial ischemic lesions. 10696524: NG-Nitro-L-arginine methyl ester-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites NO2- and NO3- and was aggravated when rats drank 0.9% NaCl in place of tap water. These results suggest that long-term inhibition of NO synthesis produces a sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension. 10719388: To evaluate the role of renal nerve activity in L-NAME-induced hypertension, we compared the blood pressure response in four groups (N = 10 each) of male Wistar-Hannover rats weighing 200 to 250 g: 1) sham-operated vehicle-treated, 2) sham-operated L-NAME-treated, 3) denervated vehicle-treated, and 4) denervated L-NAME-treated rats. Much of the hypertension caused by chronic NO synthesis inhibition is thus dependent on renal nerve activity. 10726711: OBJECTIVE: Both physiologic and pharmacological data have implicated the nitric oxide (NO) signaling cascade in the regulation of blood pressure in humans and its impairment in the pathogenesis of hypertension. 10805399: Based on these data, it is concluded that even though there is a lot of evidence in favor of the primary and causal association of endothelial dysfunction and NO in experimental hypertension, it seems still more plausible that they are causative in some types of hypertension only. 10905540: Oral administration of L-NAME may serve as a model of hypertension due to chronic NO deficiency with increased oxidative stress. 10930118: Inhibition of nitric oxide synthesis causes hypertension, myocardial damage and repair in rats. 10972689: BACKGROUND: A deficiency of the endogenous vasodilator nitric oxide (NO) has been implicated as a potential cause of hypertension in chronic renal disease (CRD) patients. 11311074: Nitric oxide deficiency as a cause of clinical hypertension: promising new drug targets for refractory hypertension. 11319669: Inhibiting NO production produces hypertension in animals and in humans and not surprisingly there has been considerable interest in establishing whether deficiencies of endothelial NO pathway activity are implicated in the aetiology of essential hypertension. 11399644: Recent studies have suggested that subtle microvascular and tubulointerstitial injury in the kidney can cause salt-sensitive hypertension. To test this hypothesis, we determined whether the mild renal disease induced by transient blockade of nitric oxide (NO) synthesis would result in salt-sensitive hypertension and whether prevention of the renal injury by coadministration of the immunosuppressive agent mycophenolate mofetil (MMF) would block the development of salt sensitivity. Mycophenolate mofetil prevents salt-sensitive hypertension resulting from nitric oxide synthesis inhibition. L-NAME treatment resulted in acute hypertension and the development of mild renal injury. 11434650: BACKGROUND: Hypertension in kidney transplant (KT) patients may result from attenuated whole-body nitric oxide (NO) content and abnormal NO-mediated vasodilation. 11688356: Cyclosporin-induced hypertension and endothelial dysfunction have been attributed to the effects of cyclosporin on factors controlling vasomotor tone. In transplanted patients with cyclosporin-induced hypertension, we have recently demonstrated upregulation of the NO system and superoxide and free radical overproduction, which, by increasing NO metabolism, could induce hypertension, vascular remodeling and chronic rejection. 11703388: We studied nitric oxide synthase (NOS) activity as a possible indicator of NO production in adrenocorticotrophin (ACTH)-induced hypertension in the rat. Previous observations of diminished NO production in ACTH- and corticosterone-induced hypertension in the rat were confirmed, but could not be explained by reduced NOS activity in the present study. Nitric oxide synthase activity in adrenocorticotrophin-induced hypertension in the rat. 11763298: Oxidative stress and impairment of synthesis or release of nitric oxide (NO) are being regarded as causative factors in the pathogenesis of hypertension, diabetes mellitus and atherosclerosis, among other conditions. 11788432: We have previously shown that reduction of this infiltrate results in prevention of salt-sensitive hypertension induced by short-term angiotensin II infusion and nitric oxide inhibition (Quiroz Y, Pons H, Gordon KI, Rincon J, Chavez M, Parra G, Herrera-Acosta J, Gomez-Garre D, Largo R, Egido J, Johnson RJ, and Rodriguez-Iturbe B. 11798798: OBJECTIVE: To investigate the changes of nitric oxide (NO) and nitric oxide synthase (NOS) in vascular smooth muscle cells (VSMCs) of the essential hypertension (EH) patients, determine the effect of arginine vasopressin (AVP) on NO synthesis, and evaluate their significance in the pathogenesis of hypertension. 12072572: The inhibition of nitric oxide (NO) synthesis by chronic administration of NG-nitro-l-arginine methyl ester (l-NAME) in rats is responsible for systemic hypertension. 12363278: In this review, the roles of nitric oxide and tetrahydrobiopterin in the pathogenesis of glucocorticoid hypertension will be discussed. Impaired vasodilation and nitric oxide synthase activity in glucocorticoid-induced hypertension. 1285942: The results from this simple experimental model suggest that chronic blockade of nitric oxide synthesis results in sustained arterial hypertension that is not enhanced by sodium loading. 14700747: We hypothesize that ANP participates in the hypertension-induced by NO synthesis blockade acting by baroreceptors input to the brain to stimulate ANP release and synthesis that reduces NO prival hypertension. 15233834: Disturbed nitric oxide (NO) synthesis leads to development of endothelial dysfunction that plays a significant role in the pathogenesis of arterial hypertension. 1590443: In conclusion, blockade of EDRF led to a sustained hypertension throughout the whole 24-h recordings. 16103275: Superoxide contributes to development of salt sensitivity and hypertension induced by nitric oxide deficiency. 16253277: The aim of this study was to investigate the as yet unknown role of nitric oxide (NO) in mechanisms of social stress-induced hypertension in rats with a family history of hypertension. 1634615: Chronic blockade of nitric oxide synthesis in the rat produces systemic hypertension and glomerular damage. 16810074: Mechanisms of hypertension induced by nitric oxide (NO) deficiency: focus on venous function. 16870316: A defect in the kidney's NO system could cause salt-sensitive hypertension. 17218445: Chronic blockade of nitric oxide leads to hypertension that is sustained throughout the period of the blockade in baroreceptor-intact animals. The lack of change in renal sympathetic nerve activity during the L-NAME-induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits. 17495855: Mice lacking mPGES-1 exhibit blunted natriuretic response paralleled with remarkably suppressed nitric oxide production, leading to salt-sensitive hypertension. 17645641: Interplay of reactive oxygen species and nitric oxide in the pathogenesis of experimental lead-induced hypertension. 17874014: In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays an important role in cardiac tissue adaptations caused by aerobic exercise. CONCLUSION: Short term NO synthesis blockade in sedentary animals induced hypertension but did not cause cardiac hypertrophy. 18234738: These findings may help explain the contribution of NO and cyclooxygenase products to the etiology and/or maintenance of Pb-induced hypertension and could ultimately lead to therapeutic advantages in plumbism. 18293204: Hypertension resulting from nitric oxide (NO) synthesis inhibition blunted systemic hemodynamic adaptations during pregnancy. 18627331: Similarly, underproduction of NO by NO synthase or enhanced breakdown of NO also leads to diseases such as hypertension, ischemic conditions, pre-eclampsia, premature delivery, among others. 18977125: This study sought to investigate the effects of administration of OC on high blood pressure resulting from nitric oxide (NO) synthesis inhibition in female Sprague-Dawley rats. 19345616: Our data show that NO is not altered in the NTS of juvenile CIH rats, suggesting that nitrergic mechanisms, at least in the NTS, are unlikely to be involved in the sympathetic excitation that generates the hypertension observed after 10 days of CIH. Changes in central regulation of sympathetic activity may underlie CIH-induced hypertension. 20219827: Inhibition of nitric oxide synthesis (NOS) induces hypertension and heavy proteinuria. 2026996: The significant role(s) could have important biomedical implications since perturbations in the biosynthesis, release or actions of NO could lead to hypertension, CNS dysfunction or increased susceptibility to infection. 20610532: A deficiency in nitric oxide (NO) generation leads to salt-sensitive hypertension, but the role of increased superoxide (O(2)(-)) in such salt sensitivity has not been delineated. 21214402: Salt and nitric oxide inhibition induced hypertension: the role of prostacycline and 8-isoprostane. 21289238: Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension. 22610475: The essential role of nitric oxide (NO) in maintaining endothelial function and the relationship between NO and reactive oxygen species are discussed in the context of the etiology of hypertension. 23095292: Reduced NO bioavailability, particularly within the renal circulation, has been identified as a key factor in the pathogenesis of hypertension. 23104937: The present study provides evidence that catechol-O-methyltransferase inhibition in pregnant rats produces arterial hypertension and endothelial dysfunction due to reduced nitric oxide bioavailability. 23221987: As VEGF increases the expression and the activity of nitric oxide synthase in endothelial cells, a decrease in the bioavailability of nitric oxide has been proposed as a key mechanism leading to hypertension during angiogenesis inhibition. 24705342: The present study was aimed to investigate the antihyperlipidemic and renoprotective potential of valproic acid against N(omega)-nitro-L arginine methyl ester hydrochloride (L-NAME) induced hypertension in male albino Wistar rats. These results suggest that VPA has enough potential to attenuate hypertension, dyslipidemia and renal damage in nitric oxide deficiency induced hypertension. 24790136: Correcting elevated blood pressure with losartan, an angiotensin II type 1 receptor antagonist, alleviated cardiac hypertrophy in Rap1b(-/-) mice, suggesting a possibility that cardiac hypertrophy develops secondary to hypertension. Defective endothelial release of dilatory nitric oxide in response to elevated blood flow leads to hypertension. 25345870: Compared with blood angiotensin-II, ALD, ACE, NOR, adrenomedullin, N-terminal fragment brain natriuretic peptide, and NO status, inappropriately elevated ET-1 plasma concentrations may play a predominant role in the pathogenesis of IDH. 25623850: SIGNIFICANCE: These findings indicate that NO induced-hypertension is associated with up-regulation of NADPH oxidase, oxidative stress production and overexpression of key inflammatory mediators. Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension. Nitric oxide (NO) inhibition with N(w)-nitro-L-arginine methyl ester (L-NAME) has previously been reported to produce hypertension, increased expression of Angiotensin II (Ang II) and renal dysfunction. The current study was designed to test the hypothesis that AT1R activation promotes renal NAD(P)H oxidase up-regulation, oxidative stress and cytokine production during L-NAME induced-hypertension. KEY FINDINGS: After two weeks, L-NAME induced high blood pressure, renal overexpression of AT1R, NAD(P)H oxidase sub-units gp91, p22 and p47, increased levels of oxidative stress, interleukin-6 (IL-6) and interleukin-17 (IL-17). 26192363: Inhibiting NO production or availability induces hypertension and proteinuria, which is prevented by concomitant blockade of the H2S producing enzyme cystathionine gamma-lyase (CSE) by d,l-propargylglycine (PAG). We hypothesized that blocking H2S production ameliorates Angiotensin II (AngII)-induced hypertension and renal injury in a rodent model. 26777256: GUCY1A3 missense and haploinsufficiency mutations disrupt NO signaling leading to MMD and hypertension, with or without achalasia. 27457113: RESULTS: NG-nitro-L-arginine-methyl ester exposure during pregnancy induced programmed hypertension in adult male offspring, which was prevented by maternal melatonin or N-acetylcysteine therapy. Next, we aimed to identify potential gatekeeper pathways that contribute to NG-nitro-L-arginine-methyl ester -induced programmed hypertension using the next generation RNA sequencing technology. Among them, genes belong to the renin-angiotensin system, and arachidonic acid metabolism pathways were potentially involved in the NG-nitro-L-arginine-methyl ester-induced programmed hypertension. Nitric oxide deficiency during pregnancy causes hypertension in adult offspring. Protective effects of melatonin and N-acetylcysteine against NG-nitro-L-arginine-methyl ester-induced programmed hypertension were associated with an increase in hydrogen sulfide-generating enzymes and hydrogen sulfide synthesis in the kidneys. 28376377: Combined oral contraceptive (COC) use or inhibition of nitric oxide (NO) synthesis has been shown to cause hypertension and insulin resistance. 28590009: Moreover, rMnSOD prevents the nephrotoxicity induced by OTA probably restoring the balance between superoxide and NO that is most probably the cause of hypertension and renal functional alterations through the inhibition of NO synthase. 28692698: Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) exhibit decreased levels of nitric oxide (NO) that may be responsible for the overexpression of Gialpha proteins that has been shown as a contributing factor for the pathogenesis of hypertension in SHR. 29632845: Conclusion: Because long-term consumption of Z. jujuba extract, especially its lowest dose, attenuated cardiovascular responses induced by L-NAME, we suggest that Z. jujuba has potential beneficial effects in prevention of hypertension induced by NO deficiency. 29934052: Taken together, these data suggested that mangiferin has played an important part in alleviating hypertension induced by hyperuricemia via increasing NO secretion and improving endothelial function. In this study, we aimed to evaluate the effect of mangiferin on alleviating hypertension induced by hyperuricemia. 29950683: We previously reported that systemic heterozygous ATP2B1-null (ATP2B1+/-) mice exhibited hypertension due to impaired endothelial nitric oxide synthase (eNOS) activity and decreased nitric oxide (NO) production. 30778103: The aim of this study was to determine whether Hhcy homocysteinylates endothelial nitric oxide synthase (eNOS) and alters caveolin-1 expression to decrease nitric oxide bioavailability, causing hypertension and renal dysfunction. 31489946: As the nitric oxide (NO) and aryl hydrocarbon receptor (AHR) signaling pathways both contribute to the pathogenesis of hypertension, we evaluated whether resveratrol, an antioxidant and an AHR antagonist, can prevent hypertension programmed by a maternal BPA and HF diet. 31731536: Collectively, the data suggested that fructose intake reduced NO levels in the NTS and caused baroreflex dysfunction, which further stimulated sympathetic nerve activity and induced the development of high BP. 31809283: We found information regarding the role of the brain-gut--bone marrow axis, the brain-gut--kidney axis, the high-salt diet, short-chain fatty acids (SCFAs), neurotransitters, such as serotonin, dopamine and norepinephrine, nitric oxide, endothelin and steroids in modulating gut microbiota and in contributing to the pathogenesis of hypertension. 7485485: To explore the relationship between insulin resistance and hypertension, we examined whether acute induction of hypertension can engender insulin resistance. For this purpose we measured rates of insulin-mediated glucose uptake in awake unstressed rats with the euglycemic hyperinsulinemic (12 microns.kg-1.min-1) clamp technique during infusions of saline alone or after induction of hypertension by bolus administration of NG-monomethyl-L-arginine (L-NMMA, 30 and 15 mg/kg), a competitive inhibitor of nitric oxide synthase. Insulin resistance after hypertension induced by the nitric oxide synthesis inhibitor L-NMMA in rats. 7503951: We proposed that defective production of nitric oxide produces salt-sensitive hypertension in the Dahl/Rapp rat. 7511764: We conclude that inhibition of the synthesis of endogenous NO causes a hypertension in pithed rats that is associated with increased vasoconstriction in response to sympathetic nerve stimulation and adrenal catecholamine release. 7515855: Thus the hypertension caused by long-term nitric oxide synthesis inhibition was not associated with the increased arterial distensibility observed in SHR despite similar blood pressure elevations, similar arterial hypertrophy, and consequently similar wall stress. 7520668: Previous studies have shown that chronic oral treatment with the NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) decreases NO synthesis and causes hypertension. 7600050: Nitric oxide in the pathogenesis of hypertension. 7909994: CONCLUSION: Chronic inhibition of nitric oxide synthesis in gravid rats leads to sustained hypertension, proteinuria, thrombocytopenia, and intrauterine growth retardation, providing a simple animal model for preeclampsia. Prolonged blockade of nitric oxide synthesis in gravid rats produces sustained hypertension, proteinuria, thrombocytopenia, and intrauterine growth retardation. 7963487: Participation of nitric oxide in the regulation of renal function: possible role in the genesis of arterial hypertension. 8203622: In these studies, we produced chronic NO blockade by oral administration of the NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME), which produced sustained hypertension and increased renal vascular resistance (RVR) in conscious rats. 8206637: To evaluate the potential role of the renal sympathetic nerves in L-NAME-induced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n = 8 each): (1) sham-operated vehicle-treated, (2) sham-operated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves. Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent. 8238200: CONCLUSIONS: Infusion of an inhibitor of nitric oxide synthesis during pregnancy causes hypertension and fetal growth retardation, without affecting gestational length. 8357952: Systemic inhibition of endothelium-derived relaxing factor (EDRF) synthesis leads to acute hypertension and increased peripheral vascular resistance. 8742954: In vivo, chronic inhibition of NO synthesis induces nephrosclerosis and hypertension. 8834165: Nitric oxide deficiency leads to hypertension and renal damage in experimental animals and may be related to the development of some hypertensive disorders in people. 8991028: A defect of NO synthesis by endothelial or renal cells could be involved in the pathogenesis of salt-sensitive hypertension whereas, in other forms of hypertension, vascular NO would have a compensatory role. 9160788: It is suggested that the disturbance in the production of nitric oxide may induce salt-sensitive hypertension and the abnormality of renal hemodynamics in the S rats. Thus, the supplementation of L-arginine normalized the abnormality of renal hemodynamics accompanying salt-induced hypertension. 9239755: Thus, the present results indicate that the prolonged blockade of nitric oxide synthesis that causes arterial hypertension is associated with an activation of the sympathoadrenal system. 9248573: Effective systemic blockade of endogenous nitric oxide production results in moderate hypertension, reduced sympathetic activity and shortened bleeding time in healthy volunteers. 9366930: Blockade of endogenous nitric oxide production results in moderate hypertension, reducing sympathetic activity and shortening bleeding time in healthy volunteers. 9396239: Although the inhibition of nitric oxide (NO) synthesis is known to induce systemic hypertension, the underlying mechanisms mediating this type of hypertension are incompletely understood. L-NAME-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites, NO2- and NO3-, and was aggravated when rats drank 0.9% saline in place of tap water. These results suggest that the inhibition of chronic NO synthesis produces sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension. 9405639: Further study into the regulation of this adventitial source of O2- is important in elucidating the mechanisms regulating the bioactivity of NO and may contribute to our understanding of the pathogenesis of hypertension. 9453322: Recent studies have indicated that nitric oxide (NO) synthesis inhibition during mid to late gestation in pregnant rats results in severe hypertension and proteinuria. 9661203: The results suggest that the rapid reactions of oxy- and deoxyhemoglobin with nitric oxide are the fundamental cause of the hypertension. 9807669: These data support a role for the NO system in cortisol-induced hypertension in humans. The nitric oxide system and cortisol-induced hypertension in humans. 9813440: These results do not support the idea of a generalized decrease in NO production being a major cause of hypertension in preeclampsia. 9890305: Chronic inhibition of nitric oxide (NO) synthesis has been shown to result in arterial hypertension and an important blunting of the pressure diuresis and natriuresis response (PDN). 9931145: A role for reduced renal nitric oxide production has been proposed as a mechanism responsible for hypertension in Dahl \salt-sensitive\ rats. 10567488: There is a growing evidence that NO is involved in neuronal death in Alzheimer's disease, and the oxidative stress caused by NO in the brain could be a pathogenic mechanism in Alzheimer's disease. 11110032: Interleukin-1 (IL-1) is known to trigger induction of inducible nitric oxide synthase (iNOS) to persistently mass produce nitric oxide (NO) to induce various diseases such as cancer, inflammation, Alzheimer's disease and eye diseases, including uveitis, retinopathy, age-related macular degeneration, glaucoma and myopia. 1381038: A possible role for nitric oxide in glutamate (MSG)-induced Chinese restaurant syndrome, glutamate-induced asthma, 'hot-dog headache', pugilistic Alzheimer's disease, and other disorders. 16253246: This is the first direct evidence demonstrating that nitric oxide induces AD-like tau hyperphosphorylation in vitro, and GSK-3beta activation is partially responsible for the nitric oxide-induced tau hyperphosphorylation. 17560043: Several studies suggest a pivotal role of amyloid beta (Abeta)(1-42) and nitric oxide (NO) in the pathogenesis of Alzheimer's disease. 20082297: The elevation of nitric oxide (NO) within the central nervous system (CNS) is known to be associated with the pathogenesis of neurodegenerative diseases such as HIV-associated dementia (HAD), brain ischemia, Parkinson's disease, and Alzheimer's disease. 22445961: The Abeta aggregate-induced neurotoxicity, inflammatory reactions, oxidative stress, and nitric oxide (NO) generation are strongly linked to the etiology of AD. 23745722: This suggests chronic loss of endothelial NO may be an important contributor to the pathogenesis of sporadic AD. 27806872: Our results showed that LPS treatment (500MUg/kg/day) for 7days disturbed memory, enhanced systemic NO production, NOS2 and Abeta 1-42 cerebral expression and generated an Alzheimer's disease (AD)-like neuronal degeneration. 29300354: The overproduction of nitric oxide (NO) and prostaglandin E2 (PGE2) by microglia may cause neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. 31531065: Nitric oxide (NO) is a key mediator that plays an important role in pathogenesis of various chronic diseases like Alzheimer's disease and Parkinson's disease. 10081624: Chronic inhibition of nitric oxide synthase (NOS) results in a persistent hypertension, while chronic blockade of endothelin ETA receptors has little effect on arterial pressure. 10981063: It is thereby involved in the long-term control of arterial blood pressure, and inhibition or deficiency of NO synthase may result in a sustained hypertension. 11304519: Decreased renal expression of nitric oxide synthase isoforms in adrenocorticotropin-induced and corticosterone-induced hypertension. Because glucocorticoids can affect the nitric oxide system at several sites, the present study tested the hypothesis that nitric oxide synthase (NOS) expression may be altered in ACTH-induced and corticosterone-induced hypertension in the rat. 11502712: BACKGROUND: Long-term inhibition of nitric oxide synthase (NOS) is known to induce hypertension and perivascular fibrosis. 11576927: Chronic inhibition of NO synthases (NOS) has been shown to cause hypertension and vasculopathy. 11717657: OBJECTIVE: The purpose of this study was to test whether omitting the vasodilator nitric oxide that is derived from any 1 of the 3 isoforms of nitric oxide synthase results in hypertension during pregnancy. 11798798: OBJECTIVE: To investigate the changes of nitric oxide (NO) and nitric oxide synthase (NOS) in vascular smooth muscle cells (VSMCs) of the essential hypertension (EH) patients, determine the effect of arginine vasopressin (AVP) on NO synthesis, and evaluate their significance in the pathogenesis of hypertension. 11881129: CONCLUSION: Blockade of NOS causes hypertension and renal damage. 12187099: Long-term inhibition of nitric oxide synthase (NOS) in rats is known to cause systemic hypertension and renal parenchymal injury. 12269387: A pharmacological inhibition of nitric oxide synthase (NOS) in rats for 4-6 weeks produces renal vasoconstriction, renal dysfunction, and severe hypertension. 12714875: Chronic inhibition of nitric oxide synthase induces hypertension and cardiomyocyte mitochondrial and myocardial collagen remodelling in the absence of hypertrophy. OBJECTIVES: To evaluate the morphometric and ultrastructural alterations of the heart produced by long-term inhibition of nitric oxide (NO) synthase with N(omega)-nitro-l-arginine methyl ester (l-NAME) and to examine whether the changes are caused by l-NAME-induced hypertension or a lack of NO. 14569001: Inhibition of nitric oxide synthases causes systemic hypertension and renal injury in rats. 15036467: A pharmacological inhibition of nitric oxide synthase (NOS) in rats produces renal vasoconstriction, renal dysfunction, and hypertension. Taken together, these results suggest that BFWE prevents the increase of SBP in the L-NAME-induced hypertension that may have been caused by enhanced generation of vascular NO and amelioration of renal functions. 16250858: Furthermore, targeted disruption of the endothelial isoform of NOS in mice causes moderate hypertension, implying that hypertension may also develop from reductions in NOS expression. 16935907: Moreover, treatment with AG and L-NIL prevented the morpho-functional changes induced by subtotal renal ablation, despite persistence of systemic hypertension, suggesting that high concentrations of nitric oxide produced by NOS-2 could act as a positive modulator of the proinflammatory and profibrotic pathways involved in the progression of renal disease. 17262047: It is therefore plausible that NOS deficiency plays a part in the pathogenesis of pyloric stenosis, hypertension and cyst development in autosomal-dominant PKD. 17965319: We hypothesize that nitric oxide synthase (NOS) uncoupling is important in the pathogenesis of interstitial lung disease-associated pulmonary hypertension, and this process can be abrogated by phosphodiesterase type 5 (PDE5) inhibition to improve pulmonary vascular remodeling and right ventricular function. 20002674: Chronic inhibition of nitric-oxide synthase induces hypertension and erectile dysfunction in the rat that is not reversed by sildenafil. STUDY TYPE: Aetiology (case control) Level of Evidence 3b OBJECTIVE To evaluate the effect of N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (HT) on erectile function in the rat and determine if the phosphodiesterase (PDE)-5 inhibitor, sildenafil, can reverse the effects of nitric oxide (NO) deficiency, as HT is a risk factor for erectile dysfunction (ED) and the NO synthase (NOS) inhibitor L-NAME induces NO-deficient HT. 20041987: Chronic L-NAME treatment induced hypertension, elevated the oxidative load and inhibited NOS activity. To elucidate the possible role of the nitric oxide (NO) pathway in the hemodynamic actions of melatonin, the effects of this indolamine on vascular function during hypertension induced by the NO-synthase (NOS) inhibitor, N(omega)-nitro-L-arginine-methyl ester (L-NAME) were investigated. Melatonin interactions with blood pressure and vascular function during L-NAME-induced hypertension. 22447945: We hypothesized that reduced PVN NO led to elevations in blood pressure during both the onset and sustained phases of hypertension due to decreased NO synthase (NOS) and increased asymmetrical dimethylarginine (ADMA; an endogenous NOS inhibitor) and symmetric dimethylarginine (SDMA). 22711313: BH4 depletion and NOS uncoupling contribute to overload-induced heart failure, hypertension, ischemia/reperfusion injury, and atrial fibrillation. 25159081: BACKGROUND: This study investigates the contribution of genetic interactions between the beta-2 adrenergic receptor (ADRB2) and nitric oxide synthase (NOS3) genes to the complex etiology of hypertension. 26694820: In addition, nitric oxide (NO), synthesized by nitric oxide synthases (endothelial and inducible), is also associated with IR when both impaired release and reduced bioavailability of all which lead to inflammation and hypertension. 28257997: Hypertension was induced by N-nitro-l-arginine methyl ester (25 mg/kg/day in drinking water), and exercise training comprised swimming 1 h/day, 5 days/week, for 6 weeks. This study aimed to assess the effect of the HO/CO system on the vascular tone in exercise-trained rats with hypertension induced by chronic NO synthase (NOS) inhibition. 28391290: As high-fat diet (HFD) is an important contributor to the development of obesity, we tested the hypothesis that pregnant rats on HFD have hypertension and endothelial dysfunction due to reduced nitric oxide synthase (NOS). 32605800: Sodium thiosulfate improves renal function and oxygenation in L-NNA-induced hypertension in rats. In experimental settings, inhibition of nitric oxide synthase causes hypertension, renal dysfunction and damage. 7558232: We also found that L-NAME-induced hypertension, once developed, is completely reversed by acute ganglionic blockade. Pharmacological inhibition of nitric oxide synthase causes sustained hypertension in many animal species. 8789388: Chronic inhibition of nitric oxide synthase (NOS) induces a sustained hypertension in rats. 9363467: A chronic model of hypertension, induced by continuous inhibition of nitric oxide synthase (NOS), was used to examine whether chronic NOS inhibition is associated with the heightened sympathetic activity and how nitric oxide (NO) produced by NOS contributes to maintain structural integrity of coronary artery and myocardial interstitium. These results suggest that, in the chronic model of hypertension induced by sustained LNAME administration, not only NO derived from endothelial NOS (NOS-3), but also the heightened sympathetic drive caused by central NOS (NOS-1) inhibition modifies progression of the disease. 9464471: It was found that L-NAME induced arterial hypertension on weeks 1-4 in control rats but not in garlic-fed rats, whose blood pressure remained essentially as the basal values. It has been reported that garlic activates nitric oxide synthase in vitro and that chronic inhibition of nitric oxide (NO) synthesis by N omega-nitro-L-arginine-methyl-ester (L-NAME) induces arterial hypertension in rats. 9688675: Systemic inhibition of nitric oxide synthase (NOS) evokes hypertension, which is enhanced by salt loading, partly via augmented sympathetic activity. 9689443: Recent studies have indicated that chronic inhibition of nitric oxide synthase induces arterial hypertension without myocardial hypertrophy. 10226765: Endothelin-1 and relaxation of the rat aorta during pregnancy in nitroarginine-induced hypertension. 10480022: Strain differences of hypertension induced by dietary NG-nitro-L-arginine in normotensive rats. 1526064: Dietary NG-nitro-L-arginine induces sustained hypertension in normotensive Wistar-Kyoto rats. Prolonged oral administration of NG-nitro-L-arginine (L-NNA) for a period of 5 weeks in 8 week old male normotensive Wistar-Kyoto (WKY) rats (n = 10), induced hypertension in all animals. 1915573: L-NG-nitro arginine produces an exaggerated hypertension in anesthetized SHR. 28487985: L-NNA was used to induce hypertension in mice, and the mice were subsequently treated with CJGJ and HLGJ. Gardenia jasminoides has therapeutic effects on L-NNA-induced hypertension in vivo. The anti-hypertensive effects of Gardenia jasminoides were determined by a L-NG-nitroarginine (L-NNA)-induced hypertension animal model. 32605800: Sodium thiosulfate improves renal function and oxygenation in L-NNA-induced hypertension in rats. In experimental settings, inhibition of nitric oxide synthase causes hypertension, renal dysfunction and damage. 34055010: Furthermore, the animal experiment indicated that after the L-NNA-induced hypertension rat model was established, CIF intervention was given by gavage for 3 weeks, and it can decrease serum concentrations of endothelin-1 (ET-1) and thromboxane B2 (TXB 2 ), increase the expression of nitric oxide (NO) and prostacyclin 2 (PGI 2 ), and improve renal, cardiac, and aortic lesions. 7532526: Enhanced vascular responsiveness to Bay K 8644 in mineralocorticoid- and N-nitro arginine-induced hypertension. The present study evaluates the response to the L-type voltage gated calcium channel agonist Bay K 8644 in two forms of experimental hypertension (mineralocorticoid- and hypertension induced by the nitric oxide synthase inhibitor N omega-nitro-L-arginine (N-Nitro arginine)) and under conditions of acute stretch. 7678095: NG-Nitro-L-arginine-induced hypertension was markedly attenuated or abolished by treatment with hexamethonium; this inhibition was still observed when the blood pressure fall caused by the ganglionic blocking agent was compensated by continuous infusion of angiotensin II. 7882578: Fish protein-rich diet attenuates hypertension induced by dietary NG-nitro-L-arginine in normotensive Wistar-Kyoto rats. 7904258: Arterial hypertension was provoked in a ramp progression by the drug NG-nitro-L-arginine alone or in association with aortic coarctation. 8566099: Chronic NO blockade was produced by oral administration of the NO synthase inhibitor NG-nitro-L-arginine for 4 weeks, which produced sustained hypertension. 11725006: Attenuation of Endothelium-Dependent Relaxation in Mesenteric Artery during Noise-Induced Hypertension. This indicates that noise-induced hypertension may be partly due to the alterations of endothelial activity. The present study was designed to determine whether there is a causal relationship between noise-induced hypertension and changes of endothelial function. 14775394: [Arterial hypertension caused by industrial noise]. 15130445: [Effects of hearing susceptibility for noise induced hypertension in fertilizer manufacture workers]. 1537714: Noise-induced hypertension and magnesium in rats: relationship to microcirculation and calcium. Experiments were designed to determine whether 1) there is a causal relationship among environmental noise stress, serum and vascular tissue (aortas and portal veins) Mg contents, and development of hypertension and 2) such noise-induced hypertension has a microcirculatory basis and what the mechanism may be. 15808811: Most genetic studies of hypertension use a candidate gene approach and two conclusions have been made: there is no association or linkage with the genes studied, or the hypertension phenotype is heterogeneous and subgroups with hypertension related to certain polymorphisms cannot be identified because of background noise. 1661766: To determine the role of noise exposure in the etiology of hypertension, a cross-sectional study was performed by measuring the blood pressure of 2124 male laborers working in a noisy factory. 16850905: The objectives of the present study were to study the (i) prevalence of hypertension and hearing impairment in iron and steel industry workers, (ii) association between hypertension and hearing impairment, (iii) association between hypertension and hearing impairment, with duration of exposure, and (iv) correlation between levels of sound and noise induced health problems viz. hypertension and hearing impairment in a cross sectional study involving Workers working in iron and steel industry at Nagpur. 2015209: A dose response relation for noise induced hypertension. 20846132: Noise induced hypertension and prehypertension in Pakistan. 23759732: A number of studies revealed that starting from 65 decibels, the noise causes hypertension for patients of more than 40 years following 5 years of exposure. The noise, through creating stress, acts on the central nervous system and on the autonomic nervous system and is likely to cause hypertension by increasing peripheral resistance, total cholesterol, fatty acids, adrenaline, cortisol and blood glucose. 25203347: Can noise cause high blood pressure? 25774612: To determine if aircraft noise exposure causes an increased incidence of hypertension among residents near airports. 27318606: Less than one-third of respondents (29%) reported loss of sleep due to noise and 8% reported hypertension, which could be related to the disturbance caused due to noise. 28554004: BACKGROUND: Environmental traffic noise is a potential cause of hypertension. 29084230: Therefore, continuous exposure to noise can have an effect on immune function, hormonal levels, and cardiovascular function, leading to hypertension and stress. 30416547: This review examines the effects of noise pollution on the cardiovascular system, with a particular focus on non-auditory effects such as noise-induced arterial hypertension. 31836979: Based on the survey, 94% of respondents reported headache, 76% sleeplessness, 74% hypertension, 74% physiological stress, 64% elevated blood pressure levels, and 60% dizziness due to noise. 32872306: The meta-analysis found a pooled effect size (ES) for hypertension (systolic/diastolic blood pressure >=140/90 mmHg) due to noise exposures >=80 dB(A) of 1.81 (95% CI 1.51-2.18). 33748836: Noise and air pollution as triggers of hypertension. 35727516: Some studies have shown that exposure to noise can cause coronary artery disease, high blood pressure, and stroke. 35931843: Epidemiological evidence indicates that high levels of noise, particularly at night, may cause arterial hypertension and endothelial dysfunction due to higher level of stress hormones and oxidative stress. 3874543: The role of noise exposure in the etiology of high blood pressure is unclear. 10204164: Increasing of the noradrenaline synthesis with daily i.p. administration of synthetic noradrenaline precursor DL-Threo on the 21-25th day of life of the rats with inherited stress-induced arterial hypertension (ISIAH) resulted in a drop of basal and stress-induced blood pressure in adult animals with no changes in response of the hypothalamic-pituitary-adrenocortical system (HPAS). 1033105: 2) TLP-607 slightly hypertension induced by dopamine, adrenaline and noradrenaline, but had no effect on hypotension induced by acetylcholine and histamine. 10400907: Induction of ecSOD by angiotensin II was not due to hypertension alone, because hypertension caused by norepinephrine (5.6 mg. kg-1. d-1) had no effect on ecSOD. 10642335: Increase in renal medullary nitric oxide synthase activity protects from norepinephrine-induced hypertension. 11507742: Methanol and dichloromethanol extracts of the leaves and stems of Mentha suaveolens Ehrh. have been tested for their effects on resting arterial blood pressure, heart rate and noradrenaline induced hypertension. Both extracts administered by i.v. bolus to urethane anaesthetized normotensive rats reduced the mean arterial blood pressure and heart rate, while only the dichloromethanol extract prevented the noradrenaline induced hypertension. 11710791: This study provides evidence that hypertension is associated with the remodeling of the human mesenteric artery and that MCTZ is as efficient in inhibiting the contractile response induced by NE on hypertensive than on normotensive arteries. 12879669: Over a specific dose range, systemic hypertension induced by adrenaline, noradrenaline and dopamine did not significantly increase cerebral blood flow under 2% isoflurane anaesthesia. 13258484: Electrocardiographic changes during norepinephrine-induced hypertension in normal man. 13404042: [Effects of heparin on the velocity of circulation and on hypertension produced by adrenalin and noradrenalin]. 13513773: The blood volumes and plasma protein during levarterenol-induced hypertension. 13597404: [Tolazoline (priscol) diminishes or reverses in the guinea pig adrenalin- & noradrenalin-induced hypertension]. 13960259: [Oscillographic behavior during experimental hypertension induced by noradrenaline in subjects with and without peripheral arterial disease]. 14300130: [INVESTIGATION OF HEMODYNAMIC CHANGES IN ACUTE ARTERIAL HYPERTENSION EVOKED BY NOREPINEPHRINE]. 14498719: [Electrocardiographic and histological findings in hypertension caused by noradrenalin in animal experiment]. 15079024: Feasibility and safety of norepinephrine-induced arterial hypertension in acute ischemic stroke. 15278610: Comparative cardiovascular effects of SNP, ATP and phentolamine during norepinephrine-induced hypertension in dogs. 15834284: DESIGN: The dose-response relationship of chronic noradrenaline infusion on arterial pressure was characterized to identify a dose that would produce sustained hypertension, and the effect of combined endothelin ETA and ETB receptor blockade (TAK-044) on the response to this dose was then examined. 16108042: This study was designed to investigate the acute effects of local application of a SMF to neck or pelvic region under pharmacologically modulated BP; norepinephrine (NE)-induced hypertension as well as an L-type voltage-gated Ca(2+) channel blocker, nicardipine (NIC)-induced hypotension in conscious rabbits. 1655648: We propose that Na+,K(+)-ATPase inhibition resulting in neuronal depolarization is responsible for the augmented norepinephrine turnover caused by bufalin and that these indirect effects of norepinephrine on the cardiovascular system may play a role in the etiology of hypertension. 16777933: During hypertension induced by aortic constriction (mean arterial pressure, MAP = 140 +/- 6 mmHg) coronary vascular resistance (CVR), reactive hyperaemia (ratio of peak in hyperaemic flow to control flow and ratio of repayment to debt) and the decrease in CVR during the peak in hyperaemic flow were comparable to those during normotension. During hypertension induced by noradrenaline (MAP = 144 +/- 6 mmHg) CVR was 16% lower (P < 0.05), reactive hyperaemia was reduced by 14-25% (P < 0.05) and the decrease in CVR during the peak in hyperaemic flow was lower than the values of these parameters during normotension. 16788141: We conclude that decreases in UT-A1, AQP2, and NKCC2/BSC1 proteins may contribute to the diuresis and natriuresis that occur following ANG II or norepinephrine-induced acute hypertension and do not appear to involve ANG II stimulation of aldosterone or thirst. Urea transporter UT-A1 and aquaporin-2 proteins decrease in response to angiotensin II or norepinephrine-induced acute hypertension. 17433074: Also, in vivo infusion with either ang II or noradrenaline caused similar hypertension and vascular hypertrophy to wild-type. 17645634: To investigate whether noradrenaline-induced hypertension induces persistent, functionally important changes to the kidney, the acute pressure-natriuresis relationship was characterized in anaesthetized rats under controlled neural and hormonal conditions following chronic (14 days) intravenous infusion of noradrenaline (48 microg/kg per h) or vehicle (0.04 mg/mL ascorbic acid and 0.156 mg/mL NaH2PO4 2 H2O in 10 IU/mL heparinized saline). 1872357: It is concluded that fetal arterial hypertension provoked by norepinephrine infusion has no effect on placental vascular resistance, umbilical blood flow, and umbilical artery pulsatility index. Fetal hypertension induced by norepinephrine infusion and umbilical artery flow velocity waveforms in fetal sheep. 18768397: By contrast, norepinephrine-induced hypertension, which is not associated with an increase in vascular superoxide anion production, is not affected in MNK(mut) mice. 192391: The same stimulation of the nerve during hypertension caused by noradrenaline injection led to the fall of arterial pressure and tachycardia. 1926237: In this study, we examined the effect of pretreatment with a calcium entry blocker, flunarizine, on the increased cerebrovascular permeability to protein that develops in norepinephrine-induced acute hypertension. 19343267: BACKGROUND: Vasopressor-induced hypertension is routinely indicated for prevention and treatment of cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). Norepinephrine-induced hypertension dilates vasospastic basilar artery after subarachnoid haemorrhage in rabbits. CONCLUSION: This study demonstrated that NE-induced hypertension causes angiographic dilatation of the BA in the SAH rabbit model. The aim of this study was to evaluate angiographic effects of normovolaemic Norepinephrine (NE)-induced hypertension therapy on the rabbit basilar artery (BA) after SAH. Based on these observations, it can be hypothesised that clinical improvement during vasopressor-induced hypertension therapy after SAH might be explained with cerebral vasodilatation mechanisms that lead to improvement of cerebral blood flow. Mechanisms underlying patients' clinical improvement during vasopressor-induced hypertension remain incompletely understood. Five days later the animals underwent follow-up angiography prior to and during NE-induced hypertension. 1950401: Large amounts of norepinephrine are released into the systemic circulation, resulting in hypertension, tachycardia, dysrhythmias and ECG changes. 20170612: CONCLUSION: These data suggest that HT induced by NE helps to maintain stable hemodynamic status and oxygen metabolism, and may protect the liver in terms of function and cellular injury after CPR. 20610: Noradrenaline (NA), 100 microgram intraventricularly (ivtr), produces an evident hypertension, lasting for up to 15 min. 20825880: BACKGROUND: The aim of this study was to study the effects of norepinephrine (NE)-induced hypertension (HT) on renal biochemistry, enzymology, and morphology after restoration of spontaneous circulation (ROSC) by cardiopulmonary resuscitation (CPR) in swine. 2089934: The pattern of Evans blue extravasation in the brain in norepinephrine-induced acute hypertension is similar to our previous observations using horseradish peroxidase as a tracer. 21122203: CONCLUSION: Hypertension induced by norepinephrine is a safe and effective method to reduce brain damages and prevent apoptosis of neurons. 2161850: In pithed rats, bromocriptine did not affect the hypertension due to exogenous noradrenaline, phenylephrine, B-HT 920, nor the bradycardia evoked by stimulation of the cardiac muscarinic receptors by carbachol. 2168774: Levels of triiodothyronine, thyroxine, insulin, glucose and free fatty acids in the blood; contents of adrenaline, noradrenaline in adrenals and glycogen in the liver; activity of phenylethanolamine-N-methyltransferase in adrenals, hexokinase and glucose-6-phosphatase in the liver were studied in male Wistar rats and rats with inherited stress-induced arterial hypertension /ISIAH/. 22826137: CONCLUSION: As compared to norepinephrine-induced hypertension, dobutamine-induced high CI did not reduce the rate of vasospasm in SAH patients. 23020995: STUDY DESIGN: Twenty chronically instrumented near-term ewes with increased placental vascular resistance after placental embolization were anesthetized and randomized to receive labetalol or pindolol for norepinephrine-induced hypertension. 23785438: These tumors release excessive epinephrine and norepinephrine resulting in hypertension and cardiovascular crises for which surgery is the only definitive treatment. 2389298: Group II (n = 6) and III (n = 6) dogs were treated with norepinephrine at the beginning of reperfusion to induce hypertension for 4 hours. 24250487: The administration of AECE (100, 200, and 400 mg/Kg/day, p.o.) for six weeks and AECE (10, 20, and 40 mg/Kg, IV) on the day of experiment in renal artery-occluded hypertensive rats and AECE (20 and 40 mg/Kg, IV) in noradrenalin-induced hypertension in rats produced significant (p < 0.05) anti-hypertensive effects. 24729712: Neurogenic orthostatic hypotension (nOH) is due to failure of the autonomic nervous system to regulate blood pressure in response to postural changes due to an inadequate release of norepinephrine, leading to orthostatic hypotension and supine hypertension. 25149991: METHODS: Effects of intravenous LKP infusion and then superimposed losartan (AT1R antagonist) on MAP, total renal (RBF, Transonic probe) and renal medullary blood flows (laser-Doppler), and on renal excretion, were examined in anesthetized (1) Wistar rats with acute norepinephrine-induced hypertension, untreated or pretreated with AT2R antagonist (PD 123319) and (2) spontaneously hypertensive rats (SHR) maintained on standard or high-sodium (HS) diet. CONCLUSIONS: LKP lowered MAP in norepinephrine-induced hypertension, probably via activation of AT2R. 25990676: Cardiac fibrosis, or accumulation of collagen in the myocardium, is seen in several models of cardiac hypertrophy, such as those induced by aging, pressure overload, and norepinephrine-induced hypertension. 26559126: Here, the role of NO-GC1 in hypertension provoked by contractile agonists angiotensin II (Ang II) and norepinephrine (NE) was evaluated in NO-GC1-deficient mice. Hypertension induced by chronic Ang II treatment did not differ between wild-type (WT) and NO-GC1 knockout mice (KO). Angiotensin II-Induced Hypertension Is Attenuated by Reduction of Sympathetic Output in NO-Sensitive Guanylyl Cyclase 1 Knockout Mice. 2705561: When cerebral blood flow in cats was decreased by hyperventilation-induced hypocapnia and increased by norepinephrine-induced hypertension, the percent changes in LD flow and H2 clearance flow changed linearly (r = 0.94, slope = 0.97). 2778312: Effects of complete renal denervation and selective afferent renal denervation on the hypertension induced by intrarenal norepinephrine infusion in conscious rats. 2801151: Regional cerebral blood flow in acute hypertension induced by adrenaline, noradrenaline and phenylephrine in the conscious rat. 29951531: However, the highest dose of norepinephrine (15 MUg/kg/h) resulted in more hypertension episodes. 30355657: Acute hypertension was induced by norepinephrine (NE) infusion and resulted in an increase in LVEDP and pulmonary artery pressure (Ppa) that were associated with a rapid fall in PaO2, and increases in lung wet/dry ratio and injury scores. 3038401: In addition, IR infusion of the angiotensin-II analogue, saralasin (2 and 10 micrograms/kg/min) showed no depressor effect in NE induced acute hypertension. In order to elucidate the antihypertensive action of angiotensin-I converting enzyme inhibitors (CEIs) in the kidney, intrarenal (IR) administration of CEIs was performed in norepinephrine (NE) or angiotensin-II (AII) induced acute hypertension in conscious unrestrained rabbits. 30822427: MAIN METHODS: The effects of ropivacaine on lung permeability were assessed in two models of acute hypertension (AH): the isolated perfused lung preparation where acute increases in left atrial pressure model the hemodynamic changes of severe hypertension, and an animal model of AH induced by norepinephrine. 3113166: Leakage of HRP occurred in both cerebral hemispheres in response to hypertension induced by the three pressor agents, but the leakage was greater on the lesioned side in response to epinephrine and norepinephrine, while in the case of angiotensin-induced hypertension side-to-side differences in permeability alterations were not observed. Unilateral locus ceruleus lesion enhances leakage of radioiodinated human serum albumin into the ipsilateral cerebral cortex of rats with norepinephrine-induced hypertension. 31608673: NE infusion evoked salt-sensitive hypertension and prevented dietary Na+-evoked suppression of NCC mRNA, protein expression, phosphorylation, and in vivo activity. 31809283: We found information regarding the role of the brain-gut--bone marrow axis, the brain-gut--kidney axis, the high-salt diet, short-chain fatty acids (SCFAs), neurotransitters, such as serotonin, dopamine and norepinephrine, nitric oxide, endothelin and steroids in modulating gut microbiota and in contributing to the pathogenesis of hypertension. 3260082: Measurements were performed and blood samples were taken in the awake state (I); 15 min after achievement of steady-state conditions with 1.68 vol.% enflurane or 1.5 vol.% isoflurane without blood pressure support (II); during norepinephrine-induced hypertension at a cerebral perfusion pressure of 110 mmHg (III); and during controlled hyperventilation at a PaCO2 of 27 mmHg and normotension (IV). 3375267: Pulmonary vascular efflux of norepinephrine in Dahl rats susceptible or resistant to salt-induced hypertension. These data indicate that impaired accumulation and efflux of norepinephrine by the lungs does not contribute to the pathogenesis of hypertension in Dahl S rats. 3536587: Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. 3594068: The effects of either hypotension induced by sodium nitroprusside or hexamethonium or hypertension produced by angiotensin II or noradrenaline on the circulating levels of methionine enkephalin ([Met]enkephalin)-like immunoreactivity (MLI), adrenaline and noradrenaline in anaesthetized greyhounds were examined. 3605371: Nonuniformity of CBF response to NE- or ANG II-induced hypertension in rabbits. 3677452: Characterization of hypertension induced by long-term intrarenal norepinephrine infusion in conscious rats. 3734443: Norepinephrine-induced hypertension in Guillain Barre syndrome. 3766759: Blood-brain barrier (BBB) permeability was increased during moderate hypertension induced by dopamine and not when induced by norepinephrine. The effects of hypertension induced by norepinephrine and dopamine infusion on the relationship between local cerebral blood flow (CBF) and local glucose use (GU) were examined in rats with the use of quantitative autoradiographic techniques. 4053309: Following hypertension, the sustained vasodilation caused by acute hypertension was inhibited significantly by topical application of superoxide dismutase and catalase, showing that it was due in part to superoxide and other radicals derived from it. The appearance of superoxide anion radical in cerebral extracellular space during and after acute hypertension induced by intravenous norepinephrine was investigated in anesthetized cats equipped with cranial windows. The results show that superoxide and other radicals generated after acute hypertension interfere with acetylcholine-induced endothelium-dependent vasodilation, probably because they destroy the endothelium-derived relaxant factor. 43064: Acute hypertension was induced by adrenaline, noradrenaline or angiotensin in awake unrestrained rats with chronic indwelling catheters in a jugular vein and in the aorta. Blood-brain barrier to albumin in awake rats in acute hypertension induced by adrenaline, noradrenaline or angiotensin. 4326850: alpha adrenoceptor blockade with phenoxybenzamine and phentolamine localized to the region of the carotid bifurcation in male cats abolished the increase in sympathetic discharge rate at high blood pressure induced by noradrenaline, but did not alter the response to angiotensin.6. 4351842: [Effects of porcine ACTH on arterial hypertension due to norepinephrine in rats]. 466431: No significant changes in DA content were observed in any region of the brain following induction of hypertension by the three different methods. NA content increased significantly in various areas: the increase of NA in the pons-medulla was common to all procedures inducing hypertension. In two substrains, selected from the Hebrew University strain, for their respective sensitivity (H) or immunity (N) to hypertension induced by DOCA--salt treatment, there were no significant increases in NA or DA in any part of the brain following DOCA--salt treatment. Noradrenaline (NA) and dopamine (DA) distribution in different brain areas was assayed following induction of hypertension. 4802784: [Effects of hydrocortisone and corticosterone on arterial hypertension induced by norepinephrine in rats]. 5509006: [Determination of adrenaline and noradrenaline in the urine of patients suffering from hypertension with special reference to the genesis of hypertension]. 5870364: Effects of hypertension induced by norepinephrine and sodium chloride upon the arteries and various organs of rats. 5975131: [The antagonistic action of lactic acid on adrenalin and noradrenalin-induced hypertension]. 6138461: Both alpha 1- and alpha 2-adrenoceptor blocking agent also significantly inhibited the hypertension induced by noradrenaline. This hypertensive effect was suppressed by an alpha 2-adrenoceptor blocking agent when an alpha 1-adrenoceptor blocking was responsible for the reversal of adrenaline-induced hypertension, and conversely. In fact, only a significant decrease of the noradrenaline-induced hypertension was observed after each alpha-blocker. In anaesthetized dog, the adrenaline induced hypertension is reversed by both alpha 1- and alpha 2-adrenoceptor blocking agents such as AR-C 239 and yohimbine. 6160942: Effect of beta-receptor-blocking agents on cardiovascular structural changes in spontaneous and noradrenaline-induced hypertension in rats. 6286176: Since alpha 2 receptors are located in proximal tubules at sites where norepinephrine induces sodium reabsorption, we postulate that this genetically determined abnormal receptor regulation could lead to exaggerated sodium retention and possibly high blood pressure. 6461018: The abrupt hypertension induced by norepinephrine is an inadequate model for the study of the effect of increased intramural tension. 6542210: In a rat model, norepinephrine (0.02 mg/kg) caused systemic hypertension and numerous pulmonary petechiae, the latter a common finding in SIDS. 6599723: To investigate the role of norepinephrine release from the sympathetic nerve endings and vascular responsiveness to endogenous and exogenous norepinephrine in the pathogenesis of hypertension, the perfused mesenteric preparations from spontaneously hypertensive rats (SHR) and DOCA-salt hypertension were used. 6742791: Norepinephrine-induced hypertension and seizures, however, caused significant increases in albumin leakage into forebrain structures ipsilateral to the lesion. 6765925: Immediately postischemia in four monkeys, intermittent arterial hypertension (i.e., 150--190 mm Hg) was induced by norepinephrine infusion for 3--5 min. 6769361: The effects of nitroglycerin (TNG) and sodium nitroprusside (SNP) on mean aortic pressure (MAP), uterine blood flow (UBF), uterine vascular conductance (UVC), and pulse rate (PR) were compared when the two agents were infused to prevent and treat hypertension induced by norepinephrine (NE) in gravid ewes. 6861444: Intrarenal infusion of noradrenaline caused hypertension at doses which did not do so when infused intravenously. 7036175: Extracellular fluid volume expansion associated with increased alpha receptor sensitivity to noradrenaline may cause hypertension in renal transplant recipients. 7049922: These findings suggest that overweight does not confer a unique aberration in the body sodium-volume state, circulating renin, aldosterone or catecholamines, or cardiovascular responses to NE or AII which result in hypertension. 7144267: The possibility is that dopamine along with noradrenaline may be playing an important role in peripheral organs, such as adrenal gland and heart, in the pathogenesis of hypertension. The noradrenaline and dopamine contents of heart and adrenal gland were estimated in rats with spontaneous, renal and stress-induced hypertension. 7223903: Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. 7440939: Norepinephrine resulted in bradycardia, hypertension and an increased placental vascular resistance. 7446169: Pial arterial vessels were inspected in hypercapnia (PaCO2 97 +/- 9 (S.E.) mmHg) and in acute hypertension induced by 5 microgram kg-1 noradrenaline i.v. 7978565: STUDY OBJECTIVE: Recent studies suggest that norepinephrine-induced hypertension early after cardiac arrest ameliorates cerebral hypoperfusion and improves neurologic outcome. CONCLUSION: In the early resuscitation period, increasing the norepinephrine dose to induce mild hypertension significantly increases oxygen use in the postischemic myocardium. Norepinephrine-induced hypertension following cardiac arrest: effects on myocardial oxygen use in a swine model. 799556: The role of noradrenaline and other transmitter hormones in the pathogenesis of hypertension. 811997: At higher doses than those required to block noradrenaline-induced hypertension, the three drugs inhibited pressor responses elicited by electrical stimulation and were equally active on peripherally- and centrally-evoked responses. Phentolamine, dihydroergocristine and isoxsuprine were compared for their effects on the blood pressure in anaesthetized normotensive rats, in rats made hypotensive by ganglionic blockade or by pithing and in rats with noradrenaline-induced hypertension. All three drugs appeared very potent in inhibiting noradrenaline-induced hypertension and caused a dose-dependent fall in blood pressure in normotensive rats, which however was less pronounced with dihydroergocristine than with phentolamine and isoxsuprine. 8186973: A decrease in the inhibitory capacities of GABA transmission in these areas, due to alterations of NE, may play a role in the genesis of hypertension. 8582488: Although many studies have examined the metabolism of catecholamines and cardiovascular responsiveness to norepinephrine in essential and various experimental hypertension, the role of sympathetic nervous system in the pathogenesis of hypertension has not been elucidated. 864477: Infusions of L-noradrenaline and angiotension produced greater hypertension, and injections of isoprenaline greater hypotension than in controls. 870220: The data indicate that chronic intrarenal infusion of norepinephrine in uninephrectomized conscious dogs results in sustained hypertension characterized by decreased renal plasma flow, normal glomerular filtration rate, positive sodium balance, and increased total peripheral resistance due to norepinephrine-dependent vasoconstriction. 8711809: Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 microns) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs). 8941043: The effects of acute norepinephrine-induced hypertension on the coronary arteries of newborn piglets. Newborn piglets were subjected to 45 min of sustained norepinephrine-induced hypertension and then monitored for 4 hr at baseline conditions. 9024144: CONCLUSIONS: Hypertension caused by chronically elevated angiotensin II is mediated in part by .O2-, likely via degradation of endothelium-derived NO. In contrast, angiotensin II-induced hypertension was associated with increased vascular .O2- production, whereas norepinephrine-induced hypertension was not. Treatment with liposome-encapsulated SOD reduced blood pressure by 50 mm Hg in angiotensin II-infused rats while having no effect on blood pressure in control rats or rats with norepinephrine-induced hypertension. 9194512: In rabbits with norepinephrine-induced acute hypertension, bolus and continuous infusion of hBNP markedly reduced blood pressure. 961912: Single injections of 1 ng/kg or more of angiotensin II or norepinephrine also increase dorsal aortic pressure but do not cause consistent diuresis and natriuresis, Continuous infusions of angiotensin II or repeated injections of norepinephrine produce sustained hypertension and more modest diuresis and natriuresis than are seen after injections of arginine vasotocin that cause less hypertension. 9854457: Eight of these underwent evaluation of EDV and endothelium-independent vasodilatation (EIDV) by means of forearm blood flow measurements during local intra-arterial infusions of methacholine (2 and 4 micrograms/min) and sodium nitroprusside (5 and 10 micrograms/min), before and after 1 h of sustained hypertension, induced by noradrenaline given intravenously. 10421092: The health consequences of obesity in adults are well established, including greater rates of hypertension, non-insulin dependent diabetes mellitus, and heart disease. 10477144: BP values in young male whites increased significantly with increasing BMI values but were independent of the C825T polymorphism, suggesting that hypertension associated with the 825T allele could be a consequence of obesity. 10480477: Time-course analysis of changes in blood pressure may reveal two components of obesity-induced hypertension, an early phase related to HFD itself and a later phase related to weight gain. To explore the mechanisms of obesity-induced hypertension we analyzed the sequential changes in cardiovascular and renal function in adult rabbits switched to high-fat diet (HFD) for 8 weeks. 10564240: Our results can be explained from an evolutionary perspective, since obesity-induced hypertension would be a much greater selective force in hominids compared with rodents. 10593542: Increasing adiposity, or obesity, is itself a direct cause of Type II diabetes, hypertension, CHD, gallbladder disease, osteoarthritis and cancer of the breast, colon, and endometrium. 10826410: In the present study, we tested the hypothesis that an increased activity of the sympathetic nervous system may contribute to the development of obesity-induced hypertension. Role of the sympathetic nervous system during the development of obesity-induced hypertension in rabbits. 10829088: Sympathetic activation appears to mediate at least part of the obesity-induced sodium retention and hypertension since adrenergic blockade or renal denervation markedly attenuates these changes. 10847146: The assumed mechanisms by which obesity leads to arterial hypertension are: insuline resistance; genetic factors (hypothesis for the sparing gene); correlations leptin-neuropeptide Y; fatty tissue as origin of local pressor and depressor humoral factors. 10900666: Obesity is determined by a polygenic constellation and produces insulin resistance, hypertension and dyslipidemia. 11126481: Excess weight is associated with an increased risk for numerous health problems, including dyslipidemia, hypertension, cardiovascular disease, type 2 diabetes, and some cancers, and it has been estimated that up to 325,000 deaths per year in the United States are attributable to obesity. 11230334: Oxidative stress in a rat model of obesity-induced hypertension. 11230354: The goal of this study was to examine the role of NO in modulating the chronic blood pressure, heart rate, and renal responses to hyperleptinemia, comparable to that found in obesity-induced hypertension. 11276398: Apart from the recent observation of obesity-associated structural changes in kidney structure that may lead to enhanced tubular sodium reabsorbtion, reports of paracrine and hormonal factors derived from adipose tissue have prompted speculations about the role of adipose tissue in the pathophysiology of obesity-induced hypertension. The mechanisms discussed herein may contribute to the typical findings in obesity-induced hypertension, including volume expansion, sodium retention, enhanced sympathetic nervous system activity, increased activity of the systemic renin-angiotensin system, low atrial natriuretic peptide levels, and disturbed glucose and insulin metabolism. New developments in mechanisms of obesity-induced hypertension: role of adipose tissue. 11411745: Sympathetic activation contributes to obesity-induced sodium retention and hypertension because adrenergic blockade or renal denervation markedly attenuates these changes. 11475857: Obesity, insulin resistance and hyperinsulinaemia are responsible for hypertension in diabetes mellitus type 2. 11485285: Loss of nocturnal dipping of blood pressure and heart rate in obesity-induced hypertension in rabbits. 11882596: We propose that because leptin produces central TRH synthesis and release, obesity may induce hypertension through TRH system activation and that the TRH-leptin interaction may thus contribute to the strong association between hypertension and obesity. 11887431: Obesity-induced HTN has some unique characteristics that differ from those observed in lean hypertensive patients. DATA SUMMARY: Obesity is a widespread and increasingly prevalent condition associated with a large number of comorbid diseases, one of the most important of which is obesity-induced hypertension (HTN). 11932566: CONCLUSION: These data suggest that exercise training, in the absence of differences in body weight, may be useful in the reduction of obesity-induced hypertension but that other therapies may be needed in order to control other cardiovascular risk factors. 12608526: Although the effects of Ang II on metabolism have not been studied widely, it is intriguing to assume that components of the RAS produced by adipocytes may play an autocrine, a paracrine and/or an endocrine role in the pathophysiology of obesity and provide a potential pathway through which obesity leads to hypertension and type 2 diabetes mellitus. 12771049: The major goal of this study was to determine whether there is increased activation of medullary neurons that participate in the central baroreceptor reflex pathway in dogs with obesity-induced hypertension, a model of hypertension that is associated with increased sympathetic activity. 12919774: AIMS: Obesity leads to hypertension and metabolic disturbances, as well as left ventricular hypertrophy and altered left ventricular geometry. 12939236: The reduction in the synthesis of these eicosanoids may play an important role in the regulation of renal function and blood pressure in obesity-induced hypertension. Downregulation of renal CYP-derived eicosanoid synthesis in rats with diet-induced hypertension. 14501164: Obesity, a state of increased adipose tissue mass, is a major cause for type 2 diabetes, hyperlipidemia, and hypertension, resulting in clustering of risk factors for atherosclerosis. 14516417: Interestingly, the degree of obesity induced hypertension was augmented when mice were studied at thermonuetrality. 14707164: Endothelin-1 appears to play an important role in the maintenance of arterial pressure in rats fed HF and NF diets, but it does not appear to contribute to increased MAP in this model of diet-induced hypertension. Endothelial dysfunction has been suggested to play an important role in the development of obesity-induced hypertension. 15007033: We conclude that obesity-induced hypertension and obesity-induced insulin resistance are not directly related. 15166905: Immediate consequences of childhood obesity include an increased prevalence of atherosclerotic plaques, hypertension, and an adverse lipid profile, with a poor self-image that limits participation in physical activity. 15241727: Although the importance of obesity as a cause of hypertension is well established, the molecular basis of the relationship between obesity and increased blood pressure remains poorly understood. 15287987: These conditions such as hypertriglyceridemia, hypercholesterolemia, obesity, and hyperglycemia might induce hypertension through various mechanisms. 15448764: Elevation of serum AGII and serum leptin levels when associated with increased BMI may contribute to the pathophysiology of obesity induced hypertension. 15506059: A sympathetic hyperactivity is a common feature in hypertension, type 2 diabetes (T2D), ageing and obesity-induced hypertension. [Role of vagosympathetic balance in obesity-induced hypertension]. 15583075: The continuing discovery of mechanisms regulating appetite and metabolism is likely to lead to new therapies for obesity-induced hypertension. 15882553: Despite the strides made toward understanding cardiac abnormalities in obesity-induced hypertension, the composition and concentration of cardiac extracellular matrix (ECM) components resulting from diet-induced obesity are largely unknown. 16105937: One of the major mechanisms leading to the development of obesity-induced hypertension appears to be leptin-mediated sympatho-activation. Obesity in humans causes hypertension, myocardial hypertrophy and coronary atherosclerosis, and increased cardiovascular morbidity and mortality that is thought to be related to sympathetic overactivity. 16105939: Leptin, a peptide hormone normally associated with body weight homeostasis, is implicated in the generation of obesity-induced hypertension. 16338246: The chief risk factors for this excess risk of death are cigarette smoking, obesity leading to dyslipidemia, insulin resistance and diabetes, and hypertension. 16352114: Obesity and hypertension both lead to cardiovascular complications. Endothelial, vascular and renal dysfunctions, all consequences of high blood pressure, further worsen hypertension. Multiple mechanisms involved in obesity-induced hypertension. 16355015: Of these elements, obesity may play the most important and pivotal role in creating the conditions that lead to hypertension in the metabolic syndrome. The cause of hypertension in the metabolic syndrome is complex and multifactorial and all of the elements of the metabolic syndrome, including obesity, insulin resistance, and the characteristic dyslipidemia probably are involved in mediating changes ultimately resulting in hypertension and modifying its course. 16514174: Our aim was to develop and characterize a model of pre-pubescent obesity-induced hypertension. Obesity-induced hypertension develops in young rats independently of the renin-angiotensin-aldosterone system. 16819529: CONCLUSION: Enhanced vascular reactivity may contribute to obesity-induced hypertension, while reductions in coronary artery relaxation would impair the ability of the heart to respond to increased myocardial demand. OBJECTIVE: To determine whether obesity-induced hypertension was associated with alterations in vascular contractility and/or cardiac function. 16896999: Obesity-induced hypertension and essential hypertension in lean patients are two different forms of hypertension. 16912512: Roles of paraoxonase and oxidative stress in adolescents with uraemic, essential or obesity-induced hypertension. Oxidative stress and the PON1 (activity and Q192R polymorphism) were analysed in adolescent patients with essential (n = 49) or obesity-induced hypertension (n = 79), uraemic patients (n = 20), and also in obese normotensive patients (n = 60) and age-matched controls (n = 57). The GSH levels were significantly lower in the patients with hypertension (p < 0.001) and obesity-induced hypertension (p < 0.05) than in the controls, while the GSSG level (p < 0.01) and the ratio GSSG/GSH (p < 0.05) was significantly higher in the uraemic hypertensive group. 17008074: CONCLUSION: Current research supports the notion of physical exercise as a potential non-pharmacological antihypertensive treatment for diet-induced obesity hypertension. The diet-induced obesity caused mild hypertension with adverse cardiovascular changes. 17190873: Neurons of the rostral ventrolateral medulla contribute to obesity-induced hypertension in rats. Activation of the sympathetic nervous system contributes to the pathogenesis of obesity-induced hypertension. 1730455: Cardiovascular regulation in obesity-induced hypertension. 1730456: Hyperinsulinemia: possible role in obesity-induced hypertension. 1730462: Although the mechanism for obesity-related hypertension has not yet been fully elucidated, recent studies have suggested that abnormalities in renal sodium handling may be involved in the pathogenesis of obesity-induced hypertension. 17429340: Our data indicate that juvenile obesity per se leads to systemic hypertension and renal structural and functional pathology. 17438305: The main goal of this study was to assess the influence of prolonged baroreflex activation on arterial pressure and neurohormonal responses in 6 dogs with obesity-induced hypertension. Prolonged activation of the baroreflex abolishes obesity-induced hypertension. 17630587: Although hypertension is recognized as one of the most serious consequences of obesity, its pathophysiology remains incompletely understood. 17680333: Approximately 80-90% of individuals with obesity-induced hypertension were in the 25.0 <or= BMI < 30.0 kg/m(2) category for both sexes in each year. The proportion of individuals with obesity-induced hypertension among total hypertensives in a general Japanese population: NIPPON DATA80, 90. Among all hypertensives, the percentage whose hypertension was due to obesity in 1980 and 1990 was 11.4% (95% confidence interval (CI): 4.7-17.7%) and 15.3% (95% CI: 6.8-23.1%) for men and 19.3% (95% CI: 12.1-25.9%) and 22.3% (95% CI: 14.6-29.3%) for women, respectively. In conclusion, we found that obesity-induced hypertension as a proportion of total hypertension increased between 1980 and 1990 for both sexes. 17880324: The health consequences of obesity include increased risk of heart disease, hypertension, diabetes, sleep apnea, cancer, osteoarthritis, and mental health problems. 17884458: We have recently shown that, in rats with obesity-induced hypertension, hyperleptinemia may produce an increase of dTRH together with an elevation of arterial blood pressure (ABP) through an increase of sympathetic activity and that these alterations were reversed by antisense oligonucleotide and small interfering RNA against preproTRH treatments. 18154717: Various diseases such as arterial hypertension, diabetes and obesity result in renal diseases which are often irreversible and resistant to currently available therapies. 18177582: This article reviews these issues and highlights the nuances and challenges in the effectiveness of weight loss for treatment of obesity-induced hypertension. 18282589: The established synergy between obesity and low nephron number on induction of high blood pressure and further decline of renal function identifies subjects with obesity, metabolic syndrome and diabetes mellitus II as particularly susceptible groups. 18378435: CONCLUSION: Our study has demonstrated that obesity plays the central role in leading to hypertension and a pro-inflammatory state, insulin resistance and dyslipidaemia. 18458706: While the physical consequences of obesity, such as arthritis, are debilitating and costly, the metabolic consequences are the drivers behind the modern epidemics of insulin resistance, diabetes, fatty liver disease, coronary artery disease, hypertension and polycystic ovary syndrome. 18677587: Obesity shows a strong association with hypertension, primarily due to secretion of an abundance of para- and endocrine peptides by the visceral adipose tissue that play a key role in the pathogenesis of high blood pressure and are responsible for the accelerated atherothrombosis encountered in overweight individuals. 18719995: Many other disorders, such as hypertension and diabetes are considered as the consequences of obesity. 18829779: Multinomial logistic regression was used to evaluate the odds for prehypertension and hypertension resulting from overweight and obesity. 18847118: Obesity is a cause of hypertension. 19107106: The rapid rise in the incidence and prevalence of obesity and the concomitant increase in the incidence and prevalence of hypertension have fueled investigation into the role of obesity in the pathogenesis of hypertension. Key changes in adipocytokine levels seen in obesity-induced hypertension include increased leptin and adiponectin levels. Another important mechanism in obesity-induced hypertension is the generation of angiotensin II and direct stimulation of aldosterone production. 19202910: Metabolic syndrome is diagnosed by the accumulation of dislipidemia, glucose intolerance and/or high blood pressure caused by visceral obesity. 19204299: CONCLUSIONS: In obesity-induced hypertension, increased oxidative stress in the brain, possibly via activation of NADPH oxidase, may contribute to the progression of hypertension through central sympathoexcitation. The present study was performed to determine whether oxidative stress could mediate central sympathoexcitation in the initial stage of obesity-induced hypertension. Sympathoexcitation by oxidative stress in the brain mediates arterial pressure elevation in obesity-induced hypertension. 19293441: BACKGROUND & OBJECTIVES: Obesity, hyperlipidaemia and hypercholesterolaemia are known risk factors in the pathogenesis of hypertension. 19383622: Obesity is a leading cause of diabetes mellitus and hypertension. 19409982: ROS contribute to the interrelationship between metabolic syndrome and salt-sensitive hypertension, which are both caused by obesity and excess salt consumption and are major threats to health in developed countries. 19443625: CONCLUSIONS: These results indicate that obese donors are not at higher risk for long-term reduced renal function compared with nonobese donors and that the increased incidence of hypertension and other cardiovascular disease risk factors in obese donors is due to their obesity and is not further exacerbated by nephrectomy. 19490286: Obesity-induced hypertension has multiple potential etiologic pathways, the most well established being increased renal sodium reabsorption with impaired pressure natriuresis via (1) activation of the renin-angiotensin system, (2) stimulation of the sympathetic nervous system, and (3) altered intrarenal physical forces. 19542189: Recent technological advances also enable the investigation of the contributions of genes to the co-morbidities of obesity, such as obesity-induced hypertension. 19603071: The objective of this study was to determine whether hypertension specifically affects the plasma lipidome independently and differently from the effects induced by obesity and insulin resistance. CONCLUSIONS/SIGNIFICANCE: Top-down shotgun lipidomics demonstrated that hypertension is accompanied by specific reduction of the content of ether lipids and free cholesterol that occurred independently of lipidomic alterations induced by obesity and insulin resistance. 19687357: BACKGROUND: Obesity causes hypertension and sympathoactivation, a process proposed to be mediated by leptin. 19809879: Metabolic consequences of obesity including insulin resistance, type 2 diabetes mellitus, hyperlipidemia, hypertension, polycystic ovarian syndrome, and non-alcoholic fatty liver infiltration are rapidly emerging in the pediatric population. 19811354: Moreover, excessive salt (8% salt diet: 8 weeks)-induced hypertension and proteinuria was accelerated in HF-fed rats. Salt sensitivity of blood pressure (BP) is speculated to be a characteristic in obesity-induced hypertension. 20002080: The metabolic consequences of obesity include dyslipidaemia, hypertension, proinflammatory atherogenesis, pre-diabetes and Type 2 diabetes. 20348094: Obesity-induced hypertension: role of sympathetic nervous system, leptin, and melanocortins. 20442753: The mechanisms through which obesity directly causes hypertension are still an area of research. Mechanisms of obesity-induced hypertension. 20514927: Role of excitatory amino acid input in rostral ventrolateral medulla neurons in rats with obesity-induced hypertension. 20645853: Excessive energy intake and obesity are major causes of hypertension. 20797323: Hypertension among the Inuit from Nunavik: should we expect an increase because of obesity? These results clearly indicate that HTN is becoming a growing health challenge in Nunavik because of pandemic obesity. 21041703: These findings offer the possibility of treating not only hypertension, but also other detrimental metabolic consequences of obesity including insulin resistance and dyslipidemia in obese populations by induction of HO-1 in adipocytes. 21388436: Interestingly, it is also suggested that, in obesity-induced hypertension models, increases in BP are caused by brain ROS-induced central sympathoexcitation. There are multiple and complex mechanisms of salt-induced hypertension; however, central sympathoexcitation plays an important role. Reactive oxygen species and the central nervous system in salt-sensitive hypertension: possible relationship with obesity-induced hypertension. Recent studies suggest that increased ROS production in the brain and central sympathoexcitation may share a common pathway that increases BP in both salt- and obesity-induced hypertension. 21457225: In animals, elevation of plasma adiponectin by either pharmacological or genetic approaches alleviates obesity-induced endothelial dysfunction and hypertension, and also prevents atherosclerosis, myocardial infarction and diabetic cardiomyopathy. 2155002: Sodium and obesity in the pathogenesis of hypertension. 21560313: There were positive interactions between family history and overweight/obesity and central obesity in the causes of hypertension. 21720269: It had also the largest population attributable fraction of hypertension due to obesity (35.5%) compared with Guadeloupe (13.3%), Martinique (12.3%) and French Guiana (23.6%). 21797044: INTRODUCTION: Obesity is often particularly burdensome for subjects at work and leads to hypertension and diabetes preceded by a low grade of inflammation. 2180241: Obesity causes a higher cardiac output and higher blood volume leading to hypertension. 22013104: These results begin to reveal the genetic architecture of obesity-induced hypertension. 22184321: Thus, we investigated the effects of global and renal specific suppression of sympathetic activity in dogs with sympathetically mediated, obesity-induced hypertension by comparing the cardiovascular, renal, and neurohormonal responses to chronic baroreflex activation and bilateral surgical renal denervation. 22254185: We compared plasma NPY and a-MSH levels between patients with or without hypertension and/or obesity and the differences in these neuropeptides between patients with or without pathological heart echo findings, aiming to investigate the possible role of these peptides in obesity induced HTN. 22291448: This dimorphism suggests sex-specific mechanisms of obesity-induced hypertension and the need for sex-specific criteria of its prevention. 22355066: We hypothesized that adrenal aldosterone production and aldosterone synthase expression would be increased in rats with obesity-induced hypertension. 2240279: The purpose of this study was to examine baroreflex sensitivity in the canine model of obesity-induced hypertension. Baroreflex sensitivity in the canine model of obesity-induced hypertension. 22517513: Obesity leads to hypertension by various mechanisms, often referred to as obesity-related hypertension. 22538946: This clinical and social problem is mainly related to the ongoing epidemic of obesity and metabolic syndrome resulting in hypertension and diabetes mellitus. 22573742: Some diseases (obesity, ascites, heart failure etc.) result in chronic AH. 22592557: Taken together, our results suggest that IDO1 activation represents a local compensatory mechanism to limit obesity-induced inflammation and hypertension. 22664863: Obesity-related hypertension in pediatric patients is becoming more prevalent around the world as a consequence of the childhood obesity epidemic. 22902874: OBJECTIVES: Sympathetic nervous system (SNS) activity is critically involved in the development and progression of obesity-induced hypertension. AT1R and oxidative stress in the RVLM might be novel treatment targets for obesity-induced hypertension through sympathoinhibition, and telmisartan might be preferable for obesity-induced hypertension. 22980162: The most important consequence of childhood obesity is its persistence into adulthood with all its health risks like dyslipidemia, hyper-insulinemia, cardiovascular diseases, type 2 diabetes, osteoarthritis, gall bladder disease, hypertension and some sex hormone- sensitive cancers. 23074483: This suggests that obesity leads to OSA, diabetes, and hypertension, rather than OSA independently causing diabetes and hypertension. 23150506: The observation of raised levels of adipokines in wild-type but not TRPV1 knockout mice is in keeping with TRPV1 involvement in stimulating the proinflammatory network that is central to obesity-induced hypertension and sensory neuronal dysfunction. 23154648: BACKGROUND/AIMS: Obesity and hypervolemic status are the main causes of hypertension in patients with chronic kidney disease (CKD). 23244451: This paper summarizes the existing literature on the main theories as to how obesity leads to hypertension as well as the literature concerning the effects of gastric bypass surgery on hypertension. 23374353: These findings provide a cellular correlate of the autonomic side effects associated with MC4R agonists and demonstrate a role for MC4Rs expressed in cholinergic neurons in the regulation of insulin levels and in the development of obesity-induced hypertension. 23536127: Understanding the pathways by which obesity contributes to increased blood pressure will hopefully pave the way to and better define the appropriate treatment for obesity-induced hypertension. 23670298: Obesity is a strong risk factor for hypertension, but the mechanisms by which obesity leads to hypertension are incompletely understood. 23716916: Patients who had nondiabetic nephropathy, uncontrolled hypertension (>125/75 mmHg) irrespective of antihypertensive drugs, excess weight due to edema or obesity due to other specific diseases, alcoholics, smokers, and patients who were on hemodialysis were excluded from the study. 23883674: The review focuses on a critical analysis of the concept of selective leptin resistance (SLR) and the role of leptin in the pathogenesis of obesity-induced hypertension in both experimental animals and humans. Finally, I review perplexing data on the effects of leptin on sympathetic activity and BP in humans and its role in human obesity-induced hypertension. 23913707: Chronic baroreflex activation restores spontaneous baroreflex control and variability of heart rate in obesity-induced hypertension. 23966059: Obesity, arterial stiffness and high aldosterone levels can interact to cause resistant hypertension (RHTN). 24010102: Obesity can cause hyperlipidemia, hypertension, cardiovascular diseases, metabolic syndrome and non-alcoholic fatty liver disease (NAFLD). 24019901: Whilst modest, our findings support the hypothesis that a reduced nephron endowment increases the susceptibility to obesity-induced kidney disease and hypertension. 24199153: We also discuss the relevance of PI3K signaling for obesity-induced hypertension through its role in mediating selective leptin resistance. 24400148: Obesity is a major cause of hypertension, but links between the obese and hypertensive states remain incompletely understood. 24497896: Obesity leads to significant systemic disorders, such as hypertension, hypercholesterolemia, hypertriglyceridemia and insulin resistance, and also increases the risk of developing cardiovascular diseases (ischemic heart disease, ischemic stroke), metabolic diseases (type 2 diabetes), certain types of cancer, and degenerative bone disorders (osteoarthritis). 24709437: BACKGROUND: Obesity-induced hypertension appears to be due, in part, to increased renal sympathetic activity. 24760503: However, our data in conscious, freely moving GHS-R deficient mice demonstrate that chronic absence of GHS-R signaling is protective against obesity-induced hypertension. Growth hormone secretagogue receptor deficiency in mice protects against obesity-induced hypertension. 24846230: This leads to a change in profile of the released adipo(cyto)kines, resulting in a decreased vasorelaxing effect of PVAT, which may be linked to obesity-induced hypertension. 24958528: It had also the largest population attributable fraction of hypertension due to obesity (35.5%) compared with Guadeloupe (13.3%), Martinique (12.3%) and French Guiana (23.6%). 24993282: Recently, we demonstrated that, in salt- and obesity-induced hypertension, hypothalamic ROS levels was elevated and intracerebroventricular antioxidants suppress BP and renal sympathetic nerve activity more profoundly, compared to their control. Thus, it is suggested that brain ROS overproduction increases BP through central symapthoexcitation in salt- and obesity-induced hypertension, which are often associated. 25016404: Hypertension is a common consequence of obesity. 25041756: CONCLUSION: Collectively, these data indicate that obesity-induced down-regulation of CAT1 expression and subsequent reduced bioavailability of nitric oxide may contribute to the development of obesity-induced hypertension. In this study, we tested the hypothesis that abnormal L-arginine transport may be a key mediator of obesity-induced hypertension. 25090962: Central nervous system dysfunction in obesity-induced hypertension. 25210844: OBJECTIVE: Obesity is a metabolic disorder that can lead to high blood pressure, increased blood cholesterol and triglycerides, insulin resistance, and diabetes mellitus. 25368023: Why obesity causes hypertension is poorly understood. Thus, we have identified a novel role for FcgammaRIIB in the pathogenesis of obesity-induced hypertension, independent of processes regulating adiposity, and it may entail an IgG-induced attenuation of endothelial NO synthase function. Recognizing known associations between CRP and obesity and hypertension in humans, in the present study we tested the hypothesis that FcgammaRIIB plays a role in obesity-induced hypertension in mice. IgG receptor FcgammaRIIB plays a key role in obesity-induced hypertension. 25487935: It was examined whether obesity affects serum levels of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6), which may lead to the consequences of obesity, such as type 2 diabetes, hypertension, and finally the metabolic syndrome. 25534200: Obesity: The many faces of leptin--a novel role for leptin signalling in obesity-induced hypertension. 25620635: We also discuss the potential underlying mechanisms by which obesity promotes other cardiovascular and renal conditions, as well as available nonpharmacologic and pharmacologic approaches for treating obesity-induced hypertension. 25653535: However, in animal studies, increased circulating adiponectin alleviates obesity-induced endothelial dysfunction and hypertension, and also prevents atherosclerosis, myocardial infarction, and diabetic cardiac tissue disorders. 25686864: The mechanisms by which obesity causes HTN are complex and involve several organic mechanisms. For both groups, healthy and a variety of diseased dogs were observed; the correlations between pathologies and obesity were studied, paying special attention to diseases whose pathophysiologies could lead to HTN. 25767285: Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms. 25860531: This review highlights recent advances that have identified novel signal transduction mechanisms within multiple hypothalamic nuclei (e.g., paraventricular nucleus, arcuate nucleus) acting to drive the pathophysiology of hypertension in neurogenic hypertension, angiotensin II hypertension, salt-sensitive hypertension, chronic intermittent hypoxia, and obesity-induced hypertension. 26078188: We recently demonstrated that female mice are resistant to the development of obesity-induced hypertension through a sex hormone-dependent mechanism that involved adipose angiotensin-converting enzyme 2 (ACE2). 26083724: HBP in about 22.9% (95% CI 21.5, 24.2%) of boys and 14.7% (95% CI 13.5, 15.8%) of girls could be attributable to overweight and obesity. 26103132: Furthermore, gene-environment interactions may have the potential to modify gene expression and epigenetic mechanisms could also contribute to the heritability of obesity-induced hypertension. New developments in the pathogenesis of obesity-induced hypertension. 26175484: Obesity in children and adolescents can result in hypertension, dyslipidemia, chronic inflammation, and hyperinsulinemia, increasing the risk of death, as children grow into adulthood, and raising public health concerns. 26186712: Augmented Endothelial-Specific L-Arginine Transport Blunts the Contribution of the Sympathetic Nervous System to Obesity Induced Hypertension in Mice. We tested the hypotheses that CAT1 overexpression prevents obesity-induced hypertension by buffering the influence of the sympathetic nervous system (SNS) on the maintenance of arterial pressure and by buffering pressor responses to stress. We conclude that CAT1 overexpression prevents obesity-induced hypertension by reducing the influence of the SNS on the maintenance of arterial pressure but not by buffering pressor responses to stress. 26295295: Obesity, insulin resistance (IR), inflammation, and hyperandrogenism may lead to polycystic ovary syndrome (PCOS) and hypertension. 26667041: The associated health consequences of obesity are pleiotropic, with individuals being more susceptible to chronic diseases such as type 2 diabetes mellitus, hypertension, and lipotoxicity-related chronic diseases. 26682787: The enigma of obesity-induced hypertension mechanisms in the youth. 26820476: CONCLUSION: These findings suggest that obesity-induced hypertension and increased RSNA are dependent on the balance between greater activation of melanocortin signalling through melanocortin receptors and lesser activation of NPY sympathoinhibitory signalling. 26882812: CONCLUSIONS: In conclusion, in regulating energy balance, perilipin, irisin, and adropin, could be of pathogenic importance in obesity-induced hypertension. 26910553: The fraction of hypertension attributable to obesity was 17.8%. OBJECTIVE To estimate the prevalence of arterial hypertension and obesity and the population attributable fraction of hypertension that is due to obesity in Brazilian adolescents. Prevalences and 95% confidence intervals (95%CI) of arterial hypertension and obesity, both on a national basis and in the macro-regions of Brazil, were estimated by sex and age group, as were the fractions of hypertension attributable to obesity in the population. 26957306: Hypertension affects over 25 % of the population with the incidence continuing to rise, due in part to the growing obesity epidemic. 27048090: Obesity is one of the direct cause of hypertension. 27160198: We investigated the chronic interactions of these reflexes in dogs with sympathetically mediated, obesity-induced hypertension based on the hypothesis that hypoxemia and tonic activation of carotid chemoreceptors may be associated with obesity. 27174097: This was associated with reversal of obesity-induced hypertension and normalization of plasma adipokine levels, including leptin and insulin. 27262997: This review highlights recent advances in our understanding of central nervous system (CNS) signaling pathways that contribute to the etiology and pathogenesis of obesity-induced hypertension. Obesity-Induced Hypertension: Brain Signaling Pathways. 27397427: We investigated the effects of metformin and celecoxib on obesity-induced adipose tissue inflammation, insulin resistance (IR), fatty liver, and high blood pressure in high-fat (HF) fed rats. 27467764: CONCLUSION: Obesity in MC4R deficiency and HFD in MC4R rats result in higher BP and placental inflammation during pregnancy. 27511280: Sex differences in obesity-induced hypertension and vascular dysfunction: a protective role for estrogen in adipose tissue inflammation? 27524223: Obesity leads to the development of cardiomyopathy directly via inflammatory mediators and indirectly by obesity-induced hypertension, diabetes and coronary artery diseases. 27550916: The present study tested the hypothesis that RDNx reduces AP and renal inflammation and improves glucose metabolism in obesity-induced hypertension. These results indicate that although renal nerves play a role in obesity-induced hypertension, they do not contribute to impaired glucose metabolism or renal inflammation in this model. 27559704: Renal simplicity denervation reduces blood pressure and renal injuries in an obesity-induced hypertension dog model. 27595156: RECENT FINDINGS: This review highlights recent advances in both clinical and basic science that have provided new insight into the distribution, function, and reinnervation of the renal sympathetic nerves, with a focus on the renal afferent nerves, in hypertension and hypertension-evoked disease states including salt-sensitive hypertension, obesity-induced hypertension, and chronic kidney disease. 27665107: Leptin as a Mediator of Obesity-Induced Hypertension. 27755119: The SNS activation found in obstructive sleep apnea (OSA), caregiving for a severely demented spouse, and obesity more specifically address whether SNS activation might lead to the metabolic syndrome and hypertension. 27771702: Summary and Key Message: Microvascular (MV) disease plays a pivotal role in progressive kidney injury from different etiologies such as hypertension, diabetes, and atherosclerosis, which are all important consequences of chronic obesity. 27827474: The prothrombotic state associated with obesity-induced hypertension is reduced by cocoa and its main flavanols. 2786848: The association of hypertension with obesity has long been recognized; however, because of the lack of suitable animal models of obesity and hypertension, the pathogenesis of the high blood pressure associated with obesity remains poorly understood. 27884224: This article updates recent literature with a focus on the function of insulin resistance, obesity, and renin angiotensin aldosterone system-mediated oxidative stress on endothelial dysfunction and the pathogenesis of hypertension. 27894066: Finally, we confirm that obesity-induced hypertension can be reversed through central treatment with TGFbeta receptor antagonist. 27940022: It is recommended that health promotion programs focus on obesity in the provinces with a higher share of hypertension due to obesity. 27940965: The prevalence of hypertension induced by obesity has grown over the years, and the role of the renin-angiotensin-aldosterone system (RAAS) in this process continues to be elucidated. 27986659: MasR agonists may be effective therapies for obesity-associated cardiovascular conditions.NEW & NOTEWORTHY MasR deficiency abolishes protection of female mice from obesity-induced hypertension. Previous studies demonstrated that protection of female mice from obesity-induced hypertension was associated with increased systemic ANG-(1-7), whereas male obese hypertensive mice exhibited increased systemic ANG II. 28262443: [Pathophysiology of hypertension secondary to obesity]. 28274841: In experimental models of hypertension with high SNS activity, blockade of the melanocortin-4 receptor (MC4R) reduces BP despite causing marked hyperphagia and obesity. 28409013: Obesity was cited as a cause of hypertension but weight control was not considered as a treatment modality even though the majority of our participants were overweight. 28537562: Obesity is the cause of many serious diseases, such as type 2 diabetes, hypertension, and non-alcoholic fatty liver disease (NAFLD). 28595525: Obesity-Induced Hypertension: New Insights. CONCLUSION: Reduction in body weight with treatment is not always associated with reduction in obesity induced hypertension. 28599248: Obesity is significantly increasing worldwide because of increased high calorie food intake and decreased physical activity leading to hypertension, dyslipidemia, atherosclerosis, and insulin resistance. 28670396: BACKGROUND: Obesity-induced hypertension (OIH) has a high morbidity and mortality, and its prevention and treatment has been a major challenge in clinical practice. 28690194: Obesity-induced hypertension, assessed by radiotelemetry, was mild and transient in the WT, while the basally hypertensive KI mice were resistant to further increases in blood pressure following high fat feeding. 28977211: OBJECTIVE: Obesity can cause systemic arterial hypertension (SAH) and type 2 diabetes mellitus (DM2) factor that is also influenced by genetic variability. 29083240: Obesity may lead to hypertension through multiple ways by different percents. 29091513: Metabolic syndrome is a serious consequence of obesity characterized by increased cardiovascular risk factors such as hypertension, dyslipidemia, and glucose intolerance. 29127233: Sympathetic hyperactivation, a common feature of obesity and metabolic syndrome, is a key trigger of hypertension. 29132429: BACKGROUND: Obesity is considered problematic not only as a major cause of diabetes, hypertension, and dyslipidemia, but also as a risk of intractable dermatosis; however influence of obesity on skin function has not been clarified. 29172730: To explore the roles of glutamate acid decarboxylase 65 (GAD65) and angiotensin II type 1 receptor (AT1R) in the action of renal sympathetic denervation (RSD) on obesity-induced hypertension in canines. Renal sympathetic denervation lowers arterial pressure in canines with obesity-induced hypertension by regulating GAD65 and AT1R expression in rostral ventrolateral medulla. 29301630: Despite our failure to contain the high prevalence of obesity, we now have a better understanding of its pathophysiology, and how excess adiposity leads to type 2 diabetes, hypertension, and cardiovascular disease. 29471100: Obesity among older adults is a major cause of physical dysfunction, hypertension, diabetes, and coronary heart diseases. 29493561: CONCLUSION: Taken together, our results suggested that enhanced CB1 receptor-mediated neurotransmissions in the RVLM may play a role in the development of obesity-induced hypertension. Thus, we hypothesized that CB1 receptor in the RVLM may play a critical role in the development of obesity-induced hypertension. 29535450: CONCLUSIONS: This study shows that MSEW promotes a sex-specific dysregulation of the adipose tissue expansion and glucose homeostasis that precedes the development of obesity-induced hypertension. A model of neglect during postnatal life heightens obesity-induced hypertension and is linked to a greater metabolic compromise in female mice. 29631680: Obesity is identified one of the most important factors leading to diabetes, heart disease and hypertension. 29634663: Epidemiology and mechanisms of obesity-induced hypertension, diabetes and dyslipidemia will be reviewed and the role of lifestyle modification and treatment strategies in obesity will be updated and analyzed. 29651318: Conclusion: Arterial hypertension is becoming an important public health problem, especially due to the childhood obesity. 29689708: Obesity may induce arterial hypertension, disorders of carbohydrate metabolism, and is a risk factor of cardiovascular disease. 29731021: Finally, obesity and the metabolic syndrome, through their effects on various hormones and inflammation, might also contribute to the pathogenesis of hypertension and diabetes. The renin-angiotensin-aldosterone system may be upregulated in diabetes, leading to hypertension through a direct effect mediated by angiotensin II, as well as indirectly through upregulation of sympathetic activity. 30042353: Food-insecure people are more likely to consume high-calorie diets that lead to obesity, which, together with a lack of vigorous physical activity, leads to hypertension and CVD. 30394777: Obesity affects all systems of the body, and the serious health consequences of obesity include an increased risk for cardiovascular disease, such as Type 2 diabetes or high blood pressure, which are occurring at ever younger ages. 30632444: In order to get a better perspective on the true nature of the obesity paradox, a Medline and Embase search of the English language literature was contacted from 2012 to 2018, using the terms, overweight, obesity, obesity paradox, CVD, HF, and hypertension. 30914014: Heart attacks, strokes, renal failures are pathologies that have mid-risk factors such as dyslipidemia, hypertension and diabetes, which in turn are caused by obesity, whose primary risk factor is represented by the diet. 30968731: Obesity-Induced Hypertension: Heavy on the Accelerator. 30987571: METHODS: We conducted a research of the relevant literature regarding obesity-induced hypertension and possiple treatment strategies. 31028563: These studies also support the concept that MC4R activation is critical for obesity-induced hypertension as well as other forms of hypertension associated with increased SNS activity. 31088773: Childhood obesity considerably influences public health because it causes stroke, hypertension and diabetes mellitus. 31271650: The mechanisms underlying high-fat diet (HFD)- or obesity-induced hypertension are not well defined, although immune system activation and inflammation have been implicated in several studies. 31330870: In obese subjects, several mechanisms may lead to hypertension such as insulin and leptin resistance, perivascular adipose tissue dysfunction, renal impairment, renin-angiotensin-aldosterone-system activation and sympathetic nervous system activity. 31545149: Leptin induced hypertension in C57BL/6J mice, which was abolished by CB denervation, Trpm 7 blockers, and Trpm7 small hairpin RNA applied to CBs. OBJECTIVE: To examine if leptin induces hypertension acting on the CB Trpm7. CONCLUSIONS: We conclude that leptin induces hypertension acting on Trmp7 in CB, which opens horizons for new therapy. RATIONALE: Obesity leads to resistant hypertension and mechanisms are poorly understood, but high plasma levels of leptin have been implicated. Leptin Induces Hypertension Acting on Transient Receptor Potential Melastatin 7 Channel in the Carotid Body. 31597453: Studies were designed to determine if alterations in IgG contribute to the pathogenesis of obesity-induced hypertension. Furthermore, in HFD-fed mice, ManNAc normalized IgG sialylation and prevented obesity-induced hypertension. We previously revealed that mice globally deficient in the inhibitory immunoglobulin G (IgG) receptor FcgammaRIIB are protected from obesity-induced hypertension. CONCLUSIONS: Hyposialylated IgG and FcgammaRIIB in endothelium are critically involved in obesity-induced hypertension in mice, and supportive evidence was obtained in humans. RESULTS: Mice deficient in B cells were protected from obesity-induced hypertension. Mice deficient in FcgammaRIIB in endothelium were protected from obesity-induced hypertension. 31695458: Regulation of alternative splicing in obesity-induced hypertension. A greater knowledge of the genetic basis for obesity-linked hypertension will assist in the development of appropriate diagnostic tests as well as the identification of new personalized therapeutic targets against obesity-induced hypertension. In order to develop new and effective therapeutic agents combating obesity-induced hypertension, a thorough understanding of the molecular events leading to adipogenesis is critical. This review examines the role played by alternative splicing (AS) as a contributing factor to the metabolic regulation of obesity-induced hypertension. 31766426: Early-onset obesity is known to culminate in type 2 diabetes, arterial hypertension and subsequent cardiovascular disease. 31801409: Furthermore, loss of endothelial FTO prevented the development of obesity-induced hypertension by preserving myogenic tone in resistance arteries. 31868518: Although there are numerous reviews focused on the role of sympathetic nerves in different models of hypertension, few have revised the contribution of afferent nerves innervating adipose tissue and their role in the development of obesity-induced hypertension. A comprehensive understanding of how multiple afferent reflexes contribute to the pathophysiology of essential and/or obesity-induced hypertension may provide significant insights to improving antihypertensive therapeutic approaches. 32008372: Conclusions: These data suggest that a spatially restricted impairment of endothelial TRPV4 channels contributes to obesity-induced hypertension, and imply that inhibiting peroxynitrite might represent a strategy for normalizing endothelial TRPV4 channel activity, vasodilation, and blood pressure in obesity. Background: Impaired endothelium-dependent vasodilation is a hallmark of obesity-induced hypertension. 32044963: SR-A1 Prevents Obesity-Associated Blood Pressure Elevation through Suppressing Overproduction of VEGF-B in Macrophages.AIMS: Dysfunctional innate immune function and inflammation contributes to the pathogenesis of obesity-associated hypertension, in which macrophage infiltration in the perivascular adipose tissue (PVAT) plays a key role. TRANSLATIONAL PERSPECTIVE: An accumulating body of evidence indicates that obesity is a major cause of hypertension. 32206601: The mechanisms through which obesity causes hypertension are complex and include sympathetic nervous system overactivation, stimulation of the renin-angiotensin-aldosterone system, alterations in adipose-derived cytokines, insulin resistance, and structural and functional renal changes. 32389344: Part 1 of this review will discuss neural mechanisms of salt-sensitive hypertension, obesity-induced hypertension, and the ability of prior experiences to sensitize autonomic networks. 32389788: The present study focuses mainly on identifying the role of HMGB1 in cardiac and renal tissue damage following obesity-induced hypertension. HMGB1 and COX2 are regulated during organ damage following obesity-induced hypertension in a metabolic syndrome mouse model. Following high-fat diet and leptin injection, mice developed obesity-induced initial hypertension and critical hypertension after 4 and 9 months, respectively. Our study shows that HMGB1 plays a key role in initiating organ damage following obesity-induced hypertension, and that once damage reaches a certain level, HMGB1 expression is downregulated. 32398603: RECENT FINDINGS: In contrast to the general nontransplant hypertensive patient population, traditional risk factors, including family history of HTN, obesity and diabetes, play a minor role in the genesis of posttransplant HTN. 32495072: Weight Loss After Bariatric Surgery Significantly Improves Carotid and Cardiac Function in Apparently Healthy People with Morbid Obesity.PURPOSE: Obesity clearly increases cardiovascular risk, often inducing high blood pressure (BP), impaired left ventricular (LV) function, and increased arterial stiffness. 32552871: All pigs were fed the high-fat diet after the operation to establish a model of obesity-induced hypertension. 3298046: Obesity-induced hypertension in the dog. To study the relationship between body weight and blood pressure, we have developed an animal model of obesity-induced hypertension. 3301356: It is estimated that as much as one-third of all hypertension may be attributable to obesity in populations where hypertension and obesity are widely prevalent. 33075125: BACKGROUND: Previous studies suggest that obesity-induced hypertension in females, but not males, is due to leptin-mediated stimulation of aldosterone secretion and subsequent activation of the mineralocorticoid receptor (MR). 33119816: The authors raised concerns regarding the lack of inclusion of obesity by several societies as a formal cause of hypertension considering not only the biologic plausibility but also the huge impact of weight loss therapies such as bariatric surgery on hypertension remission. In contrast, there is no discussion that a very rare condition-namely pheochromocytoma-is the most \typical\ cause of hypertension by promoting hypertension remission in the majority of patients after surgical procedure. If obesity becomes largely accepted by several societies as a secondary form of hypertension, this pandemic condition will be certainly the most common cause of hypertension. 33693473: BACKGROUND: Obesity and hypertension are public health priorities, with obesity considered to be a potential cause of hypertension. 33815612: Obesity is associated with the pathogenesis of type 2 diabetes, hypertension, dyslipidemia, cardiovascular diseases, cancer, and kidney diseases. 33846799: Central AT1R is involved in almost all types of hypertension, including spontaneous hypertension, salt-sensitive hypertension, obesity-induced hypertension, renovascular hypertension, diabetic hypertension, L-NAME-induced hypertension, stress-induced hypertension, angiotensin II-induced hypertension and aldosterone-induced hypertension. Present in more than one billion adults, hypertension is the most significant modifiable risk factor for mortality resulting from cardiovascular disease. 33951475: These results suggest that hyperleptinemia promotes obesity-induced hypertension via a HIF1alpha-VEGF signaling cascade in hypothalamic astrocytes while establishing a novel mechanistic link that connects hypothalamic micro-angioarchitecture with control over systemic blood pressure. 33993722: Obesity increases levels of an adipocyte-produced hormone leptin, which activates the sympathetic nervous system leading to hypertension. Pharmacological and Genetic Blockade of Trpm7 in the Carotid Body Treats Obesity-Induced Hypertension. 34240733: These results provide a potential mechanism for obesity-induced endothelial dysfunction and hypertension. 34276408: Background: Obesity can cause hypertension and exacerbates sleep-disordered breathing (SDB). Obesity-induced hypertension has been associated with hyperleptinemia. 34305591: This study has been designed to provide evidence of underlying mechanisms to the medicinal use of A. officinarum as a cardiotonic using an obesity-induced hypertension model in rats. 34311195: CONCLUSIONS: Overweight or obesity was the single most significant factor leading to hypertension and diabetes among the study population. 34436493: Obesity is associated with hormonal changes and vascular dysfunction, which eventually lead to hypertension, hyperinsulinemia, chronic kidney disease, dyslipidemia and cardiac dysfunction-all associated with increased cardiovascular risk, leading to potential cardiovascular events in early adulthood. 34568440: To be more specific, AML-related hypertension was more likely to result from obesity and renal compression by perirenal fat than from endocrine disorders or blood vessels compression. 34713714: This study provides significant novel insight into the potential renal nerve-neprilysin-GLP-1 pathway involved in renal dysfunction during obesity that leads to hypertension. 34793497: In silico trial of baroreflex activation therapy for the treatment of obesity-induced hypertension. 34951936: CONCLUSIONS: Blood pressure was positively correlated with BMI, and the risk of high blood pressure due to overweight/obesity was 10.44%. 34968205: There was a significant association between obesity and pre-existing thyroid disease and induced hypertension class III. 35043013: The combination of obesity and hypertension is associated with high morbidity and mortality; however, the mechanism underlying obesity-induced hypertension remains unclear. 35083703: Obesity is a leading cause of hypertension (i.e., high blood pressure [BP]). 35229613: Pregnane X Receptor-4beta-Hydroxycholesterol Axis in the Regulation of Overweight- and Obesity-Induced Hypertension. 35554861: The experimental stimulation of afferent excitatory signals from adipose tissue has been shown to contribute with obesity-induced hypertension as part of a mechanism called the adipose afferent reflex (AAR). 35554866: Accumulating evidence suggests that increase in sympathetic nerve activity (SNA) plays a crucial role in the pathophysiology of obesity-induced hypertension. 35556326: Hypertension is prevalent in 46% of the US adult population with 40% of cases being attributable to obesity. 35556920: Moreover, our results provide a mechanism by which hepatic lipid content can affect blood pressure, identifying potential targets for the treatment and prevention of obesity-induced hypertension. 35560307: Early life stress (ELS) is associated with increases in body mass index and systolic blood pressure in adult life, leading to obesity and obesity-induced hypertension, major risk factors for cardiovascular disease (CVD). 35560673: Endothelial dysfunction in small arteries is a hallmark of obesity-induced hypertension. 35560693: Blockade of Trpm7 in the Carotid Body area attenuated intermittent hypoxia-induced Hypertension. We hypothesize that IH causes hypertension acting on CB TRPM7. CONCLUSION: Our study has shown that inhibition of TRPM7in the carotid bodies abolished IH-induced hypertension. We discovered that obesity-induced hypertension is mediated via the transient receptor potential melastatin 7 (TRPM7) channel in the glomus cells of CB. FTY720 hydrogel abolished IH-induced hypertension by decreasing blood pressure to 106.6+/-1.6 mmHg (p<0.005) on Day 1 of IH and to 101.5+/-1.6 mmHg (p<0.001) on Day 5 of IH. In contrast, control hydrogel had no effect on IH-induced hypertension. Intermittent hypoxia (IH), a hallmark manifestation of OSA, is an established cause of hypertension. 3568029: The stroke-salt intake association in East European countries might have been modified by other factors such as increased fat intake and obesity causing high blood pressure. 35809879: With obesity, both leptin and AngII increase; therefore, the increased AT1aR activation could open the gate, allowing leptin (and insulin) to drive sympathoexcitation unabated, leading to hypertension. 36139877: Although all interventions improved endothelial function in aorta segments, only supplementation with CSAT+ (r) reduced obesity-induced hypertension, prevented endothelial dysfunction in mesenteric arteries, and decreased the vascular response of aorta segments to the vasoconstrictor AngII. 36145220: The HFD induced hypertension in SS ( p < 0.01) but not SR rats, although it increased body weight gain ( p < 0.05) and tPVAT weight ( p < 0.01) in both rats. A high-fat diet (HFD) frequently causes obesity-induced hypertension. 36323255: Notably, patients with obesity carrying Mc4r mutations are protected against obesity-induced hypertension, and MC4R agonists elevate blood pressure (BP). 36501131: The prevalence of obesity is increasing worldwide, and obesity can cause type 2 diabetes, atherosclerosis, hypertension, cardiovascular disease, and cancer. 36540483: Obesity in children may lead to hypertension, coronary disease, and a greater incidence of diabetes complications and metabolic syndrome. 36578425: Moreover, QDG treatment also demonstrated robust cardioprotective effects during obesity-induced hypertension by markedly improving cardiac function and preventing cardiac hypertrophy. Qingda granule prevents obesity-induced hypertension and cardiac dysfunction by inhibiting adverse Akt signaling activation. Mouse models of obesity via long-term feeding of high-fat high-fructose diet (HFFD) were established to examine the effect and mechanism of QDG in protecting against obesity-induced hypertension and cardiac dysfunction. Our findings thus elucidated the role of QDG in preventing obesity-induced hypertension and cardiac hypertrophy via inhibiting adverse activation of Akt signaling activation. Qingda granule (QDG) is a condensed Traditional Chinese Medicine (TCM) formula that has been used clinically for treating hypertension, however, its effectiveness in obesity-induced hypertension and cardiac dysfunction remains explored. QDG protected against obesity-induced hypertension and cardiac dysfunction was due to its ability to prevent adverse chronic activation of Akt signaling pathway during long-term feeding of HFFD. Therefore, our study provides the theoretical basis for the utilization of QDG as both a safe and effective drug in the therapeutic treatment of metabolic diseases such as obesity-induced hypertension. 36646438: Obesity increases the risk of mortality and morbidity because it results in hypertension, heart disease, and type 2 diabetes. 36671022: Our results are opening the door for more studies to investigate the effect the of SCFAs/HO-2 axis on hypertension and obesity-induced cerebrovascular diseases. 36759688: We examined the risk for diabetes, hypertension, and dyslipidemia due to obesity in individuals of this age. 37052969: Context: With the development of the Chinese economy, people's quality of life has improved, obesity caused by excessive nutrition has increased among teenagers, and the age of patients with obesity-induced hypertension has become younger and younger. Adolescent Hypertension Induced by Obesity and the Efficacy of Comprehensive Intervention. Participants with obesity-induced hypertension received a comprehensive intervention. 37198444: Mineralocorticoid receptor-associated hypertension is a broad concept of hypertension that includes not only PA, but also hypertension caused by borderline aldosteronism, obesity, diabetes, and sleep apnea syndrome. 37276817: The reproductive consequences of obesity are variable and include but not exclusively menstrual disorders; fertility difficulties; recurrent miscarriages; gestational diabetes, hypertension, and pre-eclampsia; postpartum hemorrhage; and fetal macrosomia. 37452142: Obesity may independently cause hypertension through several mechanisms including activation of the renin-angiotensin-aldosterone pathway. 37531880: Both patients had hypertension caused by PA and obesity. 37598377: Hyperandrogenism Protects Against High Blood Pressure by Nongenomic Mechanisms and Obesity Causes Hypertension in Females with Polycystic Ovary Syndrome. 37906023: BACKGROUND: Recently, an important health issue in children is obesity, leading to hypertension. 37955693: Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which mimic human type 2 diabetes, are frequently used to study obesity-induced insulin resistance (IR) and hypertension. Taken together, we hypothesized that human omentin-1 may reduce obesity-induced IR and hypertension in OLETF rats. 38126089: Obesity-induced hypertension is mediated by insulin receptor (INSR) activation in CB, and may also be by high levels of circulating leptin, which binds to the leptin receptor (LEPR b ) in CB and activates transient receptor potential channel subfamily M member 7 (TRPM7). 38572182: Pheochromocytoma and paraganglioma (PPGL) are chromaffin cell tumors that produce, store, and secrete catecholamines, leading to HT and other adrenergic manifestations. Even though primary HT, obesity, and preeclampsia are the main causes of HT in this period, other less familiar conditions must be considered during the investigation. 6352118: In addition, factors such as familial aggregation, genetic aspects, and the role of obesity in the etiology of hypertension have been considered. 7083522: The results indicate that alcohol ranks close to obesity as a potentially preventable cause of hypertension in the community. 7291956: A slight association between DISH and spondylosis, and hypertension probably due to obesity was observed. 7472117: Marked obesity is now a characteristic of many Polynesian and Micronesian populations, and must rank as a major causative factor for the diabetes and hypertension explosion. 7550525: OBJECTIVE: To investigate the role of alterations in renal haemodynamics and function and in plasma renin activity on obesity-induced hypertension. These data are consistent with the indication that change in renal haemodynamics take place at an early stage in the obesity-induced hypertension. 8031546: This study was designed to evaluate the role of fasting serum insulin and plasma renin activity in obesity-induced hypertension. 8125566: Activation of the sympathetic nervous system may play a role in obesity-induced hypertension, and there is evidence for a role of altered intrarenal physical forces caused by histological changes within the renal medulla. 8136092: Effects of captopril on sympathetic activity, lipid and carbohydrate metabolism in a model of obesity-induced hypertension in dogs. These data suggest that the beneficial effects of captopril therapy in this obesity-induced hypertension model could be based on blood pressure control, together with reduction of serum glucose, cholesterol, and sympathetic activity levels. 8282380: The purpose of this study was to determine whether obesity-induced hypertension is associated with abnormalities in the pressure-natriuresis relation. Recent studies have suggested that the kidneys may play an important role in the development of obesity-induced hypertension. Abnormal pressure natriuresis in the dog model of obesity-induced hypertension. 8349321: Obesity-induced hypertension. This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. 8500496: This would lead to the consideration of hypertension as a primary risk factor for such pathologies and not only as secondary to obesity. 8613270: We conclude that hypothalamic lesioning induces overeating and obesity and selectively in the male causes hypertension and glomerular damage as well as declines in renal function. 8743540: To investigate the role of sodium in obesity induced hypertension, Wistar fatty rats (WFR) were employed. 9140797: ACE, angiotensinogen and obesity: a potential pathway leading to hypertension. 9160781: Obesity-induced hypertension, like all forms of experimental and human hypertension studied thus far, is associated with renal dysfunction characterized by the resetting of pressure natriuresis. 9301429: Early protein restriction and obesity independently induce hypertension in 1-year-old rats. 9404404: [Left ventricular repercussion of obesity-induced arterial hypertension in the dog]. 9493563: Evidence from chronic insulin infusion studies in rats suggests hyperinsulinaemia can increase BP under some conditions; however, conflicting evidence in humans and dogs leaves in question whether hyperinsulinaemia is a factor in hypertension induced by obesity. This derangement has also been proposed as a mechanism through which insulin resistance can cause hypertension. 9534095: OBESITY AND RISK OF MORBIDITY: Obesity is becoming an increasingly important factor in the pathogenesis of hypertension, dyslipidemia and diabetes, which together with hyperinsulinemia comprise the deadly quartet of the insulin resistance syndrome. 9594558: UNLABELLED: Obesity increases the risk of developing hypertension by two-to fourfold, with more that one third of all cases of hypertension attributable to obesity. 9783499: CONCLUSIONS: Our results suggest that in the elderly the importance of obesity in the pathogenesis of hypertension depends partially on gender and it may be essential in women but not in men. 9931161: State-of-the-art-lecture: Obesity-induced hypertension: new concepts from the emerging biology of obesity. 25976367: Several preclinical and epidemiological studies have linked metabolic risk factors such as hypertension, obesity, dyslipidemia, and diabetes to the pathogenesis of AD. 28582856: Diabetes mellitus and AD have received particular attention due to their prominence in Western societies as a result of the ongoing obesity epidemic and the aging populations. 29257910: Evidence suggests that neurological diseases such as Parkinson's disease and Alzheimer's disease could be initiated by various metabolic changes, related to CNS damage, caused by obesity. 30257330: Raspberry ketone preserved cholinergic activity and antioxidant defense in obesity induced Alzheimer disease in rats. 32313838: The objectives of EMIF included providing a unified platform to support a wide range of studies within two verification programmes-Alzheimer's disease (EMIF-AD), and metabolic consequences of obesity (EMIF-MET). 32555166: Although sodium butyrate (NaB) has emerged as the potential therapeutic substance in AD, there is a lack of detailed results into what signaling pathways affect amyloidogenesis in AD induced by obesity. 33728019: In this review, we have shown that obesity may induce T2D-mediated AD and assessed the recent therapeutic advances, especially the use of anthocyanin, against T2D-mediated AD pathology. 36362376: The biological plausibility of the link between high adiposity, insulin resistance, and dementia is central for understanding AD etiology, and to form bases for prevention efforts to decrease the disease burden. 37231172: Therapeutic potential of flavonoids in the management of obesity-induced Alzheimer's disease: an overview of preclinical and clinical studies. Thus, flavonoid-rich nutraceuticals can be a potential cost-effective therapeutic option for treating obesity-induced AD, but further well-designed, randomized, and placebo-controlled clinical studies are needed to assess their optimal dosages, efficacy, and long-term safety of flavonoids in humans. Obesity has also been linked to neurological diseases such as cognitive decline, dementia, and Alzheimer's disease (AD), caused by oxidative stress, pro-inflammatory cytokines, and the production of reactive oxygen free radicals (ROS). 37686334: APOE3 carriers may be more susceptible to obesity, while the risk of AD caused by APOE2 and APOE4 may not be induced by obesity. Thus, this study innovatively utilized bioinformatics and Mendelian randomization (MR) to explore the key targets of obesity-induced AD, and investigate the causal associations between different types of obesity and key targets. Bioinformatics analysis revealed Apolipoprotein E (APOE) as the key target of obesity-induced AD. 10929786: A 47-year-old male with a history of hypertension for 7 years developed blurred vision secondary to thrombotic occlusion of the central retinal artery. 11730594: Occlusion of the portal vein in patients with normal liver is a frequent cause of hypertension in children. 11923579: Atherosclerotic occlusion of the native iliac arteries and/or transplant renal artery is a major cause of post-transplant hypertension. 13277090: Occlusion of a renal artery as a cause of hypertension. 13451899: Diagnosis of hypertension due to occlusions of the renal artery. 13582848: Human hypertension due to thrombotic occlusion of both renal arteries: report of a case cured by surgical removal of the thrombus. 13946486: [Arterial hypertension caused by obstruction of the renal artery]. 13960556: [The dye dilution curve in the anesthetized dog with reflex arterial hypertension induced by occlusion of the common carotid arteries]. 14187758: [SURGICAL TREATMENT OF HYPERTENSION CAUSED BY STENOSIS OR OBSTRUCTION OF THE RENAL ARTERY]. 14724433: METHODS: Donor hypertension was induced by partial occlusion of the right renal artery with a silver clip. 14822314: [Significance of arterial hypertension induced by occlusion of a branch of the pulmonary artery in the dog]. 15138112: BACKGROUND: Budd-Chiari syndrome (BCS) is a type of disease characterized by portal hypertension and/or hypertension of the inferior vena cava (IVC) due to the obstruction of the hepatic veins (HV) and/or intrahepatic IVC outlet. 15231948: Meconium obstruction of prematurity was more common in infants with a maternal history of pregnancy-induced or chronic hypertension, suggesting the possibility of decreased intestinal perfusion prenatally. 15399021: Hypertension due to partial renovascular occlusion; report of a case. 15579328: The most common side effect is hypokalemic hypertension, which is secondary to a block of 11beta-hydroxysteroid dehydrogenase type 2 at the level of the kidney, leading to an enhanced mineralocorticoid effect of cortisol. 16046855: Hypoxemia, acidemia, hypertension and bradycardia produced by cord occlusion was similar in the melatonin- and vehicle-treated groups. 1632246: This investigation strengthens earlier studies that hypertension is not an aetiologica factor for nasal polyposis but can develop secondary to nasal obstruction. 16513152: Its most common side effect is hypokalemic hypertension, which is secondary to a block of 11beta-hydroxysteroid dehydrogenase type 2 at the level of the kidney, leading to an enhanced mineralocorticoid effect of cortisol. 17571565: It is know that not only decreased blood flow to the kidney but also obstruction of renal outflow may, in some instances, be a cause of hypertension. 17692712: Additionally, with persistent obstruction, it has an impact on the cardiovascular system, leading to hypertension and cardiac failure as one of its causative or comorbid factors. 18069660: Ductal concretions in chronic pancreatitis (CP) are one of the causes of ductal obstruction, resulting in pancreatic ductal hypertension (PDH) and duct ectasia. 1825451: In this study, intracellular Ca2+ concentration ([Ca2+]i) dynamics were examined in paced left ventricular (LV) myocytes isolated from rats with hypertension (HYP) induced by partial occlusion of the left renal artery and from normotensive rats (Sham). 18610084: HYPERTENSION DUE TO SYPHILITIC OCCLUSION OF THE MAIN RENAL ARTERIES. 1867985: We report a case of severe hypertension in the newborn period due to obstruction of the right renal artery. 19956076: In 1934, Goldblatt et al. demonstrated that partial occlusion of the renal arteries produces hypertension in dogs, and Houssay in 1936 predicted the presence of a humoral mechanism and, with Fasciolo, demonstrated that the ischemic kidneys released a pressor substance that increased the recipient's blood pressure. 20551389: Left atrial hypertension as a result of occlusion of a patent foreman ovale. 21813395: BACKGROUND: Budd-Chiari syndrome (B-CS) refers to post-hepatic portal hypertension and/or inferior vena cava hypertension caused by obstruction of blood flow at the portal cardinal hepatic vein. 2260476: A satellite tumor which was attached to the wall of the abdominal aorta induced marked hypertension due to obstruction of the renal arteries. 22851527: BACKGROUND: Stenting of the systemic ventricular outflow tract and creation or enlargement of a ventricular septal defect using stents are potential therapeutic options in rare patients with congenital heart disease who develop significant ventricular hypertension due to outflow obstruction. 24014673: Experiments were performed before and 30.9 +/- 4.2 days after induction of hypertension, which was induced via partial, unilateral renal artery occlusion. 2447295: We report the development of hypertension in a 38-year-old man after chemotherapy that was shown to be owing to nonatherosclerotic partial occlusion of the major branches of the left renal artery. 24704054: The patient is a 75-year-old male who presented with 2 years of hypertension secondary to right renal artery occlusion incidentally found on cardiac catheterization. 27522733: Abdominal pain is the most common symptom occurring due to obstruction at the SO leading to ductal hypertension, ischemia from spastic contraction and hypersensitivity of papilla. 28218546: We present the case of a young female patient with abdominal aortic coarctation, history of acute renal failure, and critical hypertension due to pseudo-occlusion of both renal arteries. 28877534: CONCLUSIONS: Liberal use of OA, as a damage control adjunct avoided the development of intra-abdominal hypertension, reduced sepsis-related complication, and improved the clinical outcomes in peritonitis secondary to acute SMA occlusion. 29174227: Systemic hypertension, proteinuria and kidney injury - such as enlargement and glomerular fibrin deposit, capillary occlusion due to edema, and hypertrophy of endocapillary cells - are some of these changes. 2959587: Dopamine (DA) binding sites in the left and right ventricle of hypertensive rats were assessed after two weeks of induction of hypertension by left renal artery occlusion. 3107846: Ketamine anaesthesia in the pregnant ewe abolished the fetal hypertension and bradycardia produced by partial cord occlusion. 32299454: The rationale for these procedures is based on the assumption that obstruction of the pancreatic duct leads to ductal hypertension and pain. 33051862: Emboli in the pulmonary arteries lead to fibrosis, obstruction and remodeling of the pulmonary arteries which causes increased pulmonary arterial blood pressure and increased pulmonary vascular resistance. 33687105: The etiopathogenesis of pain in CP is multifactorial and includes ductal hypertension due to obstruction of pancreatic duct (PD), neuropathic causes, and extra-pancreatic complications of CP like pseudocyst and distal biliary obstruction. 36660570: Extrahepatic portomesenteric obstruction resulting in splanchnic hypertension and refractory ascites. 4683384: Hypertension due to traumatic ureteral occlusion. 4748303: Diagnosis of hypertension due to occlusion of a supplemental renal artery; its localization, treatment by removal from the body, microsurgical repair and reimplantation: a case report. 5032516: A new male pseudo-hermaphroditism associated with hypertension due to a block of 17 -hydroxylation. 5373401: [Peculiarities of the course of hypertension due to occlusion of the renal artery]. 538223: Extra-hepatic obstruction of the portal vein is a well known cause of hypertension in childhood and 55 out of the 97 patients (57 per cent) seen with this condition presented before they were 15 years old. 6139979: The high incidence of cardiac damage was attributed to systemic arterial hypertension secondary to renovascular obstructions or coarctation of the aorta. 6155747: By the use of various experimental procedures with rats, the significance of intraluminal hypertension, caused by ductal obstruction, reflux of bile and duodenal reflux were considered with regard to their capacity for producing pancreatitis. 6337956: Occlusion of the partially constricted renal artery caused severe hypertension that was initially associated with a transient decrease in levels of NE in both plasma and CSF and a sustained rise in plasma and CSF concentrations of AIIir that persisted for as long as 2 weeks after the second operation. 6618932: Occlusion of the abdominal aorta in unanesthetized ducks produced immediate development of hypertension. 6709345: [Severe hypertension caused by obstruction of the renal artery]. 7268385: Fourteen months later she presented with severe hypertension and anuria, caused by occlusion of the left renal artery. 7571186: Occlusion of the abdominal aorta represents the end stage of an atherosclerotic process and often is associated with stenosis of renal artery inducing renal failure and hypertension. 8257918: The effect of changes in left ventricular (LV) shape and dimensions due to acute arterial hypertension induced by mechanical obstruction of the aorta for 10 min on LV mass values estimated by M-mode echocardiogram was studied in 14 anesthetized dogs. 8419391: Intraosseous hypertension was produced by obstruction of venous outflow by ligation of the popliteal vein draining the proximal aspect of the tibia and occlusion of the medullary space with bone cement (groups 1 and 2). 9493555: We conclude that the augmented inflow of catecholamines to the kidney through the ARVC changes the haemodynamics of the kidney and may contribute to development of arterial hypertension due to occlusion of the adrenal vein. 9530422: These findings were all consistent with a diagnosis of postsinusoidal hypertension secondary to obstruction of hepatic venous outflow (Budd-Chiari-like syndrome). 9746110: Arterial hypertension due to occlusion of the adrenal vein in the rat is strain-dependent. OBJECTIVE: To determine whether the development of arterial hypertension due to occlusion of the central adrenal vein in the rat is strain-dependent DESIGN AND METHODS: The experiments were performed on male rats weighing 300-400 g each, of the following strains: Wistar outbred, Wistar Glaxo, Lewis, Wistar-Kyoto (WKY) rats bred for high blood pressure (138 +/- 13.2 mmHg), WKY rats bred without the control of blood pressure (118 +/- 12.9 mmHg) and borderline hypertensive rats (BHR). 9865419: In addition, they suggest that these antithrombotic drugs may overcome cases of human poisoning, with low exposures of this boletus, showing a hypertension probably due to mechanical obstruction which resists normal therapy. 10681533: By using metabolically competent rat brain slices as a model, we found that selective inhibition of protein phosphatase 2A by okadaic acid induced an Alzheimer-like hyperphosphorylation and accumulation of tau. 10774752: Previous studies have shown that okadaic acid (OA) evokes tau phosphorylation and neurofibrillary changes in vivo, and in cultured neurons, that resemble Alzheimer's disease pathogenesis. 12242084: Comparison of melatonin versus vitamin C on oxidative stress and antioxidant enzyme activity in Alzheimer's disease induced by okadaic acid in neuroblastoma cells. 15000877: Melatonin ameliorated okadaic-acid induced Alzheimer-like lesions. 22459049: Here, we showed that Drp1 phosphorylation and mitochondrial fission were also increased in rat cortical neurons treated with okadaic acid (OA), which inhibits protein phosphatase-2A (PP2A) and induces AD-like tau phosphorylation and neuronal death. 22515493: Here, we examined the efficacy of memantine (MN) pretreatment on reducing OA-induced AD-like phenotypes in rats. 23944061: [Study on protective effect of acteoside on cellular model of Alzheimer's disease induced by okadaic acid]. 25317137: In this study, we pretreated rat brain tissue sections with ginsenoside Rg1, and established brain slice models of Alzheimer's disease induced by okadaic acid. 25393881: We have investigated the protective effects of ITH91/IQM157, a hybrid of melatonin and N,N-dibenzyl(N-methyl)amine, in an in vitro model of Alzheimer's disease (AD)-like pathology that combines amyloid beta (Abeta) and tau hyperphosphorylation induced by okadaic acid (OA), in the human neuroblastoma cell line SH-SY5Y. 26295819: OKA-induced AD in zebrafish can become a cost efficient model to study drug discovery for AD. Development of a Novel and Robust Pharmacological Model of Okadaic Acid-induced Alzheimer's Disease in Zebrafish. 29475037: Lanthionine ketimine-5-ethyl ester provides neuroprotection in a zebrafish model of okadaic acid-induced Alzheimer's disease. In this study, a recently established zebrafish OKA-induced AD model was utilized to further elucidate the neuroprotective and neurotrophic properties of LKE in the context of an AD-like condition. 30127109: This demonstrated the ability of the okadaic acid-induced AD zebrafish model to be implemented in the drug discovery process for therapeutics against AD. 30392874: This further corroborates the use of GSKbeta inhibitors in the treatment against AD and bolsters the use of the OKA-induced AD-like zebrafish model for drug discovery. The GSK3beta inhibitor, TDZD-8, rescues cognition in a zebrafish model of okadaic acid-induced Alzheimer's disease. 30500552: SIGNIFICANCE: In this study, we found that the administration of the CB2 receptor agonist JWH-133 in this study reduced neurodegeneration, neuroinflammation, and spatial memory impairment in the OKA-induced Alzheimer's Disease model. 32397764: Here, we developed plasma exosomes (Exo) loaded with Que (Exo-Que) to improve the drug bioavailability, enhance the brain targeting of Que and potently ameliorate cognitive dysfunction in okadaic acid (OA)-induced AD mice. 33818056: A mouse model of okadaic-acid-induced AD-like pathology was used in vivo and in vitro . 33957218: In the present study, the effects of PF11 on AD, in particular the underlying mechanisms related with protein phosphatase 2A (PP2A), were investigated in a rat model induced by okadaic acid (OA), a selective inhibitor of PP2A. The results showed that PF11 treatment dose-dependently improved the learning and memory impairments in OA-induced AD rats. 35447926: A few studies have used OA to trigger AD in zebrafish, providing an opportunity to test in vivo the effectiveness of new drugs in treating or attenuating AD. 35575872: The pathological characteristics of Alzheimer's disease (AD) include formation of senile plaques resulting from amyloid-beta (Abeta) deposition and neurofibrillary tangles caused by tau hyperphosphorylation. The above-mentioned proteins were then evaluated in an okadaic acid (OKA)-induced AD cell model to verify the results. 36594931: This study investigated the effect of cucurbitacin E (CuE), one of the bioactive components of Ecballium elaterium , on TAU fibril formation in okadaic acid-induced AD in rats. 37100105: In the case of protein expression, the heatmap suggested an important role of some common proteins identified in both groups, which can be explored further to investigate their mechanism in OKA-induced AD pathology. To explore the driving mechanisms of AD development, we stretch out further to study time-dependant changes after Okadaic acid (OKA)-induced AD-like conditions in zebrafish. Both time course OKA-induced AD models have shown significant memory impairment, as evident from T-Maze. 10645524: OBJECTIVE: To present the importance of searching for the surgical causes of pharmacologically resistant hypertension in the neonatal population. 1230521: In patients operated for symptomatic hypertension (renovascular, adrenal, coarctation of the aorta) the assessment of the results of surgery should not be limited by the determination of the decrease or normalization of the arterial pressure alone, but should be supplemented by a general clinical evaluation of the state of the patients. 12738090: Hypertension was induced by surgery. 12768726: CONCLUSION: Mental tension in operation can induce hypertension and increase bleeding, suitable sedation is necessary. 12811396: [The impact of cardiac status and arterial hypertension on the results of surgical treatment of patients over 70 years with abdominal aortic aneurysms]. 1386326: Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. 15991502: Fear and anxiety may cause some patients to become uncooperative during the surgery and may also induce a sympathetic stress response that might cause hypertension, tachycardia with myocardial ischaemia, hyperventilation or an acute panic attack. 16860635: Paragangliomas are one of the surgical causes of hypertension. 1736266: Although an acquired coarctation of the aorta is an infrequent complication of invasive or surgical procedures, it should be identified since it represents a remediable cause of hypertension in children. 20169961: And, during surgery, the blood epinephrine concentration increased due to direct tumor manupulation by surgeon, leading to induced hypertension. 20965844: RESULTS: PDRAB infections occurred mainly in patients with severe complications, most of whom had complications by diabetes or hypertension or damaged mucosal integrity due to mechanical ventilation, surgery and catheterization. 21277182: Although vasoactive agents and sympathoexcitation have been implicated and operational in the pathogenesis of hypertension associated with OSA the exact mechanisms underlying hypertension have not been established. 2130767: In order to avoid hypoperfusion to distal organs and proximal hypertension during aortic cross-clamping, two different adjuncts were used and the effectiveness of those methods were compared according to the results of surgery. 2350475: In the patients studied, surgical or medical elimination of the mechanism responsible for the hypertension when the patients were below the age of 40 reduced diastolic blood pressure 1 to 2 years later to below 90 mm Hg in 24 of 25 patients. We have analyzed the effect of age on the response of the blood pressure to the removal of the cause of hypertension in groups of patients with primary aldosteronism, renovascular hypertension, Cushing's syndrome and hypothyroid hypertension. 2529052: Twelve weeks after surgery to induce hypertension, in vivo arteriolar and venular dimensions were measured in the cremaster muscle of rats with one-kidney, one-clip hypertension (1K1C), rats in which the clip was removed after 8 weeks (1KNT), and controls. 2635419: The first patient was a 56-year-old woman who suffered from disturbances in the calcium and potassium metabolism and high blood pressure due to a previous goiter operation during which the parathyroids had been removed. 26371949: The 2K1C operation caused significant hypertension and cardiac hypertrophy as demonstrated by respective biophysical or biochemical assays. 27379932: However, from data obtained during the last few years, we know that surgical causes of hypertension are unusual: less than 10% of the patients in a reference centre. Arterial hypertension is a very common disease, and one of the main causes of death in our countries. The first step of treatment must be the research for curable causes of hypertension. 29787305: None of the aforementioned changes in circadian rhythms were observed after the surgical induction of hypertension. 3038745: Conscious femoral arterial pressure (direct arterial puncture) and intraocular pressure (Schiotz tonometer) were measured weekly before and after the surgical induction of hypertension in 11 healthy male mongrel dogs and before and after unilateral nephrectomy in 15 normotensive control dogs. 32140200: Although surgical treatment was not performed because of the patients' nonconsenting, any other cause for the hypertension was not found by extensive work-up, supports the notion that it was either secondary to nutcracker phenomenon or idiopathic . 3237663: In the authors' opinion, raised activity of the sympathetic-adrenal and renin-angiotensin systems observed during decompensation of diffuse toxic goiter and progressing after surgery, led to the transformation of central hemodynamics of the hyperkinetic type into the hypokinetic one, causing the development of postthyrotoxic arterial hypertension. 3349640: Thus, in utero exposure of pups to a chronic HT state alters the response of the pups to the surgical induction of hypertension. After surgical induction of hypertension, HT male pups of HT dams had a significantly greater (p less than .05) BP by 14 days after surgery (194 +/- 8 mm Hg) than did HT male pups of normotensive (NT) dams (169 +/- 6 mm Hg). 3389547: Anesthesia for cerebral aneurysm surgery: use of induced hypertension in patients with symptomatic vasospasm. 3493123: [Hypertension and bleeding from the upper digestive tract secondary to an operation for patent ductus arteriosus]. 3497281: Because of the well-recognized increased incidence of hypertension in black patients, and its role as a major risk factor in coronary heart disease, the sequelae of hypertension were considered in relation to results of surgical therapy.The study population included 93 men (57 percent) and 70 women (43 percent); mean age was 59 years (fourth to ninth decade). 6693149: By 2 weeks following the surgery to induce hypertension, we found that 3A sensitivity to norepinephrine had increased and the 1As had chronically constricted. 7164729: In order to prove that the functional activity of the renal artery stenosis is the real cause of high blood pressure, we have introduced to our Department a method of renal vein catheterization by which renin activity id determined. Therefore, before venturing surgery on renal vessels, with the aim to cure renovascular hypertension, it is necessary to prove that the angiographically verified changes really cause high blood pressure. 7441266: Increasing age, hypertension, and a poor neurological state (both singly and in combination) were found to influence surgical results dramatically. 7684025: Hydrochlorothiazide was administered from 8 weeks, and LV mass and function were measured at 16 weeks after surgery to induce hypertension. 7834336: These initial experiments utilized a protocol for the induction of 1K1C hypertension which produced an initial rapid rise in blood pressure, evident by day 4 following surgery, with a corresponding inhibition of the febrile response. 8119500: Hypertension at rest and after exercise could persist despite good surgical results. 8168878: These pulmonary disturbances are strikingly correlated with operation-induced intramedullary hypertension. 8450326: Other medical and surgical interventions were used with similar frequency in both groups, except that antihypertensive agents were used less frequently in the nicardipine-treated patients (26% of the nicardipine-treated group vs. 43% of the placebo-treated group, p < 0.001), and more patients in the placebo-treated group had intentional hypervolemia, induced hypertension, and/or hemodilution administered therapeutically for symptomatic vasospasm (38% of the placebo-treated group vs. 25% of the nicardipine-treated group, p < 0.001). 8552312: One week after operation when the induced hypertension was at the initial stage, GFAP expression in the retina was reduced to half of the sham control. 8575557: In the early weeks of the experiment (weeks 2-4 post-surgery to induce hypertension), an enhanced natriuresis occurred in the 2K1C UNSAT as compared to the 2K1C CONTROL and SAT diet groups. 8586943: Evolution of arterial blood pressure after surgery leads to think that aneurysms of the renal artery cannot be held responsible for arterial hypertension: whenever a stenosis of the renal artery is associated, hypertension is of renovascular origin and is constantly cured or improved after surgery; in other patients, arterial hypertension remains unchanged after repair of the aneurysm, suggesting that hypertension is essential and simply coexists with the aneurysm without relationships of cause and effect between them. 9045280: [Hypertension, coronary disease and impact of arterial hypertension on results of coronary surgery]. 9613273: Autonomic dysreflexia is suggested by headache, sweating, bradycardia and severe hypertension and may be precipitated by surgery, especially bladder distension. 9673828: Gene expression of nNOS is altered in the hypothalamus and caudal VLM of renal hypertensive rats at 3 and 6 weeks after surgical induction of hypertension. 985072: An angiotensin II antagonist, saralasin acetate, used in six patients before operation in an attempt to identify those whose hypertension depended on angiotensin II activity, produced a depressor response correlating well with the surgical result. 10406832: Brain renin-angiotensin system and ouabain-induced sympathetic hyperactivity and hypertension in Wistar rats. In the present study, we tested whether the hypertension caused by exogenous ouabain also depends on activation of brain renin-angiotensin system. 10973588: In normotensive Wistar rats, systemic administration of exogenous ouabain for 10 days or more induces hypertension, presumably through central mechanisms. Neuronal Fos-like immunoreactivity in ouabain-induced hypertension. 11016824: Chronic hypertension induced by ouabain but not digoxin in the rat: antihypertensive effect of digoxin and digitoxin. 11179079: We concluded that peripheral administration of losartan as well as embusartan can cause sufficient central effects to prevent the sympathetic hyperactivity and hypertension induced by chronic peripheral ouabain and central sodium. Sympathetic hyperactivity and hypertension caused by chronic treatment with ouabain or sodium-rich artificial cerebrospinal fluid (aCSF) can be prevented by central administration of an angiotensin type 1 (AT(1)) receptor blocker. 11230321: Thus, RHA and the unsaturated lactone ring are crucial to the high potency of OUA as an inhibitor of the sodium pump but appear to be unrelated to its ability to induce hypertension. 11307322: The most likely candidate of the endogenous digitalis is ouabain, which causes hypertension with chronic administration. 11448869: We examined short-term potentiation [posttetanic potentiation (PTP)] and long-term potentiation (LTP) in the isolated superior cervical ganglia (SCG) from Sprague-Dawley (SD) rats given vehicle, digoxin, or ouabain by subcutaneous implants as well as in animals with ouabain-induced hypertension (OHR), and inbred Baltimore ouabain-resistant (BOR) and Baltimore ouabain-sensitive (BOS) strains of rats. 11834625: These results suggest that chronic administration of ouabain induces hypertension and regional vascular alterations, the latter possibly as a consequence of the hypertension. 11882604: In addition, recent studies suggest that the induction of sustained hypertension by ouabain analogs in rats may be independent of Na pump inhibition. 12384489: The involvement of nitric oxide (NO), prostaglandins, and calcium-dependent potassium channel (K(Ca)) activators on the negative modulation of phenylephrine-induced contractions was evaluated on the isolated aorta and caudal (CAU) artery obtained from rats treated with ouabain for 5 wk to induce hypertension. These results suggest that ouabain-induced hypertension is accompanied by increased NO release derived from endothelial NOS and neuronal NOS and increased release of an endothelial hyperpolarizing factor that presumably opens K(Ca), all of which contribute to the increased negative modulation of the phenylephrine contraction. Ouabain-induced hypertension is accompanied by increases in endothelial vasodilator factors. 12658021: We also investigated the involvement of central endothelin receptors in increased sympathetic activity and hypertension induced by chronic OUA. 12763920: Ouabain (OU) itself induces hypertension in rats and both OU and mutated adducin activate the renal Na/K-ATPase function both in vivo and in cultured renal cells (NRK). 1337913: CONTENT: Recent evidence on a number of ouabain-related issues includes (1) evidence for the existence of inhibitors of sodium pumps in mammalian plasma, (2) the identification of one of these factors as ouabain, (3) measurements of plasma levels of ouabain in man, (4) evidence that ouabain causes chronic hypertension in rats and is associated with human hypertension, and (5) data on some probable mechanisms that may mediate the pressor effect. 1473573: The following article is concerned with new reports that ouabain, a plant derivative, occurs in human beings, in whom it appears to have a hormonal function; ouabain may even play a key role in the pathogenesis of hypertension. Ouabain--a link in the genesis of high blood pressure? 14991991: CONCLUSION: The ouabain induced contraction is mainly dependent on the extracellular Ca2+ concentration, independent on the presence of endothelia of aorta, suggesting that Ca2+ antagonist may treat the hypertension induced by ouabain. 15171364: [Involvement of ouabain (digitalis-like factor) in the pathogenesis of hypertension and hypertensive target-organ damage]. 15276875: Brain Na+,K+-ATPase isozyme activity and protein expression in ouabain-induced hypertension. In normotensive rats, chronic infusion of exogenous ouabain causes hypertension involving central mechanisms. To determine whether ouabain-induced hypertension is associated with specific changes in brain Na+,K+-ATPase activity and expression, we assessed brain Na+,K+-ATPase isozyme activity and protein expression in rats treated with ouabain (50 microg/day s.c. or 10 microg/day i.c.v. for 14 days). 15302685: Ouabain-induced hypertension alters the participation of endothelial factors in alpha-adrenergic responses differently in rat resistance and conductance mesenteric arteries. 15458945: Although ouabain is known to induce hypertension, the mechanism of how this cardiac glycoside affects blood pressure is uncertain. This could play a role in the development and maintenance of ouabain-induced hypertension. 15477225: In conclusion, our results suggest that endothelin and angiotensin systems play an important role in the development of ouabain-induced hypertension. 16166162: All four agents are known to lower blood pressure in salt-dependent and ouabain-induced hypertension. 16178440: Therefore, increase of proximal reabsorption of sodium may be involved in the pathogenesis of ouabain-induced hypertension. 16250857: Ouabain itself induces hypertension and up-regulates renal Na-K pump when chronically infused at low doses into rats (OS). 16297763: Cardiotonic steroids, such as endogenous ouabain, which may contribute to the pathogenesis of salt-sensitive hypertension, seem to be necessary for NCX1-mediated hypertension. 16467498: Pharmacological agents or mutations in the alpha2 Na+ pump that interfere with the action of ouabain on the pump, and reduced NCX1 expression or agents that block NCX all impede the development of salt-dependent or ouabain-induced hypertension. 16467499: Whereas chronic administration of ouabain or ACTH caused hypertension in wild-type mice, it had no effect on blood pressure in mice with a ouabain-resistant alpha2-isoform of Na+-K+-ATPase. 16473962: We have previously described that chronic administration of ouabain induces hypertension and functional alterations in mesenteric resistance arteries. 16565308: Central and peripheral renin-angiotensin systems in ouabain-induced hypertension. 16716361: Chronic ouabain treatment produces hypertension acting on the central nervous system and at vascular levels. Ouabain-induced hypertension enhances left ventricular contractility in rats. Ouabain induces hypertension but not myocardial hypertrophy. 16857351: Current evidence demonstrates that augmented production of endogenous cardiotonic steroids (CTS) such as ouabain and marinobufagenin is involved in the pathogenesis of hypertension and other cardiovascular diseases associated with volume expansion. 16982439: [Contribution of endothelin and its receptors to ouabain-induced hypertension in rats]. OBJECTIVE: To investigate the effect of endothelin and its receptors on ouabain-induced hypertension in rats. 18346177: Normalization of HR after 30 days treatment suggests that during the period from Day 16 to Day 30 ouabain-induced hypertension is dependent, at least in part, on increased sympathetic activity. The aim of the present study was to investigate the time-course of the induction of hypertension to define when changes occur in Wistar rats treated with 25 mg/kg per day, s.c., ouabain for 3, 7, 15 or 30 days. 18806618: OBJECTIVE: Chronic administration of ouabain induces hypertension and increases the contribution of nitric oxide to vasoconstrictor responses in peripheral arteries. 18945826: Chronic exposure to ouabain, in vivo, leads to hypertension and DVR endothelial dysfunction, manifested as reduced [Ca(2+)](CYT) responses to both ouabain- and endothelium-dependent vasodilators. 18976649: Although this balance avoids changes in the phenylephrine concentration-response curves, these vascular changes might contribute to maintain the ouabain-induced hypertension. 19043981: These results indicate that hypertension induced by chronic ouabain treatment is accompanied by increased endothelial nitric oxide participation and impaired endothelium-dependent hyperpolarizing factor contribution in acetylcholine-induced relaxation. 19617413: This ouabain-induced hypertension (OH) has been attributed, in part, to the narrowing of third-order resistance arteries (approximately 320 microm internal diameter) as a result of collagen deposition in the artery media. 19626329: We propose that the ouabain-induced reduction of the renal dopamine D(1) receptor function serves as a mechanism responsible for sodium retention, and this contributes to the hypertension induced by chronic ouabain treatment. 20132239: We hypothesize that the ouabain-induced decrease in renal D(1) receptor function is responsible for the increase in renal sodium reabsorption, which eventually leads to ouabain-induced hypertension. 20211726: We discuss cardenolide structure-function relationships in an effort to understand why prolonged administration of ouabain, but not digoxin, induces hypertension, and why digoxin is actually anti-hypertensive. 21273786: CONCLUSION: Although ouabain treatment induced hypertension in all groups, a larger noradrenaline induced contraction was observed over 20 weeks of treatment. 21956536: Additionally, the hypertension induced by ouabain has been associated with central mechanisms that increase sympathetic tone, subsequent to the activation of the cerebral renin-angiotensin system. 22895622: In conclusion, GSPE antagonized ouabain-induced hypertension and vascular remodeling and is recommended as a potential anti-hypertensive agent for patients with hypertensive vascular diseases. Recent studies indicate that chronic ouabain treatment leads to hypertension and hypertensive vascular remodeling. 22987017: In conclusion, GSPE increase eNOS expression and NO production in an AMPK/SIRT1 dependent manner through KLF2 induction, and attenuate ouabain induced hypertension. 23615157: Ouabain (Oua)-induced hypertension in rodents provides a model to study cardiovascular changes associated with human hypertension. 24890163: BACKGROUND: Ouabain is a mammalian adrenocortical hormone that is involved in the pathogenesis of hypertension by inhibiting Na-K ATPase activity. 25279791: These data show that long-term administration of exogenous ouabain does not necessarily cause hypertension in rodents. 25860025: Although Rho kinase expression did not change in aortas, increased basal Rho kinase activation may contribute to the development of ouabain-induced hypertension. 26198943: The truncated fragment of the sodium pump alpha2 subunit can antagonize ouabain-induced increase of [Ca(2+)]i in the VSMCs, which provides a clue for understanding the pathogenesis of and devising a therapeutic strategy for high ouabain-induced hypertension. CONCLUSIONS: Elevations in [Ca(2+)]i in the VSMCs can be the cytological basis of high ouabain-induced hypertension. 27350568: Prolonged ouabain infusion induces hypertension in rodents, and ouabain-resistant mutation of the alpha2 ouabain binding site (alpha2R/R mice) confers resistance to several forms of hypertension. 27906749: Sodium and potassium in the pathogenesis of hypertension: focus on the brain. RECENT FINDINGS: Animal studies point to a small increase in plasma and cerebrospinal fluid (CSF) [Na], a small decrease in CSF [K], and increased levels of circulating angiotensin II, aldosterone, and endogenous ouabain as the central signals evoking hypertension. 30402867: CONCLUSIONS: We detected that GSPE could improve cerebral vascular damage through inhibiting Profilin-1 in an ouabain-induced hypertension model. Profilin-1, an Actin-binding protein, is closely involved in the remodeling of large vessels in ouabain-induced hypertension. MATERIALS AND METHODS: The blood pressure of male Sprague-Dawley (SD) rats was measured during a period of ouabain-induced hypertension. Role of GSPE in improving early cerebral vascular damage by inhibition of Profilin-1 expression in a ouabain-induced hypertension model. 4684093: Ouabain-induced hypertension in a patient with decompensated hypertensive heart disease. 7930555: Ouabain-induced hypertension in the rat: relationships among plasma and tissue ouabain and blood pressure. CONCLUSIONS: Prolonged infusion of ouabain in the normal rat raises the circulating, kidney, hypothalamic and anterior pituitary levels and induces a reversible hypertension with normal plasma renin activity. 8238491: Chronic parenteral administration of ouabain to normal rats raises plasma ouabain concentrations to low nanomolar levels and induces hypertension [C. 8728291: Prolonged administration of ouabain into the brain ventricles augments sympathetic nervous system activity and induces sustained hypertension. In rats with normal kidney function, ouabain-induced hypertension is primarily sodium-insensitive although maneuvers that hinder renal sodium excretion augment the pressor effect of this steroid. Prolonged elevation of circulating ouabain in the rat induces sustained hypertension. In these patients, and in rats with ouabain-induced hypertension, increased local generation of, or increased target organ sensitivity to, angiotensin II, or both, may contribute critically to heightened vasoconstriction and a sustained increase in blood pressure. CONTENT: This review concerns the structure of endogenous ouabain, circulating levels of this steroid in various disorders of fluid and electrolyte balance, recent evidence for the association of endogenous ouabain with human hypertension, the influence of sodium and volume factors on ouabain-induced hypertension, and possible mechanisms for the hypertensinogenic activity of ouabain. 8846513: We tested the ability of ouabain to cause chronic hypertension by continuously infusing ouabain for 28 days (miniosmotic pump implantation; i.p.). 9682908: Sustained elevation of plasma ouabain in rats induces chronic hypertension with characteristics similar to those in patients and whose severity is determined by inherited factors and renal function. 9772400: Moreover, digoxin can reverse the hypertension induced by ouabain. Aldosterone might play some role in the mechanism of ouabain-induced hypertension. 9887018: To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. 10726145: The latter are, in particular, arterial hypertension and metabolic disturbances, which either arise due to overweight, or which are fostered by it. 1387988: The number of persons who referred to overweight as one of AH causes rose 6-fold (from 2.6 to 18.1%). 18637532: Researchers should consider overweight a causative risk factor for development of hypertension in early-onset groups. 18829779: Multinomial logistic regression was used to evaluate the odds for prehypertension and hypertension resulting from overweight and obesity. 22017362: The mechanisms by which overweight and physical inactivity lead to hypertension are complex. 24805956: OBJECTIVE: The adipocytokines, leptin, adiponectin, and interleukin-6, which stimulate liver C-reactive protein (CRP) production, are regarded as potential candidate intermediates between adipose tissue and overweight-induced hypertension. 25410619: These variations could thus cause overweight and hypothetically lead to hypertension. 25723554: These variations could thus cause overweight and hypothetically lead to hypertension. 26083724: HBP in about 22.9% (95% CI 21.5, 24.2%) of boys and 14.7% (95% CI 13.5, 15.8%) of girls could be attributable to overweight and obesity. 27521927: The excess risk of hypertension attributable to overweight was 32% (24%, 40%; 8 studies, I2 = 85.5%) and that attributable to obesity was 47% (40%, 54%; 8 studies, I2 = 88.2%). 6346031: These aspects are the strength of the epidemiological association; supporting evidence from trials of weight reduction; and possible mechanisms through which overweight may cause hypertension. 8109572: The percentages of hypertension attributable to overweight (body mass index > or = 25) among the Yi farmers, Yi migrants, and Han, respectively, were 4.1%, 34.1%, and 24.0% for men and 0%, 26.2%, and 28.9% for women. 8793366: We found that 6-29% of hypertension in each population was attributable to overweight and 0-16% to obesity. 9843357: Childhood overweight is the leading cause of pediatric hypertension, and overweight children are at high risk for developing long-term chronic conditions, including adult-onset diabetes mellitus, coronary heart disease, orthopedic disorders, and respiratory disease. 10100423: [Is the lesion produced by oxidation a central part in the pathogenesis of Alzheimer's disease?]. 10699746: Oxidation has been proposed to be an important factor in the pathogenesis of Alzheimer's disease (AD) and amyloid beta is considered to induce oxidation. 12832513: This may implicate the potential contribution of RNA oxidation in the pathogenesis of AD. 12926540: This mini review gives a brief overview over the oxidation mechanism of methionine (Met), relevant for processes which may lead to the oxidation of amyloid beta-peptide (betaAP), involved in the pathogenesis of Alzheimer's disease. 15203119: In particular, it is well known that oxidation of methionine 35, is strongly related to the pathogenesis of Alzheimer's disease, since it represents the residue in the beta-amyloid peptide most susceptible to oxidation \in vivo\. 15207347: In particular, it is well known that oxidation of methionine 35, is strongly related to the pathogenesis of AD, since it represents the residue in AbetaP most susceptible to oxidation in vivo. 15635660: Metal-catalysed oxidation (MCO) may play a causative role in the pathogenesis of Alzheimer's disease (AD). 20836858: We have recently shown that the cholesterol oxidation metabolite 27-hydroxycholesterol (27-OHC) causes AD-like pathology in human neuroblastoma SH-SY5Y cells and in organotypic hippocampal slices. 21272192: All three cholesterol oxidation products implicated thus far in the pathogenesis of Alzheimer's disease, 7beta-hydroxycholesterol, 24-hydroxycholesterol, and 27-hydroxycholesterol, markedly enhance the binding of amyloid-beta (Abeta) to human differentiated neuronal cell lines (SK-N-BE and NT-2) by up-regulating net expression and synthesis of CD36 and beta1-integrin receptors. 22460333: These results provide new insights and are supportive of our hypothesis that DeMPs are a newly identified trigger of neurodegenerative diseases such as Alzheimer's disease, which are known to be associated with early stage inflammation and oxidation. 22758637: Over the last decade, growing evidence supports the idea that cholesterol oxidation products, known as oxysterols, may be the missing link between altered brain cholesterol metabolism and AD pathogenesis, as their involvement in neurotoxicity, mainly by interacting with Abeta peptides, is reported. 23261179: Aluminum may mediate Alzheimer's disease through liver toxicity, with aberrant hepatic synthesis of ceruloplasmin and ATPase7B, the resultant excess free copper causing brain oxidation, beta-amyloid aggregation and Alzheimer disease. 25261765: In this review, we will provide results from our laboratory and data from literature that converge to strongly suggest the involvement of cholesterol and cholesterol oxidation products in the pathogenesis of AD and PD. 25630716: We aimed to investigate the toxicity and mechanism of AD-like pathology caused by cholesterol oxidation metabolite 27-hydroxycholesterol (27-OHC) in astrocyte cells. 29883958: It is now established that cholesterol oxidation products (oxysterols) are involved in several events underlying Alzheimer's disease (AD) pathogenesis. 9737846: Oxidation of Met35 may have implications in the aetiology of Alzheimer's disease. 10491314: These data support the suggestion that ROS and RNS, including superoxide radicals and nitric oxide, may play an important role in development of stress-induced hypertension in ISIAH rats. Manifestation of oxidative stress in the pathogenesis of arterial hypertension in ISIAH rats. 10904027: The effects of BSO were mitigated by concomitant antioxidant therapy despite GSH depletion, which supports the notion that oxidative stress was involved in the pathogenesis of hypertension in this model. Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. 12352326: In patients with cyclosporine-induced hypertension, upregulation of the nitric oxide system and oxidative stress were shown, which could induce hypertension, remodeling, and chronic rejection by increasing nitric oxide catabolism. Oxidative stress in kidney transplant patients with calcineurin inhibitor-induced hypertension: effect of ramipril. 12574105: These findings point to interrelation between oxidative stress and inflammatory reactivity in the pathogenesis of hypertension. 12745201: BACKGROUND: Hypertension induced by oxidative stress has been demonstrated in normal rats. 14713339: As oxidative stress plays a crucial role in the development and pathogenesis of hypertension, we analyzed the redox (reduction/oxidation) status in tissues from Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). Redox imbalance in essential organs may play a crucial role in the development and pathogenesis of hypertension. 14717343: The involvement of oxidative stress in polymorphonuclear leukocytes (PMN) in the pathogenesis of hypertension remains to be elucidated. 15090865: PURPOSE OF REVIEW: Oxidative stress is frequently associated with, and is partly involved in, the pathogenesis of chronic renal failure, hypertension and their complications. RECENT FINDINGS: Recent studies have provided irrefutable evidence that oxidative stress can cause hypertension and hypertension can cause oxidative stress. 15490413: Oxidative stress in CRF plays an important role in the pathogenesis of the associated hypertension (oxidation of NO and arachidonic acid and vascular remodeling), cardiovascular disease (oxidation of lipoproteins, atherogenesis), neurologic disorders (nitration of brain proteins, oxidation of myelin), anemia (reduction of erythrocyte lifespan), inflammation (nuclear factor kappa B activation), fibrosis, apoptosis, and accelerated aging. 15569323: BACKGROUND: Chronic lead exposure causes hypertension and cardiovascular disease, which are associated with, and, in part, due to oxidative stress. 15773226: Oxidative stress has been proposed as important in the pathogenesis of hypertension. In Dahl-S rats, the high salt diet induced hypertension (139 +/- 3 mmHg in LS versus 186 +/- 2 mmHg in HS, p < .05) and significantly increased the U-8-ISO (24.9 +/- 3.6 ng/24 hr in LS versus 63.2 +/- 14.6 ng/24 hr in HS, p < .05). 15811260: Oxidative stress also participates in the pathogenesis of endothelial dysfunction and hypertension, two important factors in many patients with atherosclerosis. 15814300: Aorta coarctation results in hypertension (HTN) in the arterial tree proximal to stenosis and, as such, provides an ideal model to discern the effects of different levels of blood pressure on the vascular tissue in the same animal. Compelling evidence has emerged supporting the role of oxidative stress as a cause of HTN. 15951402: Compelling evidence has emerged pointing to the interaction of oxidative stress and renal interstitial inflammation and their mutual contribution to the pathogenesis of hypertension in experimental animals. 16183628: In almost all models of hypertension, there is oxidative stress that, if corrected, lowers BP, whereas creation of oxidative stress in normal animals can cause hypertension. 16404134: We conclude that oxidative stress within the renal medulla can induce hypertension and also make the kidney functionally more vulnerable to the effects of Ang II. 17003837: For instance, oxidative stress in the kidney and vascular tissue is the primary mediator in the pathogenesis of angiotensin-induced, and perhaps lead-induced, hypertension. Mechanisms of disease: oxidative stress and inflammation in the pathogenesis of hypertension. Animal studies have shown that oxidative stress and renal tubulointerstitial inflammation are associated with, and have major roles in, the pathogenesis of hypertension. 17023572: Since earlier studies have provided compelling evidence for the role of oxidative stress and tubulointerstitial inflammation in the pathogenesis of hypertension, we tested the hypothesis that partial SOD2 deficiency may result in hypertension. High-salt diet induced hypertension in 6-mo-old SOD2-deficient mice but not in wild-type mice. 17030113: OBJECTIVE: Red wines and grape juices contain polyphenolics with antioxidant and antiplatelet properties that may be protective against oxidative stress leading to hypertension, insulin resistance, and type 2 diabetes (T2D). 17295645: Hypertensive cerebrovascular disease is the result of hypertension-induced oxidative stress. 18227482: Recently oxidative stress has been proposed as the cause of hypertension. 18385744: These results suggest that oxidative stress could be important in the pathogenesis of hypertension. 19073140: While oxidative stress is an important factor for the development of hypertension, ABHD1 could play a protective role in the pathogenesis of hypertension. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 20668101: A positive association between renin-angiotensin system, especially AT1 receptor, and oxidative stress in the pathogenesis of hypertension and cardiovascular/renal diseases has been suggested. 20942928: The results from this study revealed that the oxidative stress mediated regulation cascade is the common mechanistic link among the pathogenesis of T2D, HT and other inflammatory diseases such as OBS. 20981034: Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. 21228777: An increasing body of evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), has a key role in the pathogenesis of hypertension. 21235900: Because oxidative stress in general participates in the pathogenesis of hypertension and atherosclerosis, the enzymes that produce reactive oxygen species may be important determinants of the course of vascular disease. 21241794: Reactive oxygen species (ROS)/reactive nitrogen species (RNS) and ROS/RNS-mediated oxidative stress have well-established roles in many physiological and pathological processes and are associated with the pathogenesis of many diseases, such as hypertension, ischemia/reperfusion injury, diabetes mellitus, atherosclerosis, stroke, cancer, and neurodegenerative disorders. 21506929: Oxidative stress has been involved in the aetiology of hypertension, insulin resistance, the metabolic syndrome, cardiovascular disease and other chronic conditions. 21831233: This results in chronic vascular inflammation, oxidative stress, activation of the renin-angiotensin-aldosterone system and sympathetic overdrive, eventually leading to hypertension. 21833043: BACKGROUND: Inflammation and oxidative stress have been identified as integral parts in the pathogenesis of hypertension. 22223042: In 2000, it was first reported that oxidative stress and arterial hypertension were produced in normal Sprague-Dawley rats by oral administration of buthionine sulfoximine (BSO), which induces glutathione (GSH) depletion, indicating that oxidative stress may induce hypertension. The contribution of several potential pathogenic factors has been evaluated in the BSO rat model, the prototype of oxidative stress-induced hypertension, including vascular reactivity, endothelium-derived factors, renin-angiotensin system activity, TXA(2)-PGH(2) production, sodium sensitivity, renal dopamine-induced natriuresis, and sympathetic tone. 22507072: Sympathetic hyper-responsiveness in hypertension may result from oxidative stress. 22648117: These changes result in insulin resistance, chronic vascular inflammation, oxidative stress, and activation of the renin-angiotensin system (RAS), eventually leading to type 2 diabetes, obesity-related hypertension, and cardiovascular disease (CVD). 22713144: The present review addresses the putative function of ROS in the pathogenesis of hypertension and focuses on the role of Noxs in ROS generation in vessels and the kidney. Although evidence from experimental and animal studies supports a role for oxidative stress in the pathogenesis of hypertension, there is still no convincing proof that oxidative stress is a cause of human hypertension. 22796706: Oxidative stress in the RVLM contributes to the enhanced central sympathetic outflow that leads to hypertension in experimental models of hypertension, such as spontaneously hypertensive rats (SHRs). 22950347: Considerable evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), plays a key role in the pathogenesis of hypertension. 23105577: This observation suggests that in hypertensive disorders of pregnancy there is an imbalance between lipid peroxidation and antioxidant vitamin status because of oxidative stress. 23472597: The cooperative roles of inflammation and oxidative stress in the pathogenesis of hypertension. CRITICAL ISSUES: Inflammation and oxidative stress thereby act as cooperative and synergistic partners in the pathogenesis of hypertension. 23600794: CRITICAL ISSUES: Although extensive experimental data support a role for increased ROS levels and altered redox signaling in the pathogenesis of hypertension, the role in clinical hypertension is unclear, as a direct causative role of ROS in blood pressure elevation has yet to be demonstrated in humans. RECENT ADVANCES: Although oxidative stress may not be the only cause of hypertension, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors, such as salt loading, activation of the renin-angiotensin-aldosterone system, and sympathetic hyperactivity, at least in experimental models. 23688014: In addition to its well-established metabolic effects, more recent evidence have depicted a rather pivotal role of leptin in inflammation, oxidative stress, endoplasmic reticulum stress, apoptosis and tissue remodeling en route to the pathogenesis of type 2 diabetes mellitus, hypertension, atherosclerosis, and insulin resistance. 23717285: In the present review, we will discuss the role of Ang II and oxidative stress in hypertension, the relationship between the BRS and the genesis of hypertension and how the oxidative stress triggers baroreflex dysfunction in several models of hypertension. 24616334: Both observational and experimental studies indicate that in particular night-time noise can cause disruptions of sleep structure, vegetative arousals (e.g. increases of blood pressure and heart rate) and increases in stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. 25097610: If oxidative stress is indeed a cause of hypertension, then, antioxidants should have beneficial effects on hypertension control and reduction of oxidative damage should result in a reduction in blood pressure. Recently it has been hypothesized that oxidative stress is a key player in the pathogenesis of hypertension. 25140155: Systemic and renal oxidative stress in the pathogenesis of hypertension: modulation of long-term control of arterial blood pressure by resveratrol. 25177555: Oxidative stress has been implicated as one of the underlying cause of hypertension. 25221387: RATIONALE: Accumulated evidence implicates sympathetic activation as inducing oxidative stress and systemic inflammation, which in turn lead to hypertension, endothelial dysfunction, and atherosclerosis in obstructive sleep apnea (OSA). 25236748: In conclusion, prenatal LPS exposure, via an increase in oxidative stress, impairs renal D1R function and leads to hypertension in the offspring. 25259742: These data demonstrate an important role for CD4(+) T cells in mediating another factor, oxidative stress, to cause hypertension during preeclampsia. 25411054: This finding may have important implications for understanding the effects of DPP4 in promoting inflammation and oxidative stress in the pathogenesis of hypertension. 25623850: SIGNIFICANCE: These findings indicate that NO induced-hypertension is associated with up-regulation of NADPH oxidase, oxidative stress production and overexpression of key inflammatory mediators. Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension. Nitric oxide (NO) inhibition with N(w)-nitro-L-arginine methyl ester (L-NAME) has previously been reported to produce hypertension, increased expression of Angiotensin II (Ang II) and renal dysfunction. The current study was designed to test the hypothesis that AT1R activation promotes renal NAD(P)H oxidase up-regulation, oxidative stress and cytokine production during L-NAME induced-hypertension. KEY FINDINGS: After two weeks, L-NAME induced high blood pressure, renal overexpression of AT1R, NAD(P)H oxidase sub-units gp91, p22 and p47, increased levels of oxidative stress, interleukin-6 (IL-6) and interleukin-17 (IL-17). 25761698: Given the role of oxidative stress and inflammation in the pathogenesis of hypertension, we conducted this study to test the hypothesis that long-term administration of resveratrol will attenuate renal inflammation and oxidative stress and, hence, progression of hypertension in the young spontaneously hypertensive rats (SHR). Compelling evidence supports the role of oxidative stress and renal interstitial inflammation in the pathogenesis of hypertension. 25872164: OBJECTIVES: We hypothesized that chronic ethanol intake enhances vascular oxidative stress and induces hypertension through renin-angiotensin system (RAS) activation. 25918583: Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels. Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction. We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia. 25936489: Of the many processes involved in the pathophysiology of hypertension, vascular damage due to oxidative stress (excess bioavailability of reactive oxygen species [ROS]) is particularly important. 26635913: Oxidative stress is associated with cardiac and vascular defects leading to hypertension and atherosclerosis, being superoxide dismutase (SOD) one of the main intracellular antioxidant defence mechanisms. 26987496: The aim of this review is to investigate the effect of oxidative stress in relation to hypertension and physical exercise, including the role of NO in the pathogenesis of hypertension. 27600468: Hyperhomocysteinemia correlates with IR, increasing oxidative stress, which causes lesions of vascular endothelium leading to endothelial dysfunction, hypertension and atherosclerosis. 27884224: This article updates recent literature with a focus on the function of insulin resistance, obesity, and renin angiotensin aldosterone system-mediated oxidative stress on endothelial dysfunction and the pathogenesis of hypertension. 27928516: Meanwhile, the oxidative stress can cause hypertension, so PSO is expected to develop a health care products for the prevention and mitigation hypertensive symptoms. 28078487: OBJECTIVE: This study aimed to investigate the role of the NADPH oxidase 4 (Nox4)-induced ROS/RhoA/ROCK pathway in CIH-induced hypertension in rats. The role of the Nox4-derived ROS-mediated RhoA/Rho kinase pathway in rat hypertension induced by chronic intermittent hypoxia. CIH elicits systemic oxidative stress and sympathetic hyperactivity, which lead to hypertension. 28189851: We tested the hypothesis that salt-sensitive hypertension is caused by renal oxidative stress by measuring the blood pressure and reactive oxygen species-related proteins in the kidneys of human G protein-coupled receptor kinase 4gamma (hGRK4gamma) 486V transgenic mice and non-transgenic (Non-T) littermates on normal and high salt diets. Thus, hGRK4gamma486V causes salt-sensitive hypertension due, in part, to defective renal antioxidant mechanisms. 28326006: Background: Recent studies indicate the important role of chronic inflammation and oxidative stress in the pathogenesis of hypertension. 28397867: Oxidative stress causes hypertension and activation of nuclear factor-kappaB after high-fructose and salt treatments. 28594709: OBJECTIVES: African-Americans have a higher prevalence of hypertension compared with whites, possibly due to elevated oxidative stress and subsequent vascular dysfunction. 28844481: These data suggest that the protective effects of tBHQ in salt induced hypertension are partly due to inhibiting oxidative stress and inflammation in PVN. Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension. Excessive oxidative stress and inflammation in hypothalamic paraventricular nucleus (PVN) are implicated in the pathogenesis of hypertension. The objective of this study was to investigate the effects of tBHQ in high salt induced hypertension and to identify whether the beneficial effects were induced by inhibiting PVN oxidative stress and inflammation. 28892880: CONCLUSION: Above findings indicate that elevation in oxidative stress and decrease in endogenous antioxidant level may be involved in the pathogenesis of hypertension. 29420965: Observational and translational studies indicate that especially nighttime noise increases levels of stress hormones and vascular oxidative stress, which may lead to endothelial dysfunction and arterial hypertension. 29624500: Oxidative stress causes endothelial dysfunction, hypertension and atherosclerosis. 29962855: The effects of supplementation with punicalagin on angiogenesis and oxidative stress in pregnant rats with induced hypertension were investigated. 30354705: Our present study indicates that maternal diabetes mellitus-programed hypertension in the offspring is caused by impaired renal D1 receptor function because of oxidative stress that is mediated by increased PKC-GRK-2 activity. 30806310: METHOD: The oxidative stress is a major cause for hypertension, hence different extracts of TA having variable marker yield were evaluated for their antihypertensive effect in buthionine sulfoxamine (BSO) induced oxidative stress based model. 31350796: CONCLUSIONS: Lancemaside A prevents hypertension in rats by inhibiting the activation of MAPK signalling and the impairment in nitric oxide bioavailability due to NOX2-mediated oxidative stress. 31591535: Reactive oxygen species (ROS)-dependent production of ROS underlies sustained oxidative stress, which has been implicated in the pathogenesis of cardiovascular diseases such as hypertension, aortic aneurysm, hypercholesterolaemia, atherosclerosis, diabetic vascular complications, cardiac ischaemia-reperfusion injury, myocardial infarction, heart failure and cardiac arrhythmias. 31781313: Obstructive sleep apnea (OSA) can lead to serious complications such as coronary heart disease and hypertension due to oxidative stress. 31880979: Here we show the nexus between high salt intake and oxidative stress causing renal tubular dopamine oxidation, which leads to mitochondrial and lysosomal dysfunction and subsequently causes renal inflammation and hypertension. 32149110: In cooperation, it contributes to chronic oxidative stress and endothelial dysfunction, which might lead to hypertension and atherosclerosis. 32226258: Numerous factors such as inflammation, oxidative stress, genetic predisposition etc. play roles in the pathogenesis of hypertension. 32345536: In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. 32349533: FUTURE DIRECTIONS: Identifying the mechanisms of renal dopamine receptors in the regulation of oxidative stress and their contribution to the pathogenesis of hypertension remains an important research focus. Increased understanding of the role of reciprocal regulation between renal dopamine receptors and oxidative stress in the regulation of blood pressure may give us novel insights into the pathogenesis of hypertension and provide a new treatment strategy for hypertension. 33070655: Oxidative stress and renal inflammation play a pivotal role in the pathogenesis of hypertension. 33076803: Patients with T2D often have hyperinsulinemia, dyslipidemia, inflammation, and oxidative stress, which then lead to hypertension, chronic kidney disease, cardiovascular disease, and increased risk of morbidity and mortality (9th leading cause globally). 33535566: The Role of the Renal Dopaminergic System and Oxidative Stress in the Pathogenesis of Hypertension. 33746706: Oxidative stress plays an important role in the pathogenesis of hypertension. 34064229: In the majority of studies, increased sympathetic activity was successfully established to escalate heart rate variability, the inflammatory process, oxidative stress, endothelial remodeling and hormonal disturbances, leading to hypertension and other cardiovascular complications. 34736077: Hypertension is one of the important causes of cardiovascular diseases, and the imbalance of vascular homeostasis caused by oxidative stress and endothelial inflammation occurs throughout hypertension pathogenesis. 34866971: Glucocorticoids (GCs) initiate oxidative stress and cause renal damage which lead to hypertension, heart failure and ultimately death. 35153813: Salt-induced hypertension and fructose-induced hypertension are manifested in different mechanisms, including Inflammation, aldosterone-mineralocorticoid receptor pathway, aldosterone independent mineralocorticoid receptor pathway, renin-angiotensin system (RAS), sympathetic nervous system (SNS) activity, and genetic mechanisms. This review describes the evolution of hypertension and cardiovascular diseases (CVDs) in Lebanon and aims to elucidate potential mechanisms where salt and fructose work together to induce hypertension. These mechanisms increase salt absorption, decrease salt excretion, induce endogenous fructose production, activate fructose-insulin-salt interaction, and trigger oxidative stress, thus leading to hypertension. High intakes of salt and sugar (mainly fructose from added sugars) have been linked to the etiology of hypertension, and this may be particularly true for countries undergoing the nutrition transition, such as Lebanon. 35326161: Hypertension remains the leading cause of disease burden worldwide. Oxidative Stress-Induced Hypertension of Developmental Origins: Preventive Aspects of Antioxidant Therapy. 36615704: This review aims to highlight the role of western diet-induced oxidative stress and inflammation in the pathogenesis of hypertension and the role of various types of diets in its prevention with reference to dietary approaches to stop hypertension (DASH) diet. 36707141: Accordingly, endogenous oxidative stress induces the progressive development of various chronic diseases like rheumatoid arthritis, cancers, cardiovascular risks, diabetes, digestive ulcers, hypertension, obesity, neurological disorders, and age-related complications. 37742912: Elevated endothelin-1 (ET-1) has been implicated in several diseases including preeclampsia, where it causes the induction of hypertension, oxidative stress, endoplasmic reticulum stress, microvascular dysfunction and tissue damage in different organs. 38163553: CONCLUSION: The irreversible oxidation of C674 is not only an indicator of increased ROS, but also further inducing oxidative stress to cause hypertension. 38545789: We hypothesized that PT fructose reabsorption by SGLT5 initiates a genetic program enhancing Ang II-stimulated oxidative stress in males and females, thereby causing fructose-induced salt-sensitive hypertension. CONCLUSIONS: SGLT5-mediated PT fructose reabsorption is required for FHS to augment Ang II-stimulated proximal nephron O 2 - production, and increases in PT oxidative stress likely contribute to FHS-induced hypertension. SGLT4 (sodium glucose-linked cotransporters 4) and SGLT5 are implicated in PT fructose reabsorption, but their roles in fructose-induced hypertension are unclear. Knocking Out Sodium Glucose-Linked Transporter 5 Prevents Fructose-Induced Renal Oxidative Stress and Salt-Sensitive Hypertension. 10507060: Oxidative stress and its sequelae are likely related to both necrotic and apoptotic mechanisms of neurotoxicity, and A beta-associated free radical oxidative stress may be of fundamental importance in Alzheimer's disease etiology and pathogenesis. 10568522: The provided data appear to be in accordance with the known alteration of GSH levels in central nervous system and strengthen the hypothesis of oxidative stress as an important, possibly crucial mechanism in the pathogenesis of AD. 10681271: Many lines of evidence suggest that oxidative stress is important in the pathogenesis of Alzheimer disease. 10850732: Because of the proximal role that oxidative stress mechanisms seem to play in the pathogenesis of Alzheimer disease, further investigation in this realm may lead to novel therapeutic strategies. 10867210: The relationships shown to exist between hemorheology, blood flow, amyloids, oxidative stress, and cognitive function suggest that these factors may be one of the mechanisms operating in the complex etiology of Alzheimer's disease. 10899439: While this suggests that oxidative stress is a proximal event in Alzheimer's disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-beta-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer's disease pathogenesis and novel therapeutic approaches. 11068183: The present study may help to explain the pathogenesis of neurodegeneration in AD disorders caused by metal-generated oxidative stress. 11079778: To begin to address these issues, we investigated p38 kinase, which is induced by oxidative stress, in the pathogenesis of AD. 11232594: This furthers the evidence that redox-active iron and subsequent Fenton reaction generating reactive oxygen are critical factors in the pathogenesis of AD. Multiple lines of evidence indicate that oxidative stress is an integral component of the pathogenesis of Alzheimer disease (AD). 11578751: On the other hand, there is cumulative evidence from studies in cultured brain cells and on brains that oxidative stress constitutes a main factor in the modification of normal signaling pathways in neuronal cells, leading to biochemical and structural abnormalities and neurodegeneration as related to the pathogenesis of Alzheimer's disease. 11640950: There are multiple lines of evidence showing that oxidative stress and aberrant mitogenic signaling play an important role in the pathogenesis of Alzheimer disease. 11708617: Oxidative stress may contribute to the aetiology of AD by dysregulation of APP metabolism. 11738475: Further, in diseases such as progressive supranuclear palsy, Huntington's, Alzheimer's and Parkinson's diseases, the aberrant activation of TGases may be caused by oxidative stress and inflammation. 11771743: Oxidative stress is considered to be crucial in the pathogenesis of Alzheimer's disease-like neurodegeneration. An elevation of carbonyl compounds that are biomarkers of and leading to oxidative stress has been demonstrated in Down Syndrome (DS) and Alzheimer's Disease (AD) brains and seems to be the result of a multifactorial process. 11884366: In addition, oxidative stress in the mitochondria is associated with the pathogenesis of Alzheimer's disease, Parkinson's disease, prion diseases, and amyotrophic lateral sclerosis (ALS) as well as aging itself. 11890747: Oxidative stress and quasi-inflammatory processes recently have been recognized as contributing factors in the pathogenesis of Alzheimer's disease (AD). 12488575: Further investigation into the role that oxidative stress mechanisms seem to play in the pathogenesis of Alzheimer disease may lead to novel clinical interventions. 12870699: There is strong evidence that oxidative stress participates in the etiology of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. 12893008: Hopefully, the following discussion will help elucidate the relationship between oxidative stress, protein modification and the pathogenesis of AD. 14656990: These results support the hypothesis that oxidative stress is an important early event in AD pathogenesis, and antioxidant therapy may be beneficial only if given at this stage of the disease process. 14661103: However, increasing evidence indicates that factors such as oxidative stress and disturbed protein metabolism and their interaction in a vicious cycle are central to AD pathogenesis. 15036353: A growing body of evidence supports an important role for oxidative stress in the pathogenesis of Alzheimer's disease. 15039034: There are many lines of evidence showing that oxidative stress and aberrant mitogenic changes have important roles in the pathogenesis of Alzheimer's disease (AD). 15096699: Although several studies show the importance of oxidative stress in the pathogenesis of Alzheimer's disease (AD), there are few evidences on the role of free radicals in Mild Cognitive Impairment (MCI). 15105265: Many lines of evidence indicate that oxidative stress is one of the earliest events in the genesis of Alzheimer's disease (AD). 15120069: A growing body of evidence suggests that oxidative stress is a common underlying mechanism in the pathogenesis of neurodegenerative disorders such as Alzheimer's, Huntington's, Creutzfeld-Jakob and Parkinson's diseases. 15141484: However, increasing evidence indicates that factors such as oxidative stress and disturbed protein metabolism and their interaction in a vicious cycle are central to AD pathogenesis. 15370876: Although the role of oxidative stress in the aetiology of Alzheimer's disease is still not clear, the detection of an increased damage status in the cells of patients could have important therapeutic implications. 15380154: There is evidence that oxidative stress, homocysteine-related vitamins, fats, and alcohol have a role in the pathogenesis of AD. 15500684: BACKGROUND: An increasing body of evidence implicates both brain inflammation and oxidative stress in the pathogenesis of Alzheimer's disease (AD). 15614428: Thus, upregulation of BACE1 transcription by oxidative stress may contribute to the pathogenesis of Alzheimer's disease. Oxidative stress has been shown to affect A(beta) generation in the AD pathogenesis and the mechanism of such effect is unknown. 15635602: Despite the mounting evidence, however, for the causal role of mitogenic abnormalities and oxidative stress in AD pathogenesis, the effect of the converging relevant pathways due to chronic stimulation in AD remains largely unknown. 15723615: Oxidative stress, bioenergetic impairment and mitochondrial failure have all been implicated in the etiology of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD), as well as retinal degeneration in glaucoma and retinitis pigmentosa. 15753151: Oxidative stress is important in the pathogenesis of Alzheimer's disease (AD). 16181112: Evidence indicates that in the initial phase of Alzheimer's disease development, amyloid-beta deposition and hyperphosphorylated tau are consequences of oxidative stress and function as a primary line of antioxidant defense. 16271804: The identification of common oxidized proteins in different brain regions of AD brain suggests a potential role for these oxidized proteins and thereby oxidative stress in the pathogenesis of Alzheimer's disease. 16298240: There is a large body of evidence highlighting the importance of oxidative stress in the pathogenesis of Alzheimer's disease (AD). 16311508: Strong evidence indicates oxidative stress in the pathogenesis of Alzheimer's disease (AD). Deregulation of GRX1 and TRX1 antioxidant systems could be important events in AD pathogenesis. 16337883: These results supported the hypothesis that oxidative stress was an early event in AD pathogenesis and that antioxidant therapy may be beneficial only if given at this stage of the disease process. 16399210: We determined whether oxidative stress is an early event in the pathogenesis of sporadic Alzheimer disease (AD), and correlated oxidative stress with neuropsychological functions and neurofibrillary pathology in AD and mild cognitive impairment (MCI). Cortical and hippocampal oxidative stress is a very early event in the pathogenesis of sporadic AD and correlates with the development of specific cognitive deficits in this condition. 16538519: Several studies have documented the involvement of oxidative stress represented by lipid peroxidation in the pathogenesis of Alzheimer's disease (AD). 16624449: Besides the genetic, biochemical and neuropathological analogies between Down's syndrome (DS) and Alzheimer's disease (AD), there is ample evidence of the involvement of oxidative stress (OS) in the pathogenesis of both disorders. 16703529: Glutamatergic excitatory neurotransmission, an important process in learning and memory, is severely disrupted in AD, probably due to the oxidative stress associated with the beta-amyloid peptide (1-42) increase. 16860790: Evidence has suggested a critical role for amyloid-beta peptide metabolism and oxidative stress in Alzheimer's disease pathogenesis and progression. 16873963: Dysfunction of mitochondria and oxidative stress in the pathogenesis of Alzheimer's disease: on defects in the cytochrome c oxidase complex and aldehyde detoxification. 16930434: This indicates that truncation of tau may precede oxidative stress in the pathogenesis of neurodegenerative diseases such as AD and other tauopathies. 17121373: This review will focus on some of the mediators of oxidative stress occurring in AD pathology and their possible role in the AD pathogenesis. 17210195: There is substantial evidence implicating increased production of the hydroxyl radical and oxidative stress in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD). 17279615: Recent studies implicating Abeta oligomers and protofibrils in the neurotoxic process that ultimately leads to AD suggest that the Abeta aggregates induced by 4-HNE may be important in the pathogenesis of AD. Although it remains an open question as to whether oxidative stress is a causative factor or a consequence of AD, we show here that 4-HNE, putatively resulting from the peroxidation of lipids, covalently modifies Abeta, triggering its aggregation. 17460216: Evidence suggests that oxidative stresses are involved in the mechanism of Abeta-induced neurotoxicity and AD pathogenesis. 17664130: Roles of amyloid beta-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment. 17707551: Recent reports on amyloid beta peptide (A beta) binding-alcohol dehydrogenase (ABAD) have revealed the link of A beta with oxidative stress derived from mitochondria in the pathogenesis of Alzheimer's disease (AD). 17761673: There is substantial evidence that oxidative stress elicited by amyloid beta (Abeta) accumulation is a causative factor in the pathogenesis of Alzheimer disease (AD). 17764625: There is evidence that oxidative stress, homo-cysteine-related vitamins, fats, and alcohol have a role in the pathogenesis of AD. 17996678: Inflammatory injury and induction of oxidative stress have been implicated as causative factors in neurodegenerative diseases such as Alzheimer's disease (AD). 18084903: Oxidative stress is considered one of the causative pathomechanisms of nervous system diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, stroke and excitotoxicity. 18297609: Several studies show the importance of oxidative stress in the pathogenesis of AD. 18427999: Glutathione S-transferase omega 1 and 2 (GSTO1 and 2) protect from oxidative stress, a possible pathogenic mechanism underlying the pathogenesis of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Alzheimer's disease. 18524497: The premise that the event that initiates plaque formation is vascular explains why the risk factors for ALDs and cardiovascular diseases overlap; why drugs and lifestyle changes with vaso-protective effects protect against dementia; and why oxidative stress is prominent early in the genesis of Alzheimer-like dementias. 18539391: The expression level of cortical glial fibrillary acidic protein (GFAP) increased in an age-related manner, in particular in 2-month PS cDKO mice, suggesting that the interaction relationship between oxidative stress and inflammatory response may be closely associated with the underlying loss-of-function pathogenesis of AD. 18565274: Cross-talk between oxidative stress and modifications of cholinergic and glutaminergic receptors in the pathogenesis of Alzheimer's disease. 18662010: There is strong evidence that oxidative stress participates in the etiology of neurodegenerative diseases such as Parkinson's, and Alzheimer's diseases. 18762245: These results are discussed with reference to the importance of Abeta42-associated oxidative stress in the pathogenesis of AD. 18780972: Oxidative stress has been shown to be a triggering event in the pathogenesis of Alzheimer's disease (AD). 18822368: Oxidative stress is one of the hypotheses involved in the etiology of Alzheimer's disease (AD). 19166318: GSH deficiency or a decrease in the GSH/glutathione disulfide ratio manifests itself largely through an increased susceptibility to oxidative stress, and the resulting damage is thought to be involved in diseases, such as cancer, Parkinson's disease, and Alzheimer's disease. 19200343: Oxidative stress is one of the earliest events in the pathogenesis of Alzheimer's disease (AD) and can markedly exacerbate amyloid pathology. 19250756: The basic pathophysiological difference is that AD is caused by oxidative stress alone, whereas PD is caused by oxidative stress plus failure of energy production. 19345730: Oxidative stress has been reported to be a common underlying mechanism in the pathogenesis of many neurodegenerative disorders such as Alzheimer, Huntington, Creutzfeld-Jakob, and Parkinson disease. 19907182: BACKGROUND/AIM: The contribution of mitochondrial dysfunction and oxidative stress to the pathogenesis of Alzheimer's disease (AD) has previously been described. 19950527: CONCLUSION: R. rosea extract can protect rats against cognitive deficits, neuronal injury and oxidative stress induced by intracerebroventricular injection of streptozotocin, and may be used as a potential agent in treatment of neurodegenerative diseases such as AD. 20026169: There is significant evidence that oxidative stress is a critical event in the pathogenesis of AD. 20236039: Genetic mutations and genetic, acquired and environmental risk factors, particularly neuroinflammation and oxidative stress, are the main causes of AD. 20302830: Oxidative stress is known to play a key role in the initiation and promotion of the neurodegeneration that characterizes the pathogenesis of Alzheimer disease (AD). 20381316: There is evidence that malnutrition, oxidative stress, and homocysteine-related vitamins play a role in the pathogenesis of AD. 20541661: Metabolic derangements and oxidative stress are early events in Alzheimer's disease pathogenesis. 20555132: Although mitochondrial dysfunction and the resultant oxidative stress are believed to play a major role in the pathogenesis of both early- and late-onset AD, it is conceivable that the altered physiological state of the cells leading to sporadic AD could involve additional mechanisms. 20564553: It is strongly suggested that D-aspartic acid (D-Asp)-containing proteins are spontaneously generated by oxidative stress and would cause many aging-related misfolding diseases, such as cataracts, prion disease, and Alzheimer's disease. 20586698: Oxidative stress is an important factor, and one that acts in the earliest stages, of Alzheimer's disease (AD) pathogenesis. 20691758: The changes in the levels of homocysteine and DHEA-S in aged rat brain have been related to associated glutathione depletion and oxidative stress and the implications of the results highlighted in the pathogenesis of Alzheimer's disease. 20933033: The Abeta aggregate-induced neurotoxicity, inflammatory reactions and oxidative stress are linked strongly to the etiology of AD. 20966918: Oxidative stress is an important determinant not only in the pathogenesis of Alzheimer's disease (AD), but also in insulin resistance (InsRes) and diabetic complications. 21357903: Oxidative stress and cell membranes in the pathogenesis of Alzheimer's disease. 21426072: BACKGROUND: beta-amyloidosis and oxidative stress have been implicated as root causes of Alzheimer's disease (AD). 21463622: Increasing evidence indicates that factors such as oxidative-nitrergic stress, glutathione depletion, impaired protein metabolism and cholinergic deficit can interact in a vicious cycle, which is central to Alzheimer's disease pathogenesis. 21551909: Moreover, since alpha1-antitrypsin, the principal inhibitor of elastase, is highly susceptible to oxidative stress, our findings suggest a link between proteolytic imbalance and oxidative stress in the pathogenesis of Alzheimer disease. 21605062: Oxidative stress is considered one of the earliest events in AD pathogenesis and is thought to contribute largely to neuronal cell death. 21631359: Punica granatum protects against oxidative stress in PC12 cells and oxidative stress-induced Alzheimer's symptoms in mice. 22008267: The down-regulation of energy metabolism in AD has been considered by many as a consequence of mitochondrion damage due to oxidative stress. 22137893: Specific adducts of lipid peroxidation have been demonstrated in intimate association with the pathological lesions of Alzheimer disease (AD), suggesting that oxidative stress is a major component of AD pathogenesis. 22172527: In addition, studies from mild cognitive impairment patients suggest that oxidative stress is an early event in the pathogenesis of AD. 22406441: Our results confirm a critical role for oxidative stress in AD pathogenesis and progression and suggest the potential usefulness of EUK-207 in AD treatment. 22430645: The activation of PARP-1 by oxidative stress seems to be an early and important event in the pathogenesis of AD. 22500616: Do proteomics analyses provide insights into reduced oxidative stress in the brain of an Alzheimer disease transgenic mouse model with an M631L amyloid precursor protein substitution and thereby the importance of amyloid-beta-resident methionine 35 in Alzheimer disease pathogenesis? 22539855: Alzheimer's disease (AD) in the early stages is characterized by memory impairment, which may be attributable to synaptic dysfunction. Oxidative stress, mitochondrial dysfunction, and Ca2+ dysregulation are key factors in the pathogenesis of AD, but the causal relationship between these factors and synaptic dysfunction is not clearly understood. 22541290: Mitochondrial abnormalities contribute to oxidative stress which is part of AD pathogenesis in DS as well as AD in the general population. 22664577: It is well known that oxidative stress is one of the earliest events in Alzheimer's disease pathogenesis, indicating that may play a key role in this disease. 22708607: Copper and oxidative stress in the pathogenesis of Alzheimer's disease. 22811764: Oxidative stress in the central nervous system is strongly associated with neuronal cell death in the pathogenesis of several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. 22998047: Consequences of oxidative stress thought to contribute to the development of a wide range of diseases including Alzheimer's disease, Parkinson's disease, diabetes, rheumatoid arthritis, neurodegeneration in motor neuron diseases and many cancer types. 23107435: Increasing evidence demonstrates that amyloid beta (Abeta) elicits mitochondrial dysfunction and oxidative stress, which contributes to the pathogenesis of Alzheimer's disease (AD). 23200807: In this review, we focus on changes in mitochondrial DNA and mitochondrial dynamics, two aspects critical to the maintenance of mitochondrial homeostasis and function, in relationship with oxidative stress in the pathogenesis of AD and PD. 23228953: There are many evidences suggesting that oxidative stress is one of the earliest events in Alzheimer disease (AD) pathogenesis and plays a key role in the development of the AD pathology. 23254632: Oxidative stress is an early event in the pathogenesis of Alzheimer's disease (AD). 23420079: Significant bodies of evidences have shown different mechanisms known to be the etiological cause of Alzheimer's disease (AD) involving amyloid-beta protein accumulation, chronic inflammatory reactions, oxidative stress, proteasome inhibition, and high-cholesterol level, but the presize etiology of AD still remains enigmatic. 23480224: BACKGROUND: Oxidative stress represents a key event in the pathogenesis of Alzheimer's disease (AD). 23849337: Another hypothesis proposed by the late Mark Smith and colleagues is that oxidative stress, rather than Abeta, precipitates the pathogenesis of AD. 24372221: Oxidative stress mediated mitochondrial and vascular lesions as markers in the pathogenesis of Alzheimer disease. 24423585: Oxidative stress plays a critical role in the etiology and pathogenesis of Alzheimer's disease (AD), and the molecular mechanisms that control the neuron response to oxidative stress have been extensively studied. These results suggested that oxidative stress alters the miRNA expression profile of hippocampal neurons, and the deregulated miRNAs might play potential roles in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD). 24788773: Thus, oxidative stress-induced HRD1 insolubilization might be involved in a vicious cycle of increased amyloid beta production and amyloid beta-induced oxidative stress in Alzheimer's disease pathogenesis. 24846973: Aggregation of Abeta induces neurotoxicities manifested by apoptosis, neuroin-flammation, oxidative stress and mitochondrial dysfunction etc., which consequently provoke the pathological progression of AD. 25322927: BACKGROUND: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer's disease (AD) pathogenesis remain elusive. 25462645: Protein carbonylation is a well-documented and quantifiable consequence of oxidative stress in several neuropathologies, including multiple sclerosis, Alzheimer's disease, and Parkinson's disease. 25511446: Although pathological hallmarks of AD are senile plaques, neurofibrillary tangles, and neuronal degeneration which are associated with increased oxidative stress, synaptic loss is an early event in the pathogenesis of AD. Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies. 25620241: The biology of NF-kappaB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. 26171115: Oxidative stress is a prominent early event in the pathogenesis of AD and is therefore believed to contribute to tau hyperphosphorylation. 26295822: Alzheimer's disease (AD) is a neurodegenerative disease characterized by deposit of amyloid plaques and neurofibrillary tangles and oxidative stress plays an essential role in the pathogenesis of AD. These results indicate that JAT may be the potential target to treat AD induced by oxidative stress and apoptosis. 26500157: This study demonstrates for the first time mitochondrial dysfunction in transgenic mice with a mutation within the Abeta peptide (the Arctic APP mutation), and confirms previous studies suggesting that mitochondrial dysfunction and oxidative stress is an early event in the pathogenesis of Alzheimer disease. 26587902: BACKGROUND: The critical role of neuro-inflammation and oxidative stress in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD) has become evident. 26629876: Oxidative stress is considered as an important factor and an early event in the etiology of Alzheimer's disease (AD). 26890100: These changes include chronic astrocytic and microglial gliosis, oxidative stress, and altered metabolism of a number of proteins associated with the pathogenesis of Alzheimer's disease. 27010693: BACKGROUND: One of the factors that contribute to Alzheimer's disease (AD) is the DNA damage caused by oxidative stress and inflammation that occurs in nerve cells. 27040443: CONCLUSION: Recent studies have shown that oxidative stress is the one of the molecular changes underlying the pathogenesis of Alzheimer's disease. 27129593: In a novel sporadic mouse model that manifests AD-like pathology caused by accelerated oxidative stress in the absence of any familial AD mutation, oral administration of NMZ attenuated hallmark AD pathology and restored biomarkers of synaptic and neuronal function. 27252059: In conclusion, oxidative stress-induced HRD1 insolubilization might be involved in a vicious cycle of increased Abeta production and Abeta-induced oxidative stress in Alzheimer's disease pathogenesis. 27351675: Our findings suggest that oxidative stress and inflammatory responses could result in abnormal SET gene expression, contributing to the tauopathy in AD pathogenesis. 27386059: BACKGROUND: Recent studies have shown that oxidative stress (OS) is the most important indicator in the pathogenesis of Alzheimer's disease (AD), but the results in previous studies are conflicting. 27498145: Evidence suggests that oxidative stress and apoptosis are involved in the mechanism of Abeta-induced neurotoxicity and AD pathogenesis. 27774420: At the same time, aggregated Abeta-induced oxidative stress is the trigger in the pathogenesis of Alzheimer's disease (AD). 27796749: Oxidative stress is considered a major contributor to the pathogenesis of AD, and accumulating evidence indicates that high levels of reactive oxygen species (ROS) are involved in Abeta-induced neurodegeneration. Amyloid-beta peptide (Abeta) is one of the major players in the pathogenesis of Alzheimer's disease (AD). 28332351: Oxidative stress is known to be induced by Abeta and NFTs, and we suggest that oxidative stress caused by metabolic alterations in the body induce brain metabolic alterations, resulting in AD. 28448946: INTRODUCTION: There is increasing evidence for the involvement of chronic inflammation and oxidative stress in the pathogenesis of Alzheimer's disease (AD). 28970897: Oxidative stress is linked to the etiology of Alzheimer's disease (AD), the most common cause of dementia in the elderly. 29090409: Oxidative stress and cytotoxic damage induced by amyloid beta (Abeta) have been considered pivotal in the pathogenesis of Alzheimer's disease (AD) and may represent a target for treatment. 29109370: Our results suggest that olive biophenols potentially serve as agents for the prevention of neurodegenerative diseases such as AD, and other neurodegenerative ailments that are caused by oxidative stress. 29112116: Increased evidence suggests neuroinflammation and oxidative stress may cause AD. 29512790: Oxidative stress may contribute to the underlying mechanisms causing Alzheimer's disease (AD). 29574628: Increasing evidence indicates that sirtuin 3 (Sirt3) has neuroprotective effects in regulating oxidative stress and energy metabolism, both of which are involved in the pathogenesis of Alzheimer's disease (AD). 29951441: This paper outlines possible protective consequences of LDR in preventing the pathogenesis of AD through mechanisms such as restoring the myelin sheath and preventing neurodegeneration caused by oxidative stress. 30112360: Alzheimer's disease (AD) and multiple sclerosis are major neurodegenerative diseases, which are characterized by the accumulation of abnormal pathogenic proteins due to oxidative stress, mitochondrial dysfunction, impaired autophagy, and pathogens, leading to neurodegeneration and behavioral deficits. 30151968: Transition-metal-catalyzed oxidative stress is a widespread concern in the pathogenesis of Alzheimer's disease. 30498443: Several factors like tau protein hyperphosphorylation, amyloid-beta (Abeta) peptide aggregation, decline in acetyl cholinesterase and oxidative stress might be contributing toward the pathogenesis of AD. 30689517: Oxidative stress has also been known as an important cause of AD. 30694418: Oxidative stress and the presence of ApoEepsilon4 allele has been reported to play a major role in the pathogenesis of AD, but the contribution of oxidative stress and ApoEepsilon4 in macrophage dysfunction leading to ineffective Abeta phagocytosis needs to be analyzed. 30729451: This combinatorial model also exhibited cognitive deficiency which was assessed by Morris water maze and avoidance tests along with enhanced oxidative stress which is thought to be a major player in AD pathogenesis. 30984280: For this reason, OS is considered a key factor in Alzheimer's Disease (AD) development and recent evidence correlated oxidative stress with vascular lesion in the pathogenesis of AD, but the mechanism still need to be fully clarified. 31006097: Oxidative stress is a key factor of and closely implicated in the pathogenesis of Alzheimer's disease (AD). 31022822: The detrimental effects of oxidative stress and chronic neuroinflammation on neuronal cell death have been implicated in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). 31057691: In this review, we outline and discuss the mitochondrial and oxidative stress factors causing degenerative diseases, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and Friedreich's ataxia. 31117312: It is believed that oxidative stress and cholinergic deficit are the leading causes of AD. 31151322: Oxidative stress is believed to be one of the main causes of neurodegenerative diseases such as Alzheimer's disease (AD). 31165850: Cholinergic dysfunction and oxidative stress are the most common causes of Alzheimer's disease (AD). 31173752: The protective effects of liraglutide on AD-like neurodegeneration induced by oxidative stress in human neuroblastoma SH-SY5Y cells. 31247877: They indeed impact the aggregation pathways of Abeta and are involved in the catalytic generation of reactive oxygen species (ROS) that participate in oxidative stress, while Abeta aggregation and oxidative stress are regarded as two key events in AD etiology. 31403949: These findings suggest that EDA possesses clinical and pathological benefits for AD with CCH in the present mouse model and has a potential as a therapeutic agent for AD with CCH via targeting multiple key pathways of the disease pathogenesis. The hallmarks of AD including amyloid-beta (Abeta)/phosphorylated tau (pTau) and pathology-related events such as neural oxidative stress and neuroinflammation play critical roles in pathogenesis of AD with CCH. 31424393: Ischemic postconditioning protects against post-ischemic excitotoxicity, oxidative stress, and inflammatory process that have also been implicated in the pathogenesis of AD. 31462605: Oxidative stress is closely related to the pathogenesis of AD. 31495239: Oxidative stress is implicated in pathogenesis of neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases. 31521745: These findings support a role for the involvement of mitochondria-derived oxidative stress in the etiology of AD and suggest that mitochondria-targeted antioxidants may lessen symptoms in AD patients. 31585875: The pathophysiology involved in AD is intra-neuronal accumulation of hyper-phosphorylated tau protein as neurofibrillary tangle and extra cellular beta amyloid plaque deposition, which is due to oxidative stress. 31607444: Dysregulation of the blood brain barrier due to oxidative stress causes neurological disorders, such as Alzheimer's and Parkinson's disease. 31686372: However, the molecular mechanisms underlying the aberrant expression levels of these proteins in the pathogenesis of AD are still not completely understood. Mitochondrial dysfunctions and oxidative stress play important roles in the early pathogenesis of Alzheimer's disease (AD), which also involves the aberrant expression levels of mitochondrial proteins. 31766696: This study presents a literature review of ANTs from different berries and their potential therapeutic value, with particular emphasis on neurodegenerative AD, which owing to oxidative stress. 31939658: Oxidative stress is known to play an important role in the pathogenesis of Alzheimer's disease. 31945778: The oxidative stress is one of the main causative factors of AD. 32035419: Oxidative stress and chronic inflammation have been suggested as causes of AD. 32124703: Oxidative stress in the pathogenesis of Alzheimer's disease and cerebrovascular disease with therapeutic implications. Oxidative stress in the pathogenesis of Alzheimer's disease and cerebrovascular disease with therapeutic implications.The significant gain in life expectancy led to an increase in the incidence and prevalence of dementia. 32171783: Indeed, the burden of amyloid beta (Abeta), neurofibrillary tangles (NFTs), neuroinflammation, oxidative stress, and dysfunction of circadian rhythms may lead to AD. 32180930: Moreover, BACE1 was also found to be closely related to AD pathogenesis caused by oxidative stress. 32277437: Uric acid and late-onset Alzheimer's disease: results from the ReGAl 2.0 project.BACKGROUND: It has been suggested that oxidative stress may have a role in the pathogenesis of Alzheimer's disease (AD). 32329360: Nutritional supplementation of GA preserve the morphological and physiological integrity of the hippocampus against environmental neurotoxins (AlCl 3 ) by mopping up free radicals associated with oxidative stress induced AD. This study aimed at investigating the neuroprotective effects of Gallic Acid (GA) against aluminum-chloride induced AD in adult Wistar rats. 32444542: Tenuifolin Attenuates Amyloid-beta42-Induced Neuroinflammation in Microglia Through the NF-kappaB Signaling Pathway.BACKGROUND: Inflammation and oxidative stress are believed to play an important role in the pathogenesis of Alzheimer's disease (AD). 32504391: Protective Effects of Co-administration of Zinc and Selenium Against Streptozotocin-Induced Alzheimer's Disease: Behavioral, Mitochondrial Oxidative Stress, and GPR39 Expression Alterations in Rats. Findings of the current study showed that ZnR/GPR39 receptor, mitochondrial dysfunction, and oxidative stress play important roles in the pathogenesis of AD. Co-treatment of Zn and Se improved the cognitive performance, mitochondrial dysfunction, and oxidative stress caused by STZ-induced AD. 32594052: Amyloid beta (Abeta)-induced neurotoxicity and oxidative stress plays an important role in the pathogenesis of Alzheimer's disease (AD). 32606694: Background: beta-Amyloid (Abeta) induces oxidative stress and inflammation of microglial cells, thus leading to Alzheimer's disease. 32730855: Oxidative stress is considered as one of the pathogenesis of Alzheimer's disease (AD) and plays an important role in the occurrence and development of AD. 32737764: Oxidative stress is thought to be central in the pathogenesis of Alzheimer's disease (AD). 32765394: Thus, ORC may exert a protective role in AD through attenuating the damage caused by inflammation and oxidative stress. 32829453: Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer's disease (AD). In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. 32920833: It has long been recognized that mitochondrial dysfunction and oxidative stress contribute to the pathogenesis of Alzheimer's disease (AD). 33052996: Oxidative stress and metal dyshomeostasis are considered as crucial factors in the pathogenesis of Alzheimer's disease (AD). 33081348: Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches. Several studies have indicated that oxidative stress plays a crucial role in the pathogenesis of AD. 33114450: Amongst the dysregulated pathophysiological pathways in AD, oxidative stress seems to play a critical role in the pathogenesis progression of AD, with a dominant role of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein-1 (Keap1)/antioxidant responsive elements (ARE) pathway. 33239403: Abeta accumulation affects mitochondrial redox balance, increasing oxidative stress status, which in turn is proposed as a primary culprit in AD pathogenesis. 33264657: Hypoxia causes oxidative stress with severe and detrimental effects on brain function and acts as a critical initiating factor in the pathogenesis of Alzheimer's disease (AD). 33476985: Oxidative stress is a prominent early event in the pathogenesis of AD and is therefore believed to contribute to tau hyperphosphorylation. 33488846: beta -Amyloid (A beta ), a strong inducer of oxidative stress, plays a crucial role in the pathogenesis of AD. 33567524: Oxidative stress has been implicated in the pathogenesis of Alzheimer's disease, and brains with the disease examined in this study also exhibited higher carbonylated proteins, as well as an increased thiol oxidation state of peroxiredoxin 6 (Prx6). 33633844: Conclusions: Our findings indicate that oxidative stress, apoptosis, and inflammation/immune system processes likely underlie the pathogenesis of AD and DS. 33679375: In this review, we focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of AD, emphasizing a framework of existing and potential therapeutic approaches. Over the last few years, remarkable efforts have been made to investigate the impact on the pathogenesis of Alzheimer's disease (AD) of various forms of mitochondrial dysfunction, such as excessive reactive oxygen species (ROS) production, mitochondrial Ca 2+ dyshomeostasis, loss of ATP, and defects in mitochondrial dynamics and transport, and mitophagy. 33774476: Oxidative stress has been implicated in the pathogenesis of Alzheimer's disease (AD). 33811448: In addition, oxidative stress is considered as an important factor in the etiology of AD and a multitude of metalloproteins and transporters are affected, leading to metal ion misregulation. 33897425: The toxic aggregates of amyloid beta (Abeta) disrupt the cell membrane, induce oxidative stress and mitochondrial dysfunction, and eventually lead to Alzheimer's disease (AD). 34107282: We have found that HSV-1 induces the main neuropathological hallmarks of AD, including the accumulation of intracellular amyloid beta (Abeta), hyperphosphorylated tau protein and autophagic vesicles, that OS exacerbates these effects, and that matrix metalloproteinase 14 (MMP-14) participates in the alterations induced by OS. 34403662: CONCLUSION: CircLPAR1 promotes Abeta25-35-induced apoptosis, inflammation, and oxidative stress via miR-212-3p/ZNF217 axis, suggesting a new insight into the pathogenesis of AD. 34662512: Expanding literature suggests that oxidative stress (OS) is a vital factor contributing to the pathogenesis of AD such that biometals (e.g., iron, zinc, copper) are believed to play a crucial role in Abeta formation and neurodegeneration. 34932880: Oxidative stress and cholinergic system dysfunction are two widely studied pathogenesis of AD. 35049930: As the major clinical indications (CI) of AD are extracellular plaques formed by beta-amyloid (Abeta) protein, intracellular neurofibrillary tangles (NFTs) formed by hyper phosphorylated tau-protein, uncommon inflammatory response and neuron apoptosis and death caused by oxidative stress, alkaloids that may decrease CI, might be used against AD. 35226474: Oxidative stress is important for the etiology and pathogenesis of Alzheimer's disease (AD). 35280979: Background/Aim: Apoptosis and oxidative stress have been considered as key events in the pathogenesis of Alzheimer's disease (AD). 35341471: The accumulation of aluminum in brain is reported to be associated with cholinergic dysfunction, oxidative stress and neuronal damage, that may ultimately cause Alzheimer's disease. 35395415: Taking oxidative stress as the central point, this review comprehensively expands on the roles of oxidative stress that are involved in the pathogenesis of AD. 35411685: SCO (1 mg/kg) was administrated intraperitoneally to induce the AD in Wistar rats. Hence, this study was designed to investigate the possible therapeutic effect of betanin against SCO-induced AD on Wistar rats. Mitochondrial dysfunction and oxidative stress are identified to contribute to the mechanisms responsible for the pathogenesis of Alzheimer's disease (AD). 35474814: Identifying specific interactive effects of MI with cellular antioxidant enzymes would represent an essential step in understanding the oxidative stress-induced AD pathogenicity. 35961386: Oxidative stress is an early event during AD pathogenesis and is associated with tau-mediated AD pathology. 36014181: The antioxidant, anti-cholinesterase, and anti-diabetic potential of the prepared nanoparticles were high in comparison to other areas of biological potential, indicating that the FeNPs are capable of targeting meditators of oxidative stress leading to diabetes and Alzheimer's disease. 36091821: Conclusion: This study suggests that AOF had the potential to treat AD by suppressing apoptosis induced by oxidative stress via the PI3K/Akt pathway. 36091826: Disturbed retinoic acid signaling causes inflammatory responses, mitochondrial impairment, oxidative stress, and neurodegeneration, leading to Alzheimer's disease (AD) progression. We outlined the physiology of retinoids in this review, focusing on their possible neuroprotective actions, which will aid in elucidating the critical function of such receptors in AD pathogenesis. 36139869: Oxidative stress in the brain is highly related to the pathogenesis of Alzheimer's disease (AD). 36476438: These molecules protect neurons against oxidative stress and deposition of amyloid-beta (Abeta) and tau proteins which play a vital role in the pathogenesis of AD. 36587558: Although the pathogenesis of AD is unclear, neurotoxicity induced by oxidative stress plays an important role in the progression of AD. 36635346: Our study identified 9 key genes associated with oxidative stress and immune reaction in AD pathogenesis. Oxidative stress and neuroinflammation play important roles in the pathogenesis of AD. 36744334: OBJECTIVE: The goal of the present study was to uncover the oxidative stress mechanisms causing AD, as well as the potential therapeutic targets and neuroprotective drugs against oxidative stress mechanisms. 36999542: Oxidative stress is an important contributor to the pathogenesis of Alzheimer's disease (AD). 37231172: Therapeutic potential of flavonoids in the management of obesity-induced Alzheimer's disease: an overview of preclinical and clinical studies. Thus, flavonoid-rich nutraceuticals can be a potential cost-effective therapeutic option for treating obesity-induced AD, but further well-designed, randomized, and placebo-controlled clinical studies are needed to assess their optimal dosages, efficacy, and long-term safety of flavonoids in humans. Obesity has also been linked to neurological diseases such as cognitive decline, dementia, and Alzheimer's disease (AD), caused by oxidative stress, pro-inflammatory cytokines, and the production of reactive oxygen free radicals (ROS). 37385075: In the present study, we reported a new phosphodiester containing diaminonaphthalene compound, POZL, designed to target the PPI interface using a structure-based design strategy to combat oxidative stress in AD pathogenesis. 37453560: Brain acetylcholine deficit and oxidative stress may be considered the key pathogenic causes for AD, even though the basic etiology is still unknown. 37465125: Oxidative stress in the brain is considered as one of the contributing factors to the pathogenesis of AD, and thus, antioxidants have attracted much interest as potential therapeutic agents against the disorder. 37516225: Amyloid fibrils are associated with various neurodegenerative diseases (ND) such as Alzheimer's disease (AD) and Parkinson's disease (PD), which are caused by oxidative stress and impaired protein homeostasis. 37718506: BACKGROUND: Oxidative stress is an early event in the development of Alzheimer's disease (AD) and maybe a pivotal point of interaction governing AD pathogenesis; oxidative stress contributes to metabolism imbalance, protein misfolding, neuroinflammation and apoptosis. 37962427: The redox-active metal ions, especially Cu 2+ , are highly correlated to Alzheimer's disease (AD) by causing metal ion-mediated oxidative stress and toxic metal-bound beta-amyloid (Abeta) aggregates. 37979715: This study provides evidence to support the essential roles of OS in pathogenesis of AD, and the application of Pls in relieving AD. 38057817: However, its effects on aluminum-induced AD model have not been studied much. A body of evidence suggest that oxidative stress and autophagy are involved in the pathogenesis of AD. 38251163: The primary pathological hallmark of Alzheimer's disease (AD) is the formation and accumulation of neurofibrillary tangles and plaques, which result from the aggregation of amyloid- beta (A beta ) induced by oxidative stress. 38396988: Oxidative stress is involved in the impaired clearance of amyloid beta (Abeta), and Abeta-induced oxidative stress causes AD by inducing the formation of neurofibrillary tangles. 38565372: Multiple complex pathways, such as oxidative stress, tau and amyloid-beta (Abeta) pathology, and cholinergic dysfunction, are involved in the pathogenesis of Alzheimer's disease. 38571463: It is one of the beneficial compounds used to prevent and treat the oxidative stress induced neurological disorders like stress, depression and Alzheimer's disease. 8871938: Despite a large amount of evidence that suggests an association between oxidative stress and the pathogenesis of AD, it is not yet known whether oxidative stress is a cause or consequence of the disorder. 8871940: We and other investigators recently demonstrated that several mechanisms related to oxidative stress and free-radical reactions could play a crucial role in the pathogenesis of AD and, specifically, in the formation of senile plaques and neurofibrillary tangles (NFT). 9562500: Recent studies have implicated increased oxidative stress in the pathogenesis of Alzheimer's disease (AD). 9887447: In this review article, we will discuss the evidence suggesting that estrogen may have a protective role against AD, mainly through its action as: a trophic factor for cholinergic neurons, a modulator for the expression of apolipoprotein E (ApoE) in the brain, an antioxidant compound decreasing the neuronal damage caused by oxidative stress, and a promoter of the physiological nonamyloidogenic processing of the amyloid precursor protein (APP), decreasing the production of the amyloid-beta-peptide (A beta), a key factor in the pathogenesis of AD. 10078973: Mutations in two related genes, presenilin 1 and presenilin 2 (PS1 and PS2), cause a subset of early-onset familial Alzheimer's disease (FAD). 10340748: Because distinct mutations in presenilin 1 and presenilin 2 are a major cause of early-onset familial Alzheimer's disease, we generated four monoclonal antibodies for the identification, localization, and investigation of presenilins in various cell lines and tissues from patients and controls. 22044463: BACKGROUND: Missense mutations in three different genes encoding amyloid-beta precursor protein, presenilin 1 and presenilin 2 are recognized to cause familial early-onset Alzheimer disease. 22702962: Mutations in genes such as those encoding amyloid precursor protein (APP), presenilin 1 and presenilin 2, are responsible for early-onset familial AD. 23142261: Mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) are responsible for early-onset autosomal dominant AD. 24838203: Mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) are responsible for early-onset autosomal dominant AD. 26141474: To date, mutations in three different genes, the Amyloid precursor protein (APP), Presenilin 1 (PS1), and Presenilin 2 (PS2), have been identified as causative in early-onset AD, making predictive testing possible. 30041064: Seizures have traditionally been related to neuronal loss in the late stages of AD as a consequence of neurodegeneration, however, recent studies indicated that seizures may contribute to the emergence of AD symptoms in early stages of the disease, mainly in familial AD. Mutations in genes encoding presenilin 1 (PSEN1), presenilin 2 (PSEN2) and amyloid precursor protein (APP) are responsible for early-onset familial AD (EOFAD). 31440394: Presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP) mutations are responsible for autosomal dominant early-onset Alzheimer's disease (AD-EOAD). 8878479: These results indicate that the presenilin mutations probably cause Alzheimer's disease through a gain of deleterious function that increases the amount of A beta42(43) in the brain. Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease. 12941610: Dominant mutations in presenilin1 (PS1) and presenilin2 (PS2) are a major cause of early-onset Alzheimer's disease. 18028191: L286P is a novel mutation in PSEN1 that causes familial early-onset AD and brain haematomas related to amyloid angiopathy. 20388456: CONCLUSIONS: E120G is a novel mutation in PSEN1 that probably causes early-onset autosomal dominant AD. 20955934: Positional cloning led to the identification of rare, disease-causing mutations in APP, PSEN1, and PSEN2 causing early-onset familial AD, followed by the discovery of APOE as the single most important risk factor for late-onset AD. 21094210: Biochemical, neuropathological, and neuroimaging characteristics of early-onset Alzheimer's disease due to a novel PSEN1 mutation. 25220527: Alzheimer's disease (AD) is the most common form of dementia characterized by deterioration of memory and other cognitive domains which leads to death in 3-9years after diagnosis. In addition to mutations in APP, PSEN1 and PSEN2 genes, that cause early onset autosomal dominant AD, several genetic risk factors for late onset AD are now known. 26830138: Over 200 highly penetrant pathogenic variants in the genes APP, PSEN1, and PSEN2 cause a subset of early-onset familial AD. 27274215: Linkage analysis was the first milestone in unraveling the mutations in APP, PSEN1, and PSEN2 that cause early-onset AD, followed by the discovery of apolipoprotein E-epsilon4 allele as the only one genetic risk factor for late-onset AD. 27535542: BACKGROUND: Pathogenic mutations in PSEN1 are known to cause familial early-onset Alzheimer's disease (EOAD) but common variants in PSEN1 have not been found to strongly influence late-onset AD (LOAD). 28131463: The Val391Gly variation widens the number of PSEN1 mutations responsible for early-onset Alzheimer's disease with extrapyramidal phenotype and would help to establish a functional map of presenilin 1 protein architecture. 29478590: Genetically, the first clues were provided by genetic linkage studies that led to the identification of APP, PSEN1, and PSEN2 mutations as the main causes of autosomal-dominant early-onset AD. 29562504: The subjects are carriers of the PSEN1 mutation, which leads to early onset Alzheimer's disease, but at the time of EEG acquisition in 1999, these subjects were cognitively unimpaired. 30168435: PSEN1, APP and PSEN2 are the major causes of monogenic EOAD while GRN, MAPT and C9ORF72 are the most frequently mutated genes in familial FTLD. 30909216: With the exception of rare mutations in APP, PSEN1, and PSEN2 genes causing autosomal dominant EOAD, little is known about the genetic factors underlying most of the EOAD cases. 31026686: The mutation E280A in PSEN1 (presenilin-1) is the most common cause of early-onset familial Alzheimer's Disease (fAD). 11093531: Thoracic paragangliomas are a rare cause of hypertension. 12381537: Pheochromocytoma and paragangliomas are rare tumors of chromaffin tissue that secrete catecholamines either intermittently or continuously, producing hypertension with a constellation of symptoms and signs that can be frightening to the patient and that continue to provide perplexing problems for clinicians. 12381541: Malignant pheochromocytomas, a group of tumors that include metastatic paragangliomas, often produce hypertension and episodic symptoms from secretion of norepinephrine and sometimes epinephrine. 15237491: A 35-year-old woman, who had a past history of hypertension due to paraganglioma of the urinary bladder and in the pelvis, was referred to us 12 years after the initial diagnosis of paraganglioma. 17142218: This report describes a patient with a rare primary functioning hepatic paraganglioma that resulted in hypertension. 18488156: Thus, in this report we present a 24-year-old female patient with onset of unregulated ectopic EPO secretion, and consecutive erythrocytosis followed by hypertension, secondary to paraganglioma of multifocal retroperitoneal localization. 22790652: Arterial hypertension caused by a paraganglioma is rare and approximately one third of all cases of paraganglioma occur as part of a hereditary syndrome. 24274233: Hypertension secondary to a periprostatic paraganglioma: case report and review of the literature. 24276837: Intracerebral hemorrhage was probably caused by severe hypertension due to paraganglioma. 29800631: However, when the tumor arises near the renal hilum, hypertension may also be secondary to renal artery stenosis, which can occur via several purported mechanisms. Classically, pheochromocytomas and paragangliomas result in hypertension secondary to an excess release of catecholamines. 31655773: Still, patients frequently come to the attention of endocrinologist when pheochromocytoma/paraganglioma is suspected as a secondary cause of hypertension. 35295164: Paraganglioma is a catecholamine-secreting tumor (CST) in extra-adrenal autonomic ganglia and a rare cause of hypertension during pregnancy. 36483865: She was found to have hypertension secondary to paraganglioma. 36856470: Pheochromocytoma and paraganglioma are rare causes of hypertension, estimated to explain 0.1-0.6% of all cases, but nonetheless an important diagnosis to make, due to serious side effects. 11684176: Experiment 2 compared letter fluency performance among NC, AD and IVD groups, and participants with dementia secondary to idiopathic Parkinson's disease (PD). 14722078: The genetic defects underlying several monogenic familial forms of AD and PD have recently been identified, however, the causes of other AD and PD cases, particularly sporadic cases, remain unclear. 20634620: Camptocormia can be due to central nervous system diseases, such as Parkinson's disease, dystonia, multisystem atrophy, or Alzheimer's disease, due to peripheral nervous system diseases, such as primary myopathy, secondary myopathy, motor neuron disease, myasthenia, or chronic inflammatory demyelinating polyneuropathy, due to side effects of drug treatment, due to disc herniation, arthritis or spinal trauma, or due to paraneoplasia. 23303475: The activity of metabotropic glutamate receptors (mGluRs) is known to be altered as the consequence of neurodegenerative diseases such as Alzheimer, Parkinson, and Huntington disease. 24503004: As the second most common age related neurodegenerative disease after Alzheimer's disease, the health, social and economic impact resulting from Parkinson's disease will continue to increase alongside the longevity of the population. 26528186: Neurodegenerative diseases such as Alzheimer's disease, Creutzfeldt-Jakob disease (CJD), Parkinson's disease, Huntington's disease, frontotemporal dementia (FTD), and amyotrophic lateral sclerosis (ALS) result from the loss of a specific subsets of neurons, which is closely associated with accumulation and deposition of specific protein aggregates. 27074540: Alzheimer's disease (AD) and Parkinson's disease (PD) are the leading causes of disability associated with neurodegeneration worldwide. 27166223: Impaired protein degradation has been discussed as a cause or consequence of various neurodegenerative diseases, such as Alzheimer's, Parkinson's and Huntington's disease. 27699087: Evidence from rodent and cell models show a number of neurotrophic and neuroprotective effects of guanosine preventing deleterious consequences of seizures, spinal cord injury, pain, mood disorders and aging-related diseases, such as ischemia, Parkinson's and Alzheimer's diseases. 28839167: The ultra-sensitive IMR assay was applied to detect the plasma tau protein levels of subjects with prevalent neurodegenerative diseases, such as Alzheimer's disease (AD), mild cognitive impairment (MCI) due to AD, Parkinson's disease (PD), frontotemporal dementia (FTD) and vascular dementia (VD). 30068225: This article reviewed the up-to-date evidence of MCI including the diagnostic criteria of MCI due to Alzheimer's disease, vascular cognitive impairment and MCI due to Parkinson disease, management and preventive intervention of MCI. 32107064: Choroid plexus volume is associated with levels of CSF proteins: relevance for Alzheimer's and Parkinson's disease.The choroid plexus (ChP) is a major source of cerebrospinal fluid (CSF) production, with a direct and indirect role in protein clearance, and pathogenesis of Alzheimer's disease (AD). 33417216: Therapeutic Efficacy of Plasmalogens for Alzheimer's Disease, Mild Cognitive Impairment, and Parkinson's Disease in Conjunction with a New Hypothesis for the Etiology of Alzheimer's Disease. 33621313: Of 4498 records identified, 17 articles met the inclusion criteria with a total of 979 participants including studies on mild cognitive impairment (MCI; n = 6), multiple sclerosis (n = 4), Alzheimer's disease (n = 5), Parkinson's disease (n = 1), and MCI secondary to Parkinson's disease (n = 1). 36717892: We summarize the impact of COVID-19 infection on symptom severity, disease progression, and mortality rate of PD and AD, and discuss whether COVID-19 infection could trigger PD and AD. 38036035: For AD and PD, an increased iron load was causative: the right pallidum for AD and the right caudate, left caudate and right accumbens for PD. 8033937: Lastly, degenerative cerebral diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, progressive supranuclear palsy and corticobasal degeneration result in more or less severe eye movement disturbances. 10909653: We investigated the possibility that a pathogenetic mechanism leading to glucocorticoid (GC)-induced hypertension or to mineralocorticoid (MC)-induced hypertension, or both, may be of critical importance in primary hypertension. 12025958: We conclude that B1 and B2 receptor mRNA are differentially expressed in the hypothalamus of SHR and may play different roles in the pathogenesis of hypertension: upregulation of B2 receptor mRNA from early age may participate in the pathogenesis of hypertension, whereas an upregulation of B1 receptor mRNA in the established phase of hypertension may reflect an epiphenomenon in essential hypertension. 13493221: [Data & hypothesis on the pathogenesis of hypertension in stenosis of the pathogenesis of hypertension in stenosis of the aortic isthmus]. 14709914: We propose strain-specific differences of stress reactivity as an important pathogenetic factor in psychosomatic disorders including stress-induced hypertension. 16207143: In this short editorial review, we summarize the recent experimental, clinical and epidemiological evidence that contributed to our understanding of the pathogenetic mechanisms that lead to hypertension associated with the alpha-adducin Gly460Trp polymorphism and its interaction with ouabain. 20026766: Although soluble fms-like tyrosine kinase 1 (sFlt-1), an antagonist of vascular endothelial growth factor and placental growth factor, has been implicated in the pathogenesis of hypertension during preeclampsia, the mechanisms whereby enhanced sFlt-1 production leads to hypertension remain unclear. 2504636: Disturbances of prostaglandin I2 (PGI2, prostacyclin) production by adipose tissue contribute to the pathogenesis of diabetic ketoacidosis and may contribute to the pathogenesis of hypertension and vascular disease. 36894160: While primary failure of trophoblastic invasion with incomplete maternal spiral artery remodeling has been considered central to the pathogenesis of pre-eclampsia, cardiovascular risk factors associated with abnormal first trimester maternal blood pressure and cardiovascular adaptation produce identical placental pathology leading to hypertensive pregnancy disorders. 37260264: BACKGROUND: Dysfunctional neurons and microglia in the rostral ventrolateral medulla (RVLM) have been implicated in the pathogenesis of stress-induced hypertension (SIH). 6839514: However, the increased reactivity to this compound in the adult hypertensive rats cannot be readily explained by the known pathogenetic factors leading to their hypertension. 7970077: There are three clinical stages of SOH: slight, moderate and severe, caused by a pathogenetic mechanism which is thought to involve the action of prostaglandins and the renin-angiotensin system leading to an alteration in capillary permeability with increased ovarian diameter. The use of gonadotropins in therapy has led to the appearance of a complication due to hyperstimulation, referred to as \syndrome due to ovarian hypertension\ (SOH). 8441251: BACKGROUND: The Dahl/Rapp strains of salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rat were developed to examine pathogenetic mechanisms that produce hypertension in response to an increase in dietary salt. 9198850: Therapy resistant forms of hypertension may be caused by many different pathogenetic mechanisms. 12446969: As evidence emerges concerning the role of insulin and insulin like growth factors (IGFs) in learning and memory, recent findings have suggested that insulin may have a significant role in the pathogenetic pathways leading to Alzheimer's disease (AD). 15760652: The pathogenesis, which is primarily responsible for Alzheimer's disease (AD) and cerebrovascular accidents (CVA), seems to involve chronic hypoperfusion. 16008818: Therefore the pathogenesis of Lytico-Bodig appears still to have most pertinence to the ongoing investigation of the pathogenesis of AD and other tauopathies. 17119287: The message between the lines of the following article is that the involvement of Al in the pathogenesis of AD should not be discarded, especially in these times when the amyloid dogma of AD etiology shows its myopia. Although objects of methodological controversies for scientists and oversimplification for lay spectators, several lines of evidence have strongly supported the involvement of Al as a secondary aggravating factor or risk factor in the pathogenesis of AD. 18827923: The pathogenesis that is primarily responsible for Alzheimer's disease (AD) and cerebrovascular accidents (CVA) appears to involve chronic hypoperfusion. 19114068: As one of the earliest pathologic changes, the aberrant re-expression of many cell cycle-related proteins and inappropriate cell cycle control in specific vulnerable neuronal populations in Alzheimer's disease (AD) is emerging as an important component in the pathogenesis leading to AD and other neurodegenerative diseases. Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease. 22610992: Given the potential relationship between insulin resistance and pathogenesis of Alzheimer's disease (AD) in elderly life, we investigated the relationship between perinatal DEHP exposure and AD pathogenesis. 22906543: The phosphoinositide 3-kinase (PI3K)/Akt pathway has been implicated in the pathogenesis of AD, however, potential functions and role of tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) in AD pathogenesis have not been fully explored. 23318673: Although the pathogenesis of sporadic Alzheimer's disease (AD) is not clearly understood, neuroinflammation has been known to play a role in the pathogenesis of AD. 23711354: Recent findings, however, have implicated altered function of ER-mitochondria contact sites and amyloid beta- and/or tau-induced defects in mitochondrial function and dynamics in the pathogenesis of AD, suggesting that mitochondrial defects may act as key mediators in the pathogenesis of AD as well. 23948893: The pathogenetic mechanism of Alzheimer's disease (AD) is still unknown; however, genetic variants play a critical role in the pathogenesis of AD. 25019275: Although the pathogenetic mechanism of AD is still unknown, genetic variants play a critical role in the pathogenesis of AD. 25809055: BACKGROUNDS AND AIMS: The pathogenetic mechanism of Alzheimer's disease (AD) is still unknown; however, gene polymorphism may play a critical role in the pathogenesis of AD. 26438898: The following topics are reviewed: a role of beta-amyloid in the pathogenesis of AD, a role of tau-protein in the pathogenesis of AD, main hypotheses of the pathogenesis, the relationship between beta-amyloid and tau-protein, the dysfunction of synapses in AD, a neuroimmune hypothesis, treatment approaches. 26849355: Alzheimer's disease (AD) is the most common cause of senile dementia. Sphingolipids are widely known to have roles in the pathogenesis of inflammatory diseases, where the precise roles for sphingolipids in inflammation-associated pathogenesis of AD are not well understood. 28745240: CONCLUSION: In light of our understanding of the duality of the role of NF-?B in the pathogenesis of Alzheimer's disease, further studies are warranted to dissect and understand the basis of the dichotomous effects of NF-?B, so that certain selective benevolent and benign attributes of NF-?B can be spared while targeting its deleterious attributes and facets that are integral in the pathogenesis of Alzheimer's disease. 30362531: This review highlights the critical linkage of autophagy in the pathogenesis of AD, and avows a new insight to search for therapeutic target for blocking Alzheimer's pathogenesis. Autophagic dysfunction in Alzheimer's disease: Cellular and molecular mechanistic approaches to halt Alzheimer's pathogenesis. 35282779: This review will highlight the pathogenesis of each of the stated microbial infection, their association in AD pathogenesis as well as the effect of chronic infection in AD progression. 36071897: Currently, the pathogenesis and underlying causative genes of AD remain unclear, and there exists no effective treatment for this disease. 36291068: The amyloid cascade hypothesis has predominately been used to describe the pathogenesis of Alzheimer's disease (AD) for decades, as Abeta oligomers are thought to be the prime cause of AD. 37163426: These results not only provide a retrospective interpretation for understanding the pathogenesis of AD, but also provide a window of opportunity for more effective preventive and identifying therapeutic strategies for stress-induced AD. 38450383: Animal models have provided important insights into the pathogenesis of AD and they have shown that different brain cell types including neurons, astrocytes and microglia have important functions in the pathogenesis of AD. 38474398: Firing Alterations of Neurons in Alzheimer's Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? 7763324: As we begin to understand some of the underlying pathogenetic mechanisms and causes of AD, this most frequent dementing condition is well suited to serve as model system to study the common principles of neurodegenerative diseases. 9539218: These results suggest that the co-injection of beta-amyloid with a small amount of ibotenic acid provides a useful model for investigation of the pathogenetic mechanisms leading to Alzheimer's disease. 9577653: Now that major genes involved in the pathogenesis of AD have been identified, future research should be directed toward elucidation of the molecular mechanisms of how these gene products are involved in the pathogenesis of AD on protein as well as cellular levels. 12914680: Although criteria for MCI are not a matter of secure agreement, a consensus is emerging that MCI is common, is associated with significant mortality and morbidity, particularly the development of AD, and is due, in large part, to the same pathologic processes responsible for Alzheimer's disease (AD). 14520653: Our findings support the hypothesis that reductions in estrogens after menopause contribute to the cascade of pathological processes leading to AD. 16926067: Our findings support the hypothesis that reductions in estrogen following menopause can contribute to the cascade of pathological processes leading to AD. 17000013: Lipoprotein receptors have important roles in pathological processes that lead to Alzheimer's disease (AD). 17168651: Since the pathological processes leading to AD are seen across the lifespan in DS, an opportunity is afforded for early pharmacological intervention in the disorder. 18537547: Although cholinergic cell loss is clearly an important attribute of the pathological process, another well-described yet underappreciated early feature of AD pathogenesis is degeneration of the locus coeruleus (LC), which serves as the main source of norepinephrine (NE) supplying various cortical and subcortical areas that are affected in AD. 19028146: This has contributed to the hypothesis that the menopause may contribute to the cascade of pathological processes leading to AD. 20182019: Evidence accumulating from biological and epidemiological studies suggests that high levels of serum cholesterol may promote the pathological processes that lead to Alzheimer's disease (AD). 22315714: As cause and effect relationships between inflammation and AD are being worked out, there is a realization that some components of this complex molecular and cellular machinery are most likely promoting pathological processes leading to AD, whereas other components serve to do the opposite. 22465174: Pretangle formation marks the beginning of the pathological process and is of particular interest because it is temporally closer to the prevailing conditions that induce the pathological process underlying Alzheimer's disease in contrast to late-stage disease. 22521584: These results suggest that alterations in the SM metabolism may contribute to early pathological processes leading to AD. 22699850: The formation of non-argyrophilic pretangles marks the beginning of the pathological process and is of increasing interest because it is temporally closer to the prevailing conditions that induce the pathological process underlying AD in contrast to late-stage disease. 22700814: CONCLUSIONS: The lack of fibrillar beta-amyloid (Abeta) as visualized by PiB PET in APParc mutation carriers suggests, given the reduced glucose metabolism and levels of Abeta(1-42) in CSF, that other forms of Abeta such as oligomers and protofibrils are important for the pathologic processes leading to clinical Alzheimer disease. 23553131: More than 100 years after description of Alzheimer's disease (AD), two major pathological processes observed already by Alois Alzheimer, remain as the main explanation of the pathogenesis of Alzheimer's disease. 23701948: We argue that the interaction between the APOE-dependent non-pathological vulnerabilities and age-related pathological changes is one mechanism that can trigger neurodegeneration, resulting in AD and other complex phenotypes. However, the biological mechanisms underlying this association are still unclear because of the complexity of the pathological processes that cause AD. 24796109: It is understood that molecules involved in this inflammation promote pathological processes leading to AD, whereas other molecules work to protect neuron/brain function from toxicity found in AD pathogenesis. 26547034: Recent studies show that the pathological processes leading to AD cause characteristic alterations in blood and brain inflammatory proteins that are associated with the progression of AD, suggesting that these markers could be used to diagnosis and monitor disease progression. 27454811: IMPORTANCE: The amyloid hypothesis posits that disrupted beta-amyloid homeostasis initiates the pathological process resulting in Alzheimer disease (AD). 28760504: Alzheimer's disease (AD), which is the most commonly encountered neurodegenerative disease, causes synaptic dysfunction and neuronal loss due to various pathological processes that include tau abnormality and amyloid beta (Abeta) accumulation. 28939668: CONCLUSIONS: Synaptic dysfunction (assessed via neurogranin) may be an early pathologic process in age-related neurodegeneration, and a sensitive marker of age-related cognitive abilities, potentially preceding or even acting independently from AD pathogenesis. 28993728: Future studies conducting comprehensive and integrative characterization of brain aging, including crosstalk with peripheral systems and factors, will be necessary to define the mechanisms underlying the shift from normal aging to pathological processes in the etiology of AD. 29150293: It is felt that the main reason for this failure is that AD appears to be a disease caused by four major pathological processes. The four major pathologic processes causing AD are: I. vascular hypoperfusion of the brain with associated mitochondrial dysfunction. 30805871: beta-secretase (BACE1) and its naturally occurring anti-sense RNA (BACE1-AS) have established role in the pathologic process leading to Alzheimer's disease. 31453786: BACKGROUND: Growing evidence suggests that pathological processes leading to Alzheimer's disease occurs gradually and begins to develop decades before the earliest clinical symptoms occur. 33268824: It is generally believed that AD is caused by multiple pathological processes resulting from Abeta abnormality, tau phosphorylation, neuroinflammation, neurotransmitter dysregulation, and oxidative stress. 35557359: Previous research has demonstrated that the pathological process leading to AD occurs years before a positive diagnosis. 37126689: Impairment of its vesicular release by beta-amyloid (Abeta) oligomers is thought to participate in pathological processes leading to Alzheimer's disease. 38396302: We review here the structure, function, and pathobiology of gamma-secretases, with a focus on how mutations in presenilin genes result in early-onset AD. The GSAS represent, in theory, a precision medicine approach to the prevention of amyloid deposition, as they specifically target a discrete aspect in a complex cell biological signalling mechanism that initiates the pathological processes leading to Alzheimer's disease. 8375434: Because of the compelling evidence indicating common clinical and pathological findings in idiopathic parkinsonism, Alzheimer's disease, and amyotrophic lateral sclerosis, we believe that these conditions result from pathological processes with more similarity than diversity. 10196523: Here we review genetic and molecular biological evidence suggesting that the peptide A beta 42 is central to the etiology of AD. 10440895: Substantial genetic and biochemical evidence implicates amyloid peptides (Abeta) in the etiology of Alzheimer's Disease (AD). 10825171: beta-(25-35) is a synthetic derivative of beta-amyloid, the peptide that is believed to cause Alzheimer's disease. 10940223: beta-Amyloid peptides are the main protein components of neuritic plaques and may be important in the pathogenesis of Alzheimer's Disease. 11409035: The extracellular deposition of short amyloid peptides in the brain of patients is thought to be a central event in the pathogenesis of Alzheimer's Disease. 11437372: Time-resolved anisotropy measurements (TRAMS) have been used to study the aggregation of the beta-amyloid (Abeta) peptide which is suspected of playing a central role in the pathogenesis of Alzheimer's Disease (AD). 11544033: In the case of amyloid precursor protein, this cleavage contributes to the generation of small, toxic amyloid peptides that trigger the pathological development of Alzheimer's disease. 11606220: Beta-amyloid peptides (Abeta) are the main protein components of neuritic plaques and are important in the pathogenesis of Alzheimer's disease. 12182949: Here, we demonstrated that PACAP also protected against neuronal toxicity induced by beta-amyloid (Abeta) peptide, aggregation of which is a causative factor for Alzheimer's disease. 12414694: Neuronal plasma membranes are thought to be the primary target of the neurotoxic beta-amyloid peptides (Abeta) in the pathogenesis of the Alzheimer's disease. 12435726: Presenilins (PS1/PS2) play a critical role in proteolysis of beta-amyloid precursor protein (beta APP) to generate beta-amyloid, a peptide important in the pathogenesis of Alzheimer's disease. 12475558: The Abeta(1-42) peptide is widely considered to be of greatest significance in relation to the pathogenesis of Alzheimer's disease. 14766758: The proteolytic processing of the precursor of the beta-amyloid peptides (APP) is believed to be a key event in the pathogenesis of Alzheimer's disease. 15126696: Data that have accumulated for well over a decade have implicated the beta-amyloid (Abeta) peptide as a central player in the pathogenesis of Alzheimer's disease (AD). Amyloid plaques, composed primarily of Abeta progressively form in the brains of AD patients, and mutations in three genes (amyloid precursor protein [APP] and presenilin 1 and 2 [PS1 and PS2]) cause early-onset familial AD (FAD) by directly increasing production of the toxic, plaque-promoting Abeta42 peptide. 15211591: The beta-amyloid peptides derived by proteolytic cleavage from the amyloid precursor protein (APP) play a major role in the pathogenesis of Alzheimer's disease (AD) by forming aggregated, fibrillary complexes that have been shown to be neurotoxic. 15248287: This cleavage is responsible for a key biochemical step in signaling from several different cell-surface receptors, and it is also crucial in generating the neurotoxic amyloid peptides that are central to the pathogenesis of Alzheimer's disease. 15314264: Because accumulation of beta-amyloid (Abeta) peptide appears central to AD pathogenesis, large efforts have been directed at understanding and interfering with Abeta production or aggregation. 15326604: In the present study the transition from ideal alpha-helical to beta-hairpin conformations is revealed by long timescale molecular dynamics simulations in explicit water solvent, for two well-known amyloidogenic peptides: the H1 peptide from prion protein and the Abeta(12-28) fragment from the Abeta(1-42) peptide responsible for Alzheimer's disease. 15544501: These studies together with findings that A beta is neurotoxic in vitro, provide evidence that some aggregates of this peptide are the key to the pathogenesis of AD. A small fraction of early onset familial AD (FAD) is caused by mutations in genes, such as the beta-amyloid precursor protein (APP) and presenilins that increase the load of A beta in the brain. 15878503: The polymerization of beta-amyloid (A beta) peptides into fibrillary plaques is implicated, in part, in the pathogenesis of Alzheimer's disease. 15909112: Peptides derived from proteolytic processing of the amyloid precursor protein (APP) are important for the pathogenesis of Alzheimer's disease (AD). 16033885: Accumulation of beta-amyloid (Abeta) peptides in the cerebral cortex is considered a key event in the pathogenesis of Alzheimer's disease (AD). 16830133: The data are also consistent with the concept that a focally dysfunctional blood-brain barrier (BBB) that is unable to regulate the influx/efflux of neurotoxic amyloid peptides may participate in the pathogenesis of AD lesions. 16880006: Beta-amyloid peptides (Abeta) have been genetically implicated as the cause of Alzheimer's disease, but the causality of amyloid deposited as plaques has been challenged. 17276414: Disruption of this homeostasis due to aging, injury or toxicant exposure may contribute to accumulation of beta-amyloid peptides in the brain fluids, leading to AD. 17348862: Excessive production and/or accumulation of beta-amyloid (Abeta) peptides that are proteolytically derived from the beta-amyloid precursor protein (APP) have been linked to the pathogenesis of AD. 17385278: Reportedly, beta-amyloid peptides (Abeta40 and Abeta42) induce the neurodegenerative changes of Alzheimer's disease (AD) both directly by interacting with components of the cell surface to trigger apoptogenic signaling and indirectly by activating astrocytes and microglia to produce excess amounts of inflammatory cytokines. 17559680: Mutations in amyloid precursor protein (APP) and presenilins alter APP metabolism resulting in accumulation of Abeta42, a peptide essential for the formation of amyloid deposits and proposed to initiate the cascade leading to AD. 17881287: Cellular cholesterol accumulation enhances the deposition of insoluble beta-amyloid peptides, which is considered a hallmark in the pathogenesis of AD. 18220930: In particular, a selective reduction of the longer Abeta(1-42) peptide which is widely believed to be causative of AD is currently seen as an attractive approach for a disease-modifying therapy. 18221260: AIMS: The deposition of amyloid peptides (A beta) in the cortex and hippocampus is the primary trigger of Alzheimer's disease (AD). 18232509: Extensive studies suggest that the conversion of beta-amyloid (Abeta) peptide from soluble forms into fibrillar structure is a key factor in the pathogenesis of Alzheimer's disease (AD). 18284028: Amyloid beta (Abeta) is a peptide integral in the pathogenesis of AD. 18341423: The most studied hypothesis of development of the disease is that of the amyloid cascade, which states that overproduction of amyloid-beta peptide, or failure to clear this peptide, leads to Alzheimer's disease primarily through amyloid deposition, which is presumed to be involved in neurofibrillary tangle formation; these lesions are then associated with cell death, which is reflected in memory impairment, the hallmarks of this dementia. 18544674: Increasing evidence suggests that the elevation of beta-amyloid (Abeta) peptides in the brain is central to the pathogenesis of Alzheimer's disease (AD). 18634756: Androgen deprivation increases plasma Abeta levels, which indicate that androgens may reduce the levels of soluble Abeta, the peptide widely implicated in the initiation of AD pathogenesis; however, the underlying mechanisms are still poorly understood. 19237574: Insulin modulates metabolism of beta-amyloid precursor protein (APP) in neurons, decreasing the intracellular accumulation of beta-amyloid (Abeta) peptides, which are pivotal in AD pathogenesis. 19238376: A peptide with 42 amino acid residues (Abeta42) plays a key role in the pathogenesis of the Alzheimer's disease. 19442147: It is believed that the production and accumulation of beta-amyloid (Abeta) peptide is a critical step to the pathogenesis of Alzheimer's disease (AD). 19509405: Excessive production of beta-amyloid (Abeta) peptides from proteolytic cleavage of amyloid precursor protein is believed to play a central role in the pathogenesis of Alzheimer's disease (AD). 19595795: Thus, the aggregation kinetics of these peptides is central to understanding the etiology of AD. 19939231: Pathological, genetic, biochemical and pharmacological studies support the hypothesis that brain accumulation of oligomeric species of beta-amyloid (Abeta) peptides may cause Alzheimer's disease (AD). 20371995: Increasing evidence suggests that the elevation of beta-amyloid (Abeta) peptides in the brain is central to AD pathogenesis. 20388523: The amyloid cascade hypothesis states that overproduction of amyloid-beta peptide (Abeta/AbetaP) or failure to clear this peptide, leads to Alzheimer's disease (AD) primarily through amyloid deposition, presumed to be involved in neurofibrillary tangle formation; these lesions are then associated with cell death which is reflected in memory impairment, the hallmarks of this dementia. 20418805: The anomalous folding and polymerization of the beta-amyloid (Abeta) peptide is thought to initiate the neurodegenerative cascade in Alzheimer's disease pathogenesis(1). 21383152: Amyloid-beta (Abeta), a peptide central to the pathogenesis of AD, has profound vascular effects mediated, for the most part, by reactive oxygen species produced by the enzyme NADPH oxidase. 21740063: The latter could represent a two-dimensional (2D) seeding template for the formation of toxic oligomeric Abeta in the pathogenesis of AD. Interactions of beta-amyloid (Abeta) peptides with neuronal membranes have been associated with the pathogenesis of Alzheimer's disease (AD); however, the molecular details remain unclear. 21813692: The concentration of amyloid-beta (Abeta) within the brain extracellular space is one determinant of whether the peptide will aggregate into toxic species that are important in Alzheimer's disease (AD) pathogenesis. 21855336: Aggregation and fibril formation of beta-amyloid peptides (Abeta) is the key event in the pathogenesis of Alzheimer's disease. 21889458: Assembly of beta-amyloid (Abeta) peptide into toxic oligomers is widely believed to initiate Alzheimer's disease pathogenesis. 21939202: The beta amyloid (Abeta) peptide aggregates to form beta-rich structures that are known to trigger Alzheimer's disease. 22206488: Alzheimer's disease (AD) is characterized by pathological aggregation of beta-amyloid peptides and MAP-Tau protein. beta-Amyloid (Abeta) is a peptide responsible for extracellular Alzheimer's plaque formation. 22351782: Accumulation of the neurotoxic beta-amyloid (Abeta) peptide in the brain is central to the pathogenesis of Alzheimer disease. 22468783: In addition, the behavioral deficits accompanying Abeta(1-40)-induced AD were attenuated by inhalation of EOCO. OBJECTIVE: The aggregation and formation of beta-amyloid peptides (Abeta) into fibrils are central events in the pathogenesis of Alzheimer's disease (AD), and overproduction and aggregation of Abeta into oligomers have been known to trigger neurotoxicity. 22552903: One important CSF biomarker is the amyloid beta 42 (Abeta(42)) peptide, a key player in AD pathogenesis. 22610977: Aggregated amyloid peptides (AP), major components of senile plaques, have been considered to play a very important and crucial role in the development and neuro-pathogenesis of Alzheimer's disease (AD). 22711819: The aggregation and deposition of amyloid-beta (Abeta) peptides are believed to be central events in the pathogenesis of Alzheimer's disease (AD). 22947874: The amyloid-beta(25-35) peptide plays a key role in the etiology of Alzheimer's disease due to its extreme toxicity even in the absence of aging. 23245572: Aggregation and fibril formation of beta-amyloid peptides (Abeta) are central events in the pathogenesis of AD. 23262458: Aggregation of amyloid-beta (Abeta) peptides into oligomers and amyloid plaques in the human brain is considered a causative factor in Alzheimer's disease (AD). 23410038: The subsequent release of Abeta (amyloid beta) peptides is thought to be the major cause of the neurodegenerative Alzheimer's disease. 23425062: INTRODUCTION: Genetic, physiological, and biochemical data indicate that agglomerates of the 42-amino acid form of the amyloid-beta (Abeta(42)) peptide are strongly linked to Alzheimer's disease (AD) etiology and thus represent a particularly attractive target for the development of an effective disease-modifying approach for AD treatment. 23573456: Substantial evidence implicates beta-amyloid (Abeta) peptides in the etiology of Alzheimer's disease (AD). 23614719: Amyloid-beta (Abeta) peptides represent key players in the pathogenesis of Alzheimer's disease (AD), and mounting evidence indicates that soluble Abeta oligomers mediate the toxicity. 23708321: Aggregation of the beta-amyloid (Abeta) peptide into toxic oligomers is considered the primary event in the pathogenesis of Alzheimer's disease. 23719722: These results, in conjunction with the finding that insulin mitigates hippocampal synapse vulnerability to beta amyloid, a peptide thought to be causative in the development of AD, provide a strong rationale for hypothesizing that pharmacological strategies bolstering brain insulin signaling, such as intranasal administration of insulin, could have significant potential in the treatment and prevention of AD. 24192706: BACKGROUND: Accumulation of beta-amyloid peptides (Abeta) and its progressive deposition into amyloid plaques are key events in the aetiology of Alzheimer's disease (AD). 24410826: The beta-amyloid (Abeta) peptide has been postulated to be a key determinant in the pathogenesis of Alzheimer's disease (AD). 25504599: Copper-amyloid peptides are proposed to be the cause of Alzheimer's disease, presumably by oxidative stress. 25621019: beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the beta-secretase enzyme required for the production of the neurotoxic beta-amyloid (Abeta) peptide that is widely considered to have a crucial early role in the etiology of Alzheimer's disease (AD). 25809804: A growing body of evidence suggests that beta-amyloid peptides (Abeta) are unlikely to be the only factor involved in Alzheimer's disease (AD) aetiology. 26749845: In this study, we first provided evidence that A. arborescens extract protects IMR32, a neuroblastoma human cellular line, from toxicity induced by beta amyloid, the peptide responsible for Alzheimer's disease. 26827638: There is a vast literature on the role of beta amyloid (Abeta) peptides in the pathogenesis of Alzheimer's disease. 27030769: The accumulation of amyloid-beta (Abeta) peptides cleaved from amyloid precursor protein (APP) in the brain is a key event in AD pathogenesis and we also found that ABCA7 deficit exacerbated brain Abeta deposition in amyloid AD model APP/PS1 mice. 27044452: Over the past two decades, many studies have identified significant contributions of toxic beta-amyloid peptides (Abeta) to the etiology of Alzheimer's disease (AD), which is the most common age-dependent neurodegenerative disease. 27118677: This is important for understanding the Abeta25-35-Flavonoid (A-F) interaction as a therapeutic strategy to inhibit the neurotoxic effects that this peptide causes in AD, which currently is still considered an ambiguous process. 27565738: (A?) peptide, a key protein in Alzheimer's disease pathogenesis. 27721583: PURPOSE: This study is aimed at investigating the mechanism of reserpine action, which alleviates the toxicity of amyloid beta (Abeta) (AD-causing peptide) in Caenorhabditis elegans [1, 2]. 27807285: beta-Amyloid (Abeta) peptides are thought to be critically involved in the etiology of Alzheimer's disease (AD). 28145081: AIMS: To clarify the correlation between chronic sleep restriction (CSR) and sporadic Alzheimer disease (AD), we determined in wild-type mice the impact of CSR, on cognitive performance, beta-amyloid (A?) peptides, and its feed-forward regulators regarding AD pathogenesis. 28193770: Aggregation of the beta-amyloid (Abeta) peptide within the brain is thought to be an initiating event in AD pathogenesis. 28795459: The oligomerization and fibrillation of beta-amyloid (Abeta) peptides are important events in the pathogenesis of Alzheimer's disease. 28978359: (A?) peptides in plaques in the brain parenchyma and in cerebral blood vessels is considered to be a key event in Alzheimer's disease (AD) pathogenesis. 29337241: In conclusion, elevated brain Abeta levels and Abeta42:40 ratio apparent in the early stages of AD could perturb intraneuronal trafficking, augment the anomalous accumulation of amyloid peptides in AD brain, and drive AD pathogenesis. 2950070: The following account traces the history of NPY and appraises some of the literature in an attempt to raise some speculation concerning its function; several reviews on this peptide already exist (Emson and de Quidt 1984; Solomon 1985; Allen and Bloom 1986; Gray and Morley 1986), Particular attention is paid to studies which have recently suggested that NPY might be involved with the pathogenesis of two neurodegenerative disorders, Huntington's chorea and Alzheimer's disease. 29568268: Both peptides show enhanced aggregation and neurotoxicity in comparison to full-length Abeta, suggesting that these amyloid peptides may play an important role in the pathogenesis of AD. 30605056: We review the role of the most important proteins and peptides in AD pathogenesis. 30624452: Fibrillation of amyloid peptides induces human diseases such as Alzheimer's disease, which has become a huge challenge. 31048034: Pre-administered IP before an ICV injection of amyloid Abeta25-35 peptide, a pharmacological model of Alzheimer's disease, OZP002 prevented the learning deficits induced by the peptide after one week in the Y-maze, passive avoidance and novel object tests. 31138770: Compelling evidence implicates self-assembly of amyloid-beta (Abeta 1-42) peptides into soluble oligomers and fibrils as a major underlying event in Alzheimer's disease (AD) pathogenesis. 31749959: Failure to clear these peptides appears to cause the development of Alzheimer's disease (AD). 32093407: One- and Two-Electron Oxidations of beta-Amyloid 25-35 by Carbonate Radical Anion (CO 3 *- ) and Peroxymonocarbonate (HCO 4 - ): Role of Sulfur in Radical Reactions and Peptide Aggregation.The beta-amyloid (Abeta) peptide plays a key role in the pathogenesis of Alzheimer's disease. 32827572: Accumulation of amyloid peptides in the brain plays a key role in the pathogenesis of Alzheimer's disease (AD). 32845146: The Abeta 21-30 peptide fragment is a decapeptide fragment of the complete Abeta42 peptide which is a hypothesized cause of Alzheimer's disease via amyloid fibrillogenesis. 32857496: Deposition and aggregation of beta-amyloid (Abeta) peptides are demonstrated to be closely related to the pathogenesis of Alzheimer's disease (AD). 32973564: Though accumulation of neuron-derived Abeta peptides is considered the primary influence driving AD and CAA pathogenesis, recent studies highlighted the importance of the physiological role of the beta-amyloid precursor protein (APP) in endothelial cell homeostasis, suggesting a potential role of this protein in maintaining vascular stability. 33642533: Extracellular Zn 2+ dynamics, which serves bidirectionally and involved in cognitive activity and cognitive decline, is modified by extracellular glutamate signaling and the presence of amyloid-beta 1-42 (Abeta 1-42 ), a causative peptide in Alzheimer's disease (AD) pathogenesis. 33668038: Extracellular aggregation of the beta-amyloid (Abeta) peptide into toxic multimers in the brain is a prominent event occurring in the pathogenesis of Alzheimer's disease (AD), and a large amount of Abeta in the blood is derived from platelets. 33959916: These small peptides are attributed to the pathogenesis of both AD and CAA, suggesting an important index for disease stage and progression. 34219248: Age, hypercholesterolemia, and vitamin D deficiency are risk factors that increase the brain accumulation of pathogenic beta-amyloid peptides (40 and 42), precursors leading to Alzheimer's disease (AD) in humans. 34669098: Moreover, plant-based foods containing flavonoids were previously reported to show neuroprotective effects by modulating self-aggregation of amyloid-beta (Abeta)/or tau peptide into oligomers and fibrils, associated with the pathogenesis of AD. 34852746: BACKGROUND: Alzheimer's disease (AD) is a chronic neurodegenerative disease where no specific disease-modifying treatment is currently available. beta-secretase (BACE1) is considered the potential and rationale target because it is involved in the rate-limiting step, which produces toxic Abeta42 peptides leading to deposits in the form of amyloid plaques extracellularly leading to AD. 35006003: This study provides new molecular leads on altered protein dynamics relevant to neurodegeneration, neuroplasticity, and AD progression induced by Abeta42 toxicity. Production and deposition of beta-amyloid peptides (Abeta) are among the major hallmarks of the pathogenesis of Alzheimer's disease (AD). 35109277: ApoE binds to Sortilin, which mediates uptake of ApoE containing lipoproteins into neurons, and to amyloid-b (Ab) peptide, which is thought to play important roles in the pathogenesis of AD. 35263093: Aggregation of beta-amyloid (Abeta42) peptide in the neural extracellular space leads to cellular dysfunction, resulting in Alzheimer's disease (AD). 35309680: Methods: Intracerebroventricular amyloid-beta [Abeta(1-42)] peptide was used to induce AD in Abeta rats. 35908946: Furthermore, human Abeta 1-42 , a causative peptide in Alzheimer's disease pathogenesis captures extracellular Zn 2+ and readily taken up into hippocampal neurons followed by intracellular Zn 2+ dysregulation. 36641678: To date, conflicting pathogenic and neuroprotective roles for this peptide and its analogs for AD pathogenesis have been described. 37076912: CONCLUSIONS: In conclusion, 5-mer peptides prevent short-term memory deficit in Abeta25-35 induced AD model mouse by reducing the aggregated Abeta25-35. 37214891: Aggregation of Abeta peptides has been known as a key contributor to the etiology of Alzheimer's disease. 37265546: Aggregation of Abeta peptides is an initial event of AD pathogenesis. 37413816: Aggregation of Abeta peptides is a key contributor to the etiology of Alzheimer's disease. 37625763: Amyloid beta (Abeta), a peptide produced by the proteolytic processing of amyloid precursor protein (APP), is known as a key mediator of brain damage involved in the pathogenesis of Alzheimer's disease (AD). 37741318: AIMS: Evidence indicates accumulating Abeta peptides in brain activates immune responses in neuronal and peripheral system, which may collaboratively influence pathogenesis of Alzheimer's disease (AD). 38142891: This review briefly elaborates on the pathogenesis of AD and analyzes the regulatory effects of endogenous and exogenous peptides on the pathogenesis of AD, thereby providing new therapeutic targets for AD and a theoretical basis for the application of bioactive peptides as adjunctive therapies for AD. 38241093: Beta amyloid peptide Abeta 1-42 (Abeta42) has a unique dual role in the human organism, as both the peptide with an important physiological function and one of the most toxic biological compounds provoking Alzheimer's disease (AD). 38292476: The self-assembly of Abeta peptides into toxic oligomers and fibrils is the primary cause of Alzheimer's disease. 38578892: However, the poor track record of clinical trials based on this hypothesis suggests that the accumulation of these peptides is not the only cause of AD. 38630150: In the present study, we firstly found that Abeta peptides induced AD-like neuroinflammation upregulation and downregulated the level of autophagy. 11062294: Plasma ACE activity was determined before the induction of hypertension. 12517680: Assuming that this is a low-renin model of hypertension, the protective effect of OMA may be due to an increase in vasodilator peptides produced by both ACE and NEP inhibition. 1338766: We have found no evidence to support linkage between the ACE locus and hypertension, which suggests that mutations at the ACE locus do not commonly contribute to the pathogenesis of hypertension in our test population. 15451554: This study assessed the alterations of circulatory and tissue angiotensin converting enzyme (ACE) activity during development of lead induced hypertension. 1659958: This study was undertaken to examine the possibility that the level of angiotensin-converting enzyme (ACE) increases in vascular tissue, and that this may participate in the pathogenesis of hypertension in spontaneously hypertensive rat (SHR). 16671560: Activity of angiotensin-converting enzyme in hereditary stress-induced arterial hypertension. 21115616: Intrarenal angiotensin-converting enzyme induces hypertension in response to angiotensin I infusion. 27468663: BACKGROUND: Angiotensin-1-converting enzyme (ACE) is a crucial player in vascular homeostasis and in the pathogenesis of atherosclerosis and hypertension. 28770441: Genetic predisposition to the risk of developing hypertension due to angiotensin-converting enzyme (ACE) gene insertion(I)/deletion(D) polymorphism (through altered serum ACE activity) is well documented among various populations. 2983030: The low activity of ACE in the cerebral microvessels of young SHR indicates that in this animal model of hypertension the function of ACE is genetically altered in the cerebral microvessels, which may be correlated with the alteration of the cerebral microcirculation and pathogenesis of hypertension. 30059342: The role of angiotensin-converting enzyme (ACE) in both hypertensive and fibrotic conditions suggests ACE may be a common mechanism for the pathogenesis of both hypertension and keloids. 3038407: Possible role of vascular angiotensin converting enzyme in the genesis of hypertension. 31802381: Angiotensin converting enzyme (ACE) gene has emerged as an important player in the pathogenesis of hypertension and consequently stroke. 35655475: The renin-angiotensin system (RAS) is involved in body fluid regulation, but one of its enzymes, angiotensin-converting enzyme (ACE), indirectly causes hypertension by constricting blood vessels. 36245815: Angiotensin converting enzyme (ACE) is a key enzyme and mediator in the aetiology of high blood pressure (HBP) and hypertension. 7739115: The Angiotensin I-converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular diseases. 7955173: BACKGROUND: The angiotensin I-converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular disease. 8065033: The Angiotensin I-converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular diseases. 8258668: However, we found no support for the hypothesis that vascular ACE is responsible for high blood pressure in SHRSP. 8704029: A positive correlation with angiotensin converting enzyme activity in hypertensive patients was demonstrated and this further supports the possible involvement of prolyl oligopeptidase in the renin-angiotensin system and in the pathogenesis of hypertension. 13002117: Establishment of hypertension in rats; hypertension caused by perinephritis. 15435010: [Greater frequency of hypertension caused by perinephritis or desoxycorticosterone in the diabetic rat]. 213977: PRA significantly decreased after the production of perinephritis and decreased somewhat further during the induction period of the hypertension after contralateral nephrectomy. 2448370: Uptake of 45Ca was measured in rings of thoracic aorta from rabbits with hypertension, induced by cellophane perinephritis (Page hypertension: one-kidney, one wrap). 2955170: This collagen skeleton was studied at three periods of perinephritis-induced hypertension with hypertrophy: at 4 weeks (evolutionary); at 32 weeks with mild to moderate hypertension (early compensatory); and at 80 weeks with moderately severe hypertension (late compensatory). 5674509: [Angiographic and microangiographic study of the kidney druing the development of hypertension due to sclerous perinephritis in dogs]. 7378120: Young pigs with hypertension of 10 weeks duration, resulting from cellophane perinephritis, were injected with 125I-labelled low-density lipoprotein ([125I]LDL) before being killed 24 h or 48 h later. 7919055: Hypertension and left ventricular hypertrophy was induced by unilateral nephrectomy plus wrapping of the contralateral kidney in cellophane. This study has shown that hypertension induced by perinephritis caused left ventricular hypertrophy which was associated with a prolongation in ventricular refractoriness in the rabbit. 9100054: We suggest that this case is a new example of hypertension secondary to constrictive perinephritis (Page kidney). 967886: These studies provide strong evidence that the renin-angiotensin system is not involved in maintaining the elevated arterial pressure in dogs with chronic hypertension produced by cellophane perinephritis. 9740170: Page kidney is the name ascribed to a rare syndrome of hyperreninemic hypertension caused by unilateral compressive perinephritis. 99915: [The beagle as a hypertensive animal. Experimental hypertension due to aseptic perinephritis]. 10684495: BACKGROUND: Restraint-stress and administration of drugs that precipitate hypertension induce heat-shock protein (HSP) expression in the aorta. 11318279: The risks to the patient's well-being increase with the addition of systemic medication, and long-term steroid use can cause hypertension, induce or exacerbate diabetes, cause premature osteoporosis, cushingoid features, peptic ulceration and aseptic necrosis of the femoral head. 11468997: [Secondary forms of hypertension, 3: Hypertension caused by drugs]. 1221278: However, close patient supervision is essential when these drugs are used as they cause hypertension in the supine position in subjects with poor baroreceptor function. 1242329: This drug produced hypertension and a strong irritation on the treated eye as well as a hypotensive effect on the contralateral one. 14857836: [Pressoreceptors of the aorta in high blood pressure produced by drugs and aortic clamp]. 15288871: Failure to administer these drugs appropriately may result in haemodynamic instability (hypotension and hypertension) and in extreme cases death. 15383526: Although cyclosporin A (CsA), an inhibitory ligand of cyclophilin A, is a widely used immunosuppressive drug, it causes arterial hypertension in part by impairing eNOS-dependent vasodilation. 15676113: Hypertension may be induced by administering inotropic drugs and, in certain cases, cardiac output optimization using dobutamine also is necessary. 1632999: In univariate analyses, variables significantly associated with better pharmacy compliance were perceived lifetime treatment of hypertension, greater than 5-year history of medication use, perceived cause of hypertension other than diet, use of more than one hypertension drug, lack of reported departure from the prescribed medication regimen, absence of drug abuse history, and race (Caucasian). In multivariate analyses, the best predictive model of pharmacy compliance included three variables: drug abuse history, perceived cause of hypertension, and pattern of medication use. 16710829: Since in our patient hypertension persisted despite apparent achievement of dry weight and maintenance of antihypertensive medications, we did some extensive investigations to disclose any secondary causes of hypertension (other than ESRD); we also evaluated whether the optimal dry weight was really achieved and maintained, and if the pharmacokinetics of the antihypertensive drugs was influenced by dialysis. 16856546: Because this drug often causes hypotension, hypertension and bradycardia, it should be used under the control by skilled medical teams. 16945059: According to premarketing studies, at least 1% of ziprasidone-treated patients exhibited hypertension; however, this figure is not necessarily attributable to the drug. 17712719: We tested immunosuppressive drugs that cause hypertension, and substances that interfere with steroidogenesis or influence glucose homeostasis for their ability to influence the inhibition of 11beta-HSD isozymes. 18078444: The administration of melatonin, as a result of its antioxidant features, has been reported to reduce hypertension and cardiotoxicity induced by clinically used drugs. 18404258: In addition, although delivered within the vitreous, anti-VEGF drugs could pass into the systemic circulation, which could potentially result in hypertension, proteinuria, increased cardiovascular events and impaired wound healing. 185040: Estrogenic compounds are the most important group of drugs that can induce hypertension. Other drugs may cause hypertension. 18854766: Aspects characterizing this psychological attribute, such as knowledge (comprehensibility), capacity (manageability), and motivation (meaningfulness) may be important determinants of adherence behaviour for asymptomatic illnesses, such as hypertension, in which patients often do not feel or perceive the immediate consequences of skipping medication doses. 19376375: Hypertension induced by immunosuppressive drugs: a comparative analysis between sirolimus and cyclosporine. 19505280: In those children requiring pharmacologic therapy, the choice of medication should be guided by the etiology of HTN, the needs of the child and the risk and benefit profiles of the various drug classes. 20018933: OBJECTIVE: Drugs that activate peroxisome proliferator-activated receptor (PPAR) gamma improve glucose sensitivity and lower blood pressure, whereas dominant-negative mutations in PPARgamma cause severe insulin resistance and hypertension. 20203454: These factors may include BP measurement issues, poor adherence to antihypertensive medications, therapeutic inertia on the part of clinicians, lifestyle changes, secondary causes of hypertension, or ingestion of substances that interfere with BP control. Patients who demonstrate a deterioration in BP control should be questioned about adherence, recent changes to diet and lifestyle, signs and symptoms of secondary causes of hypertension, and use of any concomitant medications or other substances that may be known to increase BP or interfere with antihypertensive therapy. 20608581: Discontinuation of monoamine oxidase inhibitor drugs sometimes results in flu-like symptoms, dysphoria, restlessness, tachycardia, hypertension, and a delirium-like state. 20817652: The efficacy of antihypertensive medications for this cause of hypertension has not been demonstrated. CONCLUSIONS: This is the first data that demonstrates individual classes of antihypertensives are effective in bevacizumab-induced hypertension. The management of bevacizumab-induced hypertension is important in order to avoid dose interruption/discontinuation and/or end organ damage. 21234416: Management includes lifestyle and dietary modification, elimination of medications contributing to resistance, and evaluation of potential secondary causes of hypertension. 21477148: Drugs which potentially may induce tachycardia or hypertension could precipitate acute cardiac failure in these patients and should be avoided. 22002334: Several drugs can cause hypertension and/or blunt the effect of antihypertensive treatment. Purpose of this review is to examine the most common causes of resistant hypertension that are due to drugs or abuse of substances along with their underlying pathophysiological mechanisms. 22303736: [Obstructive sleep apnea and drugs as causes of treatment-resistant hypertension]. 22736265: Arterial hypertension, drugs inducing hypertension or drug side effects may cause PRES but sometimes the reason remains unknown. 22926348: Some psychoactive medications cause weight increase, insulin resistance, dyslipidemia, impairment glucose tolerance/ type II diabetes and hypertension. 23189886: Choice of a drug depends on the underlying cause of hypertension and presence of comorbidity, if any. 23784914: Cancer therapy using old (e.g., mitotic spindle poisons) as well as new (e.g., monoclonal antibody) drugs may cause arterial hypertension through different mechanisms; sometimes the increase of blood pressure levels may be responsible for chemotherapy withdrawal. 2394832: A 11 beta-OHSD deficiency has been invoked as a cause of the syndrome of apparent mineralocorticoid excess, and 11 beta-OHSD inhibition by liquorice has been invoked to explain the hypertension induced by this drug. They reinforce the notion that a defect in 11 beta-OHSD plays a major role in the syndrome of apparent mineralocorticoid excess and liquorice-induced hypertension. 24250913: Therefore, physicians are supposed to be more vigilant in examining these patients and take care not to prescribe medications that may provoke hypertension. 2455198: Increased cerebral pressor activity can cause hypertension in some patients with the Guillain-Barre syndrome, where disinhibition of cerebral centres may result from an afferent baroreflex lesion. The use of drugs (including alcohol), or at times their withdrawal, results in hypertension through neurogenic mechanisms. 24567018: The condition, which is mostly associated with severe arterial hypertension, has also been reported to be induced by several medications. 24850069: OBJECTIVES: The use of atypical antipsychotic drugs in patients with psychiatric illness may result in dyslipidemia, hypertension, glucose intolerance, and abdominal obesity, which are together referred to as metabolic syndrome (MS). 25068014: The economic burden due to hypertension may be attributable not only to antihypertensive medication but also to the very expensive procedures required for cases of cardiovascular disease that occur more frequently in hypertensive compared with normotensive individuals. 26316767: The importance of distinguishing this group from the other groups of PH is that there are PAH-specific drugs that target the molecular pathways that are pathogenic in the vascular derangements, leading to arterial hypertension, which should not be used in the other forms of PH. 26403331: It is clear that noncompliance with medication is in part responsible, but nonetheless there is a clear and unmet clinical need to find alternative means to improve BP control in such patients.In recent years, several nonpharmacological device-based technologies for hypertension have been trialed. 26873693: BACKGROUND: Adherence to medication has been repeatedly proposed to represent a major cause of treatment-resistant hypertension (TRH); however, treatment decisions such as treating TRH with renal denervation depend on accurate judgment of adherence. 2696254: Medication, and above all, continual alcohol consumption, play an increasing role in the etiology of hypertension. 28864378: Following induction of hypertension, the rats were assigned into the following 6 subgroups: an l-NAME alone group and treated groups receiving the following drugs intraperitoneally for 6 weeks; vals, vit D, COQ10 and combination of vals with either vit D or COQ10. 29237149: It is unknown whether hypertension is due to RA-related medications or the disease itself. 29291681: One of the main causes of secondary hypertension, frequently ignored, is represented by certain categories of drugs, that can induce hypertension, increase the blood pressure values in previously controlled hypertension, decrease the effects of antihypertensive medication or induce a hypertensive emergency. 29980915: No significant improvements were observed on clotting factors; this fact might depend on persistence of typical alteration of CD, such as obesity and hypertension, and reflects also on the worsening in glucide metabolism induced by the drug. 30393374: This study aims to investigate why certain drugs tend to cause iatrogenic hypertension (HTN) and focus on drug targets that are implicated in these conditions. 31285418: The drug safety evaluation revealed that both of these drugs caused hypertension and mild liver and kidney damage. 31655781: Recognition of common medications causing drug-induced hypertension is important to effectively control blood pressure. 31748121: In particular, Session II not only focused on arterial thrombosis and venous thromboembolism, but also hypertension or cardiomyopathy or atrial fibrillation induced by many otherwise life-saving drugs. 31823067: RECENT FINDINGS: Common causes of secondary hypertension include medication-induced hypertension, renal parenchymal disease, renovascular hypertension, obstructive sleep apnea, and primary aldosteronism. 32415493: HTs are the approved drugs that can cause hypertension as an AE. Data science-driven analyses of drugs inducing hypertension as an adverse effect. Data science-driven analyses of drugs inducing hypertension as an adverse effect.The utilization of approved medication is a requisite to combat certain diseases for health; however, the undesirable adverse effects (AEs) due to medication are generally unavoidable. Hypertension is one of such AEs resulting from approved medication in which blood pressure in the arteries gets elevated and is a risk factor for several diseases including heart and kidney failure. 32525967: Most patients (2,469; 79.4%) had >=1 underlying condition, including hypertension, cardiovascular disease, diabetes, chronic kidney disease, or immunosuppression due to medications or disease. 32606881: Individuals aged younger than 20 years old or older than 50, having a dermatologic disease other than vitiligo, being afflicted with the diseases which may lead to secondary hypertension, pregnancy, taking substances, and medication which can lead to hypertension were chosen as the exclusion criteria in this study. 34193741: Control rates did not significantly differ by age, number of drugs, or cause of hypertension. 34775477: In the discovery set, rs444904 (G > A) in PIK3R5 was associated with an increased risk of sorafenib-induced hypertension (p = 0.006, OR = 3.88 95% CI 1.54-9.81). In the replication set, rs427554 (G > A) in PIK3R5 (in complete linkage disequilibrium with rs444904) was associated with an increased risk of bevacizumab-induced hypertension (p = 0.008, OR = 1.39, 95% CI 1.09-1.78). This study aimed to identify predictive biomarkers of hypertension induced by these drugs using a discovery-replication approach. 35179707: PURPOSE OF REVIEW: While vascular endothelial growth factor receptor inhibitors (VEGFRis) have dramatically improved cancer survival, these drugs cause hypertension in a majority of patients. 35437784: There are no validated markers of hypertension induced by these drugs. 36360828: Angiotensin-converting enzyme inhibitors (ACEi) were the most popular medications irrespective of the etiology of AH or age. 36764674: AIM: Cyclosporin A (CsA) is a widely used immunosuppressive drug that causes hypertension and hyperkalemia. 37302940: The relationship between cancer and HT is multifactorial: common risk factors, neoplasia that cause HT through hormonal secretion, and, especially, chemotherapy drugs that cause HT. 37499767: Virtual screening and biological evaluation to identify pharmaceuticals potentially causing hypertension and hypokalemia by inhibiting steroid 11beta-hydroxylase. 37605933: However, these drugs often cause persistent hypertension owing to excess sympathetic outflow, which is maintained by N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory input to the hypothalamic paraventricular nucleus (PVN). 611664: In 1 patient, marked hypertension was induced by propranolol and the drug had to be withdrawn. 6134277: [Arterial hypertension induced by drugs acting on the nervous system]. 6285670: Rats receiving captopril for 12 weeks remained normotensive, whereas withdrawal of the drug resulted in hypertension. 6340942: OC medication is the most prevalent cause of hypertension in young women. 6758716: We administered both drugs to rats using a dosage schedule which we had shown to produce hypertension and tachycardia when clonidine, but not guanfacine, was stopped after 3 weeks treatment. 6759964: [Arterial hypertension induced by drugs]. 7093482: The drug provokes negligible hypertension, raises the systolic and cardiac outputs, and enhances myocardial contractility. 7554000: Pressor agents were avoided as indirect-acting drugs can produce severe hypertension. 7777726: Hypertension induced by drugs and other substances. 8246369: Both cyclosporine and prednisone can cause hypertension. The higher the dose of either drug, the more likely they will cause hypertension. 8821553: In hexamethonium (10 mg kg-1, i.v.) pretreated rats, these five drugs induced dose-related hypertension which was reduced by pretreatment with prazosin (0.1 mg kg-1, i.v.). 10850725: The development of additional drugs requires greater basic research on the pathogenesis of AD. 11212463: The prevalence of opioid administration, other drugs known to cause hallucinations, brain tumours, liver metastases, bone metastases, lung metastases, known renal failure, eye disease, Alzheimer's disease, Parkinson's disease, other neurodegenerative disorder, psychiatric disorder and epilepsy were also recorded. 15025506: Thus, 1 has been suggested to play a role in the degeneration of serotonergic neurons in brain disorders such as Alzheimer's disease or evoked by amphetamine drugs. 15917096: Considering the increase of Abeta42 plasma levels as a risk factor for AD, any changes induced by medication by long-term use in the peripheral and possibly also in the central compartment, could be of clinical relevance. 16553493: Drugs that target metal beta-amyloid interactions can effect Alzheimer's disease. 16863459: Although donepezil was originally developed to inhibit the breakdown of the neurotransmitter acetylcholine as symptomatic therapy for AD, recent studies raise the possibility of other effects this drug has on the pathogenesis of AD. 20298170: These treatments are symptomatic, whereas drugs under development are supposed to modify pathological steps leading to AD, thus acting on the evolution of the disease. 21095183: Accordingly, these receptors may become therapeutic targets for the development of novel drugs to be used for reducing the inflammation induced injuries in asthma, rheumatoid arthritis, Alzheimer's disease, cardiovascular diseases and traumatic shock. 21765871: These treatments are symptomatic, whereas drugs under development are intended to modify the pathological steps leading to AD, thus acting on the evolution of the disease. 22442659: To combat this disease, the few therapies that are available rely on drugs that increase neurotransmission; however, this approach has had limited success as it has simply slowed an imminent decline and failed to target the root cause of AD. 23299047: These treatments are symptomatic, whereas drugs under development are supposed to modify pathological steps leading to AD, thus acting on the evolution of the disease. 23762322: Among these medications, some might benefit, while others might exacerbate, the pathogenesis of AD. Alzheimer's disease (AD) is rapidly becoming one of the leading causes of disability and mortality in the elderly. 24353405: Treatment with acetylcholinesterase inhibitors or memantine aims at slowing progression and controlling symptoms, whereas drugs under development are intended to modify the pathologic steps leading to AD. 24379759: Thus, a platform of knowledge is provided for laboratory protocols that could be used to assess the efficacy of drugs designed to improve memory performance in rodents, including rodent models of neurodegenerative diseases that cause cognitive deficits, and Alzheimer's disease in particular. 28587340: The rats in the drug and control groups were treated to induce AD. 28955143: In the past 20 years, many new drugs that focus on the pathogenesis of Alzheimer's disease have been assessed in clinical trials. 29692948: Furthermore, we propose potential new drug targets that may modulate diverse pathways responsible for AD. 30124447: Here, we treated animals with intracerebroventricular streptozotocin (STZ, 2 mg/kg), a drug that has been described to cause Alzheimer-like behavioral and histopathological impairments. 30988761: As potential AD treatment drugs, SA and TB compounds have been demonstrated to alleviate the oxidative stress induced by Abeta25-35 via the regulation of intracellular calcium homeostasis and Calnexin, preventing AD development. 31092147: In this review, we advance the hypothesis that neuroinflammatory responses resulting from mast cell activation along with the accompanying risk factors such as age, gender, food habits, emotional status, stress, allergic tendency, chronic inflammatory diseases, and certain drugs can accelerate brain injury-associated neuroinflammation, neurodegeneration, and AD pathogenesis. 33515559: However, these medications were gradually discovered to be ineffective in removing the root of AD pathogenesis but merely targeting the symptoms so as to improve a patient's cognitive outcome. 35053277: Besides the mechanistic link, an overview of clinical studies utilizing vitamin B supplementation are given, and a potential link between diseases and medication resulting in a reduced vitamin B12 level and AD are discussed. 35204697: In summary, DOTA repositions promising drugs that target important biological pathways and are predicted to improve patient cognition, circadian rhythms, and AD pathogenesis. 35257810: Despite tremendous effort being involved, several anti-AD drugs come into clinical trials but with a moderate-to-poor success rate due to the complex AD pathogenesis and the blood-brain barrier (BBB). 36683856: We depict the cellular source, culture condition, differentiation methods, transfection methods, drugs inducing AD, general approaches (evaluation methods and metrics), and in vitro cellular models used in parallel with PC12 cells. 36931947: However, it was progressively found that these drugs did not address the underlying causes of AD pathogenesis; rather, they focused on the symptoms in order to enhance patients' cognitive outcomes. 37122620: The study provides a valuable epigenetic resource for identifying DNAm-based diagnostic biomarkers, developing effective drugs, and studying AD pathogenesis. 37183545: Then, via molecular docking, we further screened these drugs by examining their interaction with islet amyloid polypeptide (IAPP) and Abeta42 peptide, the key components involved in the pathogenesis of T2D or AD. 37824197: CONCLUSIONS: GBA interactions, along with systemic inflammation and the adverse effects of medication, might be a cause of MCI and AD development in patients with IBD. 16808550: Although heart failure is predominantly caused by cardiovascular conditions such as hypertension, coronary heart disease and valvular heart disease, it can also be an adverse reaction induced by drug therapy. 17589923: Moreover, chemotherapy under AT-II induced hypertension may have a better effect on the treatment of metastatic liver tumors. 2012403: A case of local recurrence of rectal cancer was successfully treated by UFT combined with two-route CDDP chemotherapy under the AT-II induced hypertension. [A case of local recurrence of rectal cancer successfully treated by UFT combined with two-route CDDP chemotherapy under the AT-II induced hypertension]. 2334169: These studies might suggest that intraarterial chemotherapy by induced hypertension with angiotensin II was useful on treatment of malignant brain tumors. 23572315: Recent reports of chemotherapy-induced hypertension as a common adverse effect of angiogenesis inhibitors and immunosuppressants clarify the need for routine blood pressure (BP) monitoring and guideline-based management of hypertension as an integral strategy to preserve LV function. 25217090: Hypertension induced by chemotherapeutic and immunosuppresive agents: a new challenge. 2782895: [Two-route chemotherapy under AT-II induced hypertension using totally implanted injection port system in liver metastases derived from digestive cancers]. 32027948: Clinically, recombinant human EPO (rhEPO_ additionally is an important anti-anemia agent for chronic kidney disease (CKD), myelodysplastic syndrome (MDS) and chemotherapy, but induces hypertension, and can exert certain pro-tumorigenic effects. 33081013: Conventional chemotherapy, adjunct treatments, and novel targeted therapies collectively caused new onset hypertension in 33-68% of treated patients. 35497107: All six patients had hypertension due to renal disease, except one girl with chemotherapy-induced hypertension. 3566300: Furthermore, we obtained an optimal increase in the lifespan of rats bearing limb tumors when we tried TRC in combination with the angiotensin II (AT-II)-induced hypertension method. 37189272: The median time to peak and lowest BP was at least 2 weeks and 3 weeks, respectively, for all groups, suggesting that a BP lowering effect was observed following the offset of the initial chemotherapy-induced hypertension. The significant increase in SBP can be attributed to chemotherapy-induced hypertension by 5-FU or other drugs in the chemotherapeutic regimens. 6793249: It was concluded that high blood pressure is a strong determinant in predisposing lymphocytes to increased genetic risk from induced DNA damage and that this relationship is not statistically affected by hypertensive drug therapy. 10215161: The results of the present study, together with those of previous studies from our laboratory in which we determined the effects of phenylephrine-induced hypertension on brain Fos expression [Li and Dampney (1994) Neuroscience 61, 613-634; Potts et al. (1997) Neuroscience 77, 503-520], indicate that in conscious rabbits circulating angiotensin II activates primarily circumventricular neurons within the organum vasculosum of the lamina terminalis and subfornical organ, but not the area postrema, and this in turn leads to activation of neurons in other forebrain regions, including the median preoptic, supraoptic, paraventricular and suprachiasmatic nucleus as well as the bed nucleus of the stria terminalis. 10415373: Furthermore, angiotensin II may have neurotoxic effect to use as the pressor agent for induced hypertension after cerebral ischemia. Mild phenylephrine-induced hypertension treatment (21+/-4 mmHg) during post-cerebral ischemia-reperfusion improved the survival ratio and reduced cerebral edema, which was also associated with an increase in local CBF and a recovery of brain energy metabolism. However, intense phenylephrine-induced hypertension, angiotensin II-induced hypertension, or hypotension worsen the survival rate and produced extra cerebral edema, that were also associated with deterioration of brain energy metabolism. 10614985: 5.58 +/- 0.08 beats/min per mmHg in B2+/+, P < 0.01), as well as by an exaggerated tachycardic response to chronic hypertension induced by clipping of the left renal artery (60 +/- 3 vs. 15 +/- 3 beats/min in B2+/+, P < 0.01). In B2-/- mice, the presence of an alteration in baroreceptor regulation of HR was supported by a reduced gain in the HR responses to acute nitroprusside-induced hypotension or phenylephrine-induced hypertension (slope of the regression line: 0.82 +/- 0.07 vs. 10644582: Baroreflex response slope during PE-induced fetal hypertension was lower in LTOT than in Cntl fetuses. 10670796: METHODS: During carotid crossclamping, treatment included either phenylephrine-induced hypertension without shunting (Group XC; n = 11) or insertion of a shunt (Group S; n = 12). 10969303: Phenylephrine-induced hypertension increased MAP by 20% (79 +/- 9 to 95 +/- 6 mmHg; P = 0.001) but did not affect CBF. 11124468: Acute hypertension was induced by phenylephrine. 11220382: In nine swine, mean arterial pressure (MAP) (range, 33-200 mm Hg) was altered; phenylephrine was used to induce hypertension, and a nitroprusside-esmolol combination or systemic hemorrhage was used for hypotension. 11753003: METHODS: Cerebral blood flow was measured (intraarterial (133)Xe technique) in sedated human subjects undergoing cerebral angiography during sequential infusions of (1) intracarotid saline, (2) intravenous phenylephrine to induce systemic hypertension, (3) intravenous phenylephrine with intracarotid nitroprusside (0.5 microg x kg(-1) x min(-1)), and (4) intracarotid verapamil (0.013 mg x kg(-1) x min(-1)). 12015837: Hypertension was induced by intravenously administered phenylephrine, norepinephrine, and/or dopamine, and hypervolemia was achieved by intravenously administered crystalloid and colloid solutions. 12450025: After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). 12493505: Proximal LITA and H-graft flows were measured at baseline and during pacing-induced tachycardia, phenylephrine-induced hypertension, and nitroprusside-induced hypotension. 12717712: Fos expression by glutamatergic neurons of the solitary tract nucleus after phenylephrine-induced hypertension in rats. Awake rats were subjected to phenylephrine- (PE-) induced hypertension (N=5) or received saline (N=5). 1353421: TAT and VT induced by up to three extrastimuli were studied during hypertension (control), during normotension produced most frequently by nitroprusside infusion (3-6 micrograms/kg/min), and during further hypertension most frequently produced by phenylephrine infusion (1-5 micrograms/kg/min). 1414328: We compared the risk of intracranial hemorrhage after phenylephrine-induced hypertension, combined with a hypovolemic, hypotensive insult followed by rapid volume replacement in two groups of newborn beagle puppies (one group on a piston pump HFO and the other on CMV). 1436509: We found that the cerebral blood flow was substantially increased, but was maintained at the same level (17 rats) as that observed under phenylephrine-induced hypertension (26 rats). 14617591: This phenylephrine-induced hypertension significantly increased SaO(2) and MD (92.0 +/- 7.5 vs 95.0 +/- 5.0% and 1318 +/- 344 vs 1533 +/- 425 cm x min(-1), respectively). 14994188: [unlike nifedipine (0.8 mg/kg i. v.) and yohimbine (1 mg/kg i. v.), respectively] but markedly attenuated [like prazosin (0.2 mg/kg i. v.)] the hypertension evoked by phenylephrine (PE, 25 microg/kg, i. v.), a selective alpha (1)-adrenergic receptor agonist and, like ketanserin (1 mg/kg i. v.), the second phase (rise in MAP) of the cardiovascular response caused by 5-hydroxytryptamine (5-HT, 0.3 mg/kg i. v.). 15243307: SSR149744C, which has no or low affinity for alpha 1 and beta 1 adrenergic and angiotensin II AT1 receptors, reduced isoproterenol-induced tachycardia and phenylephrine- or angiotensin II-induced hypertension in anaesthetized dogs. 1537703: Phenylephrine-induced hypertension acutely decreases genioglossus EMG activity in awake humans. 15699457: Soluble epoxide hydrolase is a main effector of angiotensin II-induced hypertension. AUDA (130 microg/mL in drinking water) did not affect blood pressure in normotensive animals but markedly lowered it in mice with angiotensin II-induced hypertension (1 mg/kg per day). Intravenous application of AUDA (8 mg/kg) acutely lowered blood pressure and heart rate in animals with angiotensin II-induced hypertension but failed to affect blood pressure in animals with phenylephrine-induced hypertension (29 mg/kg per day). These data demonstrate that the decrease in blood pressure observed after sEH inhibition in angiotensin II-induced hypertension can be attributed to an initial reduction in heart rate followed by pressure diuresis resulting from increased perfusion of the kidney. 15815256: Does phenylephrine-induced hypertension during focal cerebral ischemia aggravate brain edema? 15815377: The authors investigated the effects of phenylephrine-induced hypertension on the development of cerebral edema and neuronal dysfunction during focal cerebral ischemia. The data indicate that, in this model, induced hypertension established soon after the onset of ischemia can serve to reduce the area of histochemically detectable neuronal dysfunction, and that not only is edema formation not aggravated, but it is actually reduced. The influence of phenylephrine-induced hypertension during focal cerebral ischemia on the formation of brain edema. 15815446: Focal cerebral ischemia in rats: effect of phenylephrine-induced hypertension during reperfusion. 1614584: During carotid endarterectomy (CEA), phenylephrine infusions are commonly used to induce hypertension during carotid clamping in an attempt to increase collateral cerebral blood flow and prevent cerebral ischemia. Based on these findings, in order to decrease the incidence of both MI and cerebral infarction after general anesthesia for CEA, we recommend the restrictive use of phenylephrine-induced hypertension for specific instances of slowly or poorly reversible cerebral ischemia, as shown on the electroencephalogram. 1670915: To investigate the mechanisms by which bupivacaine may act within the CNS to produce cardiovascular toxicity, we studied four groups of halothane-anesthetized rabbits in which infusion of intracerebroventricular (icv) bupivacaine or intravenous (iv) phenylephrine resulted in dysrhythmias and hypertension. In group 4 (n = 6), iv phenylephrine-induced dysrhythmias and hypertension were not affected by icv midazolam. 16948598: OBJECTIVE: To examine the agreement between direct arterial blood pressure measurements obtained from 2 arteries and indirect blood pressure measurements obtained with an oscillometric blood pressure monitor (OBPM) during normotension and phenylephrine-induced hypertension in dogs. Accuracy of an oscillometric blood pressure monitor during phenylephrine-induced hypertension in dogs. 1711760: The data indicate that phenylephrine-induced hypertension instituted 2 h after MCAO does not aggravate edema in the ischemic core, that it improves edema in the periphery of the ischemic territory, and that it reduces the area of histochemical neuronal dysfunction. 1727143: The effect of phenylephrine-induced hypertension on CBF was investigated after 120 min of middle cerebral artery occlusion in rats. 17899189: Cold medication containing oral phenylephrine as a cause of hypertension in children. 18340095: Hypertension was induced by phenylephrine infusion starting 10 or 60 minutes after ischemia to raise blood pressure by 30% for the duration of ischemia; control groups received saline infusion. 1860718: Furthermore, acute hypertension induced by angiotensin II or phenylephrine did not affect the plasma irET-1 concentration in rats. 19004376: In conclusion, atrial fibrillation can be maintained for at least 40 min after cessation of rapid atrial pacing in dogs with phenylephrine-induced hypertension. 19407951: (4) The disruption of the blood-brain barrier (BBB) permeability in rats was caused by phenylephrine-induced hypertension, and the effect of intravenous injection of HHI-I on the BBB permeability was determined using Evans blue as the marker. 21176164: RESULTS: Compared to untreated DM rats, DMC significantly elevated the ratio of DeltaHR/DeltaMABP by enhancing the compensatory reduction in HR (-DeltaHR) in response to PE-induced hypertension (+DeltaMABP) (P < 0.05). 2146892: Infusion of phenylephrine and sodium nitroprusside (100 micrograms/ml) produced sustained hypertension (avg MAP 166 mmHg) and hypotension (avg MAP 49 mmHg), respectively. 21705025: CONCLUSION: The present study suggests that phenylephrine induced-hypertension can result in early motor restoration without serious side effects in progressing lacunar infarction. 2216612: At anticonvulsant dosage, phenobarbital sodium decreased mean arterial blood pressure transiently during steady state and significantly reduced total cerebral blood flow during phenylephrine-induced hypertension without reducing mean arterial blood pressure. In this study cerebral blood flow values in steady state and during phenylephrine-induced hypertension with and without phenobarbital pretreatment were measured in newborn beagles. 22473212: Prophylactic phenylephrine infusion can cause hypertension if increasing arterial pressure does not trigger a timely reduction in the rate of administration. 22564915: Intravenous phenylephrine produced arterial hypertension and increased myocardial metabolic demands. 22577457: The injection of phenylephrine was performed by the device after a period of recording BP, mean arterial pressure (MAP), heart rate (HR) and baroreflex sensitivity (BRS) in order to induce acute hypertension before and after injecting naloxone. 22824983: Lastly, acute hypertension during pregnancy caused greater edema formation in both brain cortices that was not attributed to changes in sympathetic innervation. In the present study, we examined the effect of pregnancy on the effectiveness of cerebral blood flow autoregulation using laser Doppler flowmetry and edema formation by wet:dry weight in acute hypertension induced by phenylephrine infusion in the anterior and posterior cerebrum from nonpregnant (n=8) and late-pregnant (n=6) Sprague-Dawley rats. 22954904: Phenylephrine-induced hypertension during transient middle cerebral artery occlusion alleviates ischemic brain injury in spontaneously hypertensive rats. 2298475: The characteristics and extent of rapid or acute resetting of the aortic baroreceptors were studied in long-term renal hypertensive rats during 30 minutes of sustained hypertension produced by phenylephrine infusion. 23366854: CONCLUSION: Acute hypertension induced by phenylephrine produces an increase in the coronary wall elastic modulus with a concomitant decrease in the fractal nature of the aortic pressure, suggesting that coronary stiffening is associated with an unwrinkled aortic pressure. 2375408: They also indicate that the addition of phenylephrine-induced hypertension to hemodilution therapy results in a further reduction of ischemic injury without exacerbating cerebral edema. 2385118: Completeness of denervation was evaluated by recording hemodynamic responses to sodium nitroprusside-induced hypotension, phenylephrine-induced hypertension, and direct cardiac autonomic nerve stimulations acutely (group I, n = 11) and 2 weeks after denervation (group II, n = 5). 2452247: Phenylephrine-induced hypertension was associated with a 30% reduction in the electrochemical peak corresponding to norepinephrine. 24573182: However, in juvenile rats, PE-induced hypertension evoked comparable bradycardia in OZR and LZR with similar or augmented c-Fos expression in NTS of the OZR. 2503766: Clearance of DHPG from arterial plasma was prolonged by phenylephrine-induced hypertension and by nitroprusside-induced hypotension. 2724147: Phenylephrine-induced hypertension reduced the catechol peak and increased the indole peak. 27841023: Although when evaluated in anesthetized rats, only the HSMHF group presented augmented blood pressure, evaluation in conscious animals revealed that both the MHF and HSMHF diets, but not the HS alone, were able to induce tachycardia and hypertension. In conclusion, a MHF diet containing 6% fructose was enough to render the renal vascular bed hyperreactive to phenylephrine and to induce both hypertension and tachycardia. 2801151: Regional cerebral blood flow in acute hypertension induced by adrenaline, noradrenaline and phenylephrine in the conscious rat. 2815189: Phenylephrine-induced hypertension reduces ischemia following middle cerebral artery occlusion in rats. For example, in the coronal section in the center of the middle cerebral artery distribution, local cerebral blood flow was 0-6 ml/100 g/min in 6.7 +/- 1.4% of the section in normotensive rats but was in that range in only 1.7 +/- 0.6% of the section during phenylephrine-induced hypertension (p less than 0.05). We studied the influence of phenylephrine-induced hypertension on the area of ischemia during brief middle cerebral artery occlusion. 29158260: In addition to these age-related changes, systemic stimulation with the alpha1-adrenergic receptor agonist phenylephrine, which induces sustained hypertension and hypertrophy development, induced expression of fetal cardiac genes that was more pronounced in adult Fhod3-deleted mice than in the control mice, suggesting that Fhod3 modulates hypertrophic changes in the adult heart. 29297736: Similarly, in nestin/hRAMP1 mice, hypertension caused by Ang II or phenylephrine was greatly attenuated, and associated autonomic dysregulation and increased sympathetic vasomotor tone were diminished or abolished. We previously reported that expression of hRAMP1 in all tissues favorably improved autonomic regulation and attenuated hypertension induced by angiotensin II (Ang II). 30648306: In addition, the in vivo results showed that HG could decrease the blood pressure in normotension, spontaneous hypertension, and PE-induced hypertension models. 31189595: Ang II-induced myogenic response and hypertension were greater in Apln -/y mice, however, an equivalent hypertension induced by phenylephrine, an alpha-adrenergic agonist, did not cause AAA or rupture in Apln -/y mice. 31645472: CONCLUSION: Among patients with noncardioembolic stroke who were ineligible for revascularization therapy and those with progressive stroke, phenylephrine-induced hypertension was safe and resulted in early neurologic improvement and long-term functional independence. After adjustment for age and initial stroke severity, induced hypertension increased the occurrence of the primary (odds ratio 2.49, 95% confidence interval [CI] 1.25-4.96, p = 0.010) and secondary (odds ratio 2.97, 95% CI 1.32-6.68, p = 0.009) efficacy endpoints. 3364465: The characteristics of rapid or acute resetting of the aortic baroreceptors were studied in anesthetized rats during 30 minutes of sustained hypertension produced by phenylephrine infusion. 3443545: Increased outputs of lymphocytes in lymph efferent from the lymph nodes of sheep during systemic arterial hypertension induced by phenylephrine or dopamine. 3596775: In WKY, acute, phenylephrine-induced hypertension increased pial arteriolar pressure by 47 +/- 7 mm Hg (mean +/- SE) and pial venous pressure by 20 +/- 2 mm Hg. 414854: This study was designed to evaluate the effects of nitroglycerin and phenylephrine-induced arterial hypertension on regional myocardial blood flow in awake dogs with acute occlusion of the left circumflex coronary artery. 469730: In both fetal and adult sheep, actue hypertension due to I.V. injection of angiotensin II was not associated with a consistent and progressive bradycardia, such as was seen with acute hypertension caused by phenylephrine. 6466984: Acute hypertension as a result of phenylephrine infusions reduced the size of this response in individual Wistar Kyoto rats. 6487416: Hypertension produced by phenylephrine facilitated the HR CR and changed the BP CR to a pressor-only response on selected trials in which baseline BP increases and baseline HR decreases were within restricted limits. 6668383: With phenylephrine, the heart rate response to induced hypertension consisted solely of reflex sinus bradycardia in 67% of the trials, whereas non-sinus cardiac arrhythmias developed during the period of reflex bradycardia in 33% of the trials. 6773436: Nitroglycerin therapy for phenylephrine-induced hypertension in pregnant ewes. 6831291: The efficacy of verapamil was independent of the accompanying reduction in blood pressure and systemic vascular resistance as subsequent phenylephrine induced hypertension could not reinstitute these arrhythmias. 7091392: When testing for the effects of baroreceptor reflexes on the sympathetic pathway phenylephrine-induced hypertension decreased, but moderate hemorrhage increased the amount of preganglionic activity at rest and during FN stimulation. 7191672: Effect of sodium nitroprusside on directly measured myocardial oxygen consumption during phenylephrine-induced hypertension in dogs anesthetized with halothane. 7205667: Phenylephrine (0.2-25 micrograms/kg per min continuous) produced (i) hypertension, (ii) no observed effects upon aerobic or anaerobic metabolism and (iii) progressive tissue oedema; these effects were similar in susceptible and normal muscle. 7323490: Most of these effects of angiotensin II were opposite to the effects of hypertension caused by phenylephrine and aortic balloon inflation. 7461796: Spontaneously hypertensive rats (SHR) and normotensive rats (WKY), 3-4 months of age, were anesthetized and acute hypertension was produced by infusing phenylephrine intravenously (i.v.). 7477892: In confirmation of our previous study, hypertension produced by phenylephrine resulted in the neuronal expression of Fos (a marker of neuronal activation) in the nucleus of the solitary tract, area postrema, the intermediate and caudal parts of the ventrolateral medulla parabrachial complex, and in the central nucleus of the amygdala. 7478238: Experimental hypertension at a similar level induced by i.p. phenylephrine also resulted in induction of c-fos IR in NTS. 7583277: Permeability of the blood-brain barrier was quantitated by the formation of venular leaky sites and clearance of fluorescent-labeled albumin (FITC-albumin) before and during phenylephrine-induced acute hypertension. 7673376: To test this possibility, pentobarbital-anesthetized rats were subjected to either hypoxic hypoxia (PaO2 approximately 30 mm Hg), hemorrhagic hypotension (MABP approximately 70 and 50 mm Hg), or phenylephrine-induced hypertension (MABP approximately 125 and 145 mm Hg). 7731395: The influence of aging and/or hypertension caused no alterations of the alpha 1-agonist response provoked by phenylephrine in aortic rings. It is concluded that (1) the responsiveness of resistance arteries to adrenoceptor stimulation only changes with elevated blood pressure and (2) hypertension in combination with aging induces an endothelial dysfunction in conduit arteries but not in resistance vessels. 7844257: Phenylephrine-induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to non-aminergic neurons, whose distribution in the NTS conformed to the termination patterns of primary baroreceptor afferents, and in the ventrolateral medulla overlapped in part with those of vagal cardiomotor and depressor neurons. 8001214: Cardiac morbidity was most likely precipitated by the interaction of phenylephrine-induced hypertension with a cocaine-depressed myocardium. 8021468: Inducing acute hypertension (coronary pressure 200 mmHg) pharmacologically with angiotensin II also augmented constriction to serotonin, whereas phenylephrine-induced hypertension did not. 8047983: RESULTS: Alpha 1 stimulation with phenylephrine resulted in marked hypertension, a reflexive bradycardia, and marked induction of aortic HSP70 mRNA. 8092519: RESULTS: Phenylephrine-induced hypertension resulted in an increase in OFF CFR. Phenylephrine-induced hypertension caused an opposite effect on the CFR of rostral ventromedial medulla neurons as compared with a noxious stimulus such as heat or maintenance of tourniquet inflation. 8112392: I.v. infused salbutamol (2-128 micrograms/kg per min, each dose for 5 min) dose dependently decreased MAP in vehicle-treated rats; the depressor responses were potentiated by hypertension induced by phenylephrine. 8188982: Sensitivity of cardiac component of baroreflex (CCB), expressed as a slope of the regression line was determined from relationships between systolic arterial pressure (SAP) and HR period (HRp) during phenylephrine (Phe)-induced hypertension and sodium nitroprusside (SN)-induced hypotension. 8223935: The cardiac-related component of renal sympathetic nerve activity was abolished as well as the sympatho-inhibitory effects that accompany the phenylephrine (5-10 micrograms/kg i.v.)-induced hypertension. 8574657: In addition, we examined changes in pial arteriolar and pial venular pressure before and during phenylephrine-induced acute hypertension. Permeability of the blood-brain barrier was quantitated by the formation of venular leaky sites and clearance of fluorescent-labeled albumin (FITC-albumin) before and during phenylephrine-induced acute hypertension. 8717156: Phenylephrine-induced hypertension was associated with decreased DOPAC and HVA concentrations in adult (P < 0.05) and old (P < 0.05) rats, respectively. 8724428: In SHR, phenylephrine-induced hypertension produced no significant changes in the extracellular norepinephrine (NE) and dihydroxyphenylacetic acid concentrations, whereas a significant increase in the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) concentration was observed. Wistar normotensive rats, in response to phenylephrine-induced hypertension, showed a significant increase in extracellular NE and 5-HIAA concentrations. 8809800: Baroreceptors were activated by phenylephrine-induced hypertension. 8853351: Heme-L-lysinate also lowered arterial pressure in deoxycorticosterone acetate-salt hypertensive rats and in rats with phenylephrine-induced hypertension, indicating that the vasodepressive actions of heme may be extended to other hypertensive models. 8955532: Permeability of the blood-brain barrier was quantitated by clearance of fluorescent-labeled dextran before and during phenylephrine-induced acute hypertension in rats treated with vehicle and Hoe-140 (0.1 microM). 909667: During phenylephrine-induced hypertension in 6 near-term pregnant ewes, nitroprusside rapidly lowered the blood pressure to control values with no accompanying change in uterine blood flow. 9368553: CONCLUSIONS: The results suggest that careful use of phenylephrine induced hypertension is not associated with an increase in morbidity or mortality in acute stroke. 9412514: In situ expression of c-fos observed in response to phenylephrine (PE)-induced hypertension provided a basis for characterizing the organization and neurotransmitter specificity of neurons at nodal points of medullary baroreflex circuitry. 9422904: We have compared the effects of inhaled nitric oxide (iNO) and i.v. nitroglycerin (ivGTN) on the haemodynamic response to phenylephrine-induced hypertension (PEHT) in anaesthetized pigs. 9506701: In addition, arterial baroreflex regulation of HR was markedly blunted in TG mice in response to both nitroglycerin-induced hypotension and phenylephrine-induced hypertension. 9728324: Systemic hypertension induced by phenylephrine (3-300 nmol kg-1), angiotensin II (0.1-3.0 nmol kg-1) and arginine vasopressin (0.03-1.0 nmol kg-1) was accompanied by constriction of the mesenteric artery. 9728831: IMPLICATIONS: Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma. Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats. UNLABELLED: Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. Phenylephrine-induced hypertension does not improve outcome after closed head trauma in rats. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). 9779193: To test autoregulation, hypertension was induced using phenylephrine. 10024986: Although intracranial hemorrhage associated with neurofibromatosis type 1 is a rare condition, fine telangiectatic collateral vessels caused by occlusive cerebrovascular disease, intracranial aneurysms, brain tumors, or hypertension caused by pheochromocytoma or stenosis of the renal artery should be considered as the cause of hemorrhage. 10095836: Arterial hypertension in patients with neurofibromatosis is most often due to an associated pheochromocytoma. 10096149: Pheochromocytomas have been estimated to be present in approximately 0.3% of patients undergoing evaluation for secondary causes of hypertension [41]. 10338428: Posttraumatic hypertension secondary to adrenal hemorrhage mimicking pheochromocytoma: case report. 10417977: A 6 year-old boy with von Hippel-Lindau (VHL) disease presented with hypertension due to bilateral pheochromocytomas. 10771134: Pheochromocytomas can cause hypertension, cardiovascular disease (frequent cause of death), kidney disease, stroke, cancer, amyloid formation and can mimic many other diseases, including acute pancreatitis, carcinoid, neuroblastoma, psychiatric illness, hypercalcemia, retinal vascular lesions, and diabetes mellitus. 10965221: Octreotide is useful for controlling blood pressure before surgery in some patients with uncontrolled hypertension caused by a pheochromocytoma. 10981118: Pheochromocytomas are the cause of hypertension in 0.1% to 0.2% of hypertensive patients. 11129996: CONCLUSION: This case emphasizes that in a patient with NF1 a phaeochromocytoma must be considered as a possible cause of hypertension. The levels of epinephrine and dopamine were elevated, suggesting an orthotopic phaeochromocytoma as the cause of the hypertension. 11167434: Intravenous magnesium sulphate infusion proved successful in controlling hypertension caused by a phaeochromocytoma in the postpartum period. 11233314: Pheochromocytoma is one of the main curable etiologies of high blood pressure, although its diagnosis and therapeutic management can be problematical: an incorrect diagnosis or inappropriate treatment may lead to fatal complications. 11375292: BACKGROUND: Pheochromocytoma is a rare cause of hypertension resulting from increased catecholamine secretion. 11572908: Hypertension due to phaeochromocytoma--an unusual cause of multiorgan failure. 11584528: [Secondary hypertension, 4: Pheochromocytoma as etiology of hypertension]. 11800059: Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. 11826768: Pheochromocytoma is a rare cause of hypertension. 12003709: Pheochromocytomas, although a rare cause of hypertension, are dangerous tumors that require consideration among large numbers of patients. 12195418: Pheochromocytoma and primary hyperaldosteronism are well-known causes of hypertension. 12381537: Pheochromocytoma and paragangliomas are rare tumors of chromaffin tissue that secrete catecholamines either intermittently or continuously, producing hypertension with a constellation of symptoms and signs that can be frightening to the patient and that continue to provide perplexing problems for clinicians. 12381539: Pheochromocytomas are dangerous tumors that, although a rare cause of hypertension, require consideration among large numbers of patients. 12381540: Pheochromocytoma is a rare, surgically correctable cause of hypertension. 12442092: Pheochromocytoma, hypercorticism, primary aldosteronism or glucocorticoid-remediable aldosteronism can be present or diagnosed at any term and may cause severe hypertension. Hypertension may be pregnancy-induced, essential or secondary to endocrine disorders. 12566722: Phaeochromocytoma is a tumour of the adrenal medulla, which, although rare, is a major cause of correctable hypertension with a prevalence of 0.1-0.5% in the hypertensive population. 1257835: However, a complete evaluation revealed pheochromocytoma as the primary cause of the hypertension. 12783740: Pheochromocytoma is a catecholamine-producing tumor and a rare cause of hypertension. 13047737: [Arterial hypertension caused by pheochromocytoma]. 13073553: [Hypertension due to adrenal pheochromocytoma]. 13119113: [Pharmacological tests in hypertension due to chromaffin tumors]. 13324246: [Permanent arterial hypertension caused by pheochromocytoma]. 13381917: Hypertension during operation due to unsuspected phaeochromocytoma associated with neurofibromatosis. 1340739: Pheochromocytoma is a cause of hypertension that frequently can be cured by surgery. 13562726: Hypertension due to adrenal tumor (pheochromocytoma); case report. 13629288: [Permanent symptomatic arterial hypertension caused by a pheochromocytoma; radiological & biological data]. 13755524: Paroxysmal and persistent hypertension as the result of pheochromocytoma. 1404141: Our case demonstrates pheochromocytoma can be a cause of hypertension in SLE. 14041880: [Evaluation of the determination of total methoxynoradrenaline and methoxyadrenaline in the urine in the diagnosis of cases of hypertension caused by pheochromocytoma]. 14364275: [Permanent but instable arterial hypertension, due to a pheochromocytoma; excision and cure]. 14431834: [Continuous arterial hypertension caused by pheochromocytoma]. 14472734: [Arterial hypertension in a young woman due to a pheochromocytoma. Recovery by means of surgical ablation of the tumor]. 14489826: [Permanent arterial hypertension caused by pheochromocytoma in a 25-year-old man]. 14594571: The classic disorder of the adrenal medulla resulting in hypertension is pheochromocytoma, although hypertension in obesity might also be associated with catecholamine secretion. 14605591: Pheochromocytomas are rare tumours of catecholamine-producing chromaffin cells leading to hypertension and symptoms of catecholamine excess. 14688974: This case is relevant to current practice regarding similarity between mercury intoxication and hypertension secondary to pheochromocytoma. 14737986: BACKGROUND: Phaeochromocytoma is a rare surgically treatable cause of hypertension. 1488333: Pheochromocytoma was the cause of arterial hypertension observed in 0.9% of children treated in 1982-1989. 14953598: Intermittent hypertension due to phaeochromocytoma. 15022406: Pheochromocytoma, though an uncommon cause of hypertension, can be a lethal condition. 15024897: Pheochromocytomas are rare, but because they are a curable cause of hypertension and potentially fatal if not found, important to diagnose. 15157558: Pheochromocytoma is a lethal tumor of chromaffin cells of the adrenal medulla that produces episodes of hypertension with the symptoms of palpitations, severe headaches, and sweating. 15171431: [Hypertension secondary to pheochromocytoma]. 15201507: Pheochromocytoma is one of the potentially fatal causes of childhood hypertension. 15405713: Sustained hypertension due to pheochromocytoma; report of case cured by removal of tumor. 15587184: Pheochromocytoma causes severe hypertension and sometimes tachycardia leading to intracranial hemorrhage or adrenaline-induced severe hypovolemia. 1597727: Pheochromocytomas are potentially curable causes of hypertension. 16202853: CONCLUSIONS: Although rare, pheochromocytoma can cause severe peripartum hypertension. BACKGROUND: Pheochromocytoma, a rare and usually curable cause of hypertension, is characterized by symptoms and signs related to increased catecholamine secretion. 16428577: Pheochromocytoma is a rare catecholamine-producing tumor that can cause severe hypertension and other systemic disturbances. 17102071: Pheochromocytoma (Pheo) is a rare cause of hypertension (HTN). 17119341: Pheochromocytoma (PHEO) is considered to be a rare cause of hypertension. 17432020: Pheochromocytoma is a catecholamine producing tumour that can cause severe hypertension and other systemic disturbances. 1745805: Pheochromocytoma is a catecholamine secreting tumor which has been traditionally considered as a potentially curable cause of hypertension. 17474956: Ganglioneuromas (GN) are neural crest cell-derived tumors which may coexist with pheochromocytomas, secrete various neuropeptides or the symptoms may mimic that of a pheochromocytoma, producing hypertension or a hypotensive crisis during anesthesia for these tumors. 18022420: Pheochromocytoma is an unusual cause of surgical hypertension and is extremely rare in the pediatric population. 18051232: Neurofibromatosis arterial hypertension caused by pheochromocytoma is extremely rare, less frecuent than 1% in childrens less than 10 years old, and young adults. 18344633: Pheochromocytoma is an infrequent secondary cause of arterial hypertension, often associated with paroxysmal headache, sweating, weight loss, and palpitations. 18458953: Phaeochromocytoma is a rare cause of hypertension in children, but important to be recognised, as hypertension can be severe and surgery is often curative. 18846988: Chromaffinoma of the adrenal medulla (pheochromocytoma--PHEO) is a rare cause of arterial hypertension which is diagnosed incidentally or run in a family as a component of disease syndromes of the genetic origin. 1914202: Assessment of catecholamine production and excretion is important in the laboratory detection of pheochromocytoma, a rare but curable cause of hypertension. 20241875: Hypertension in children caused by pheochromocytoma; report of 3 cases and review of the literature. 2031541: There was a significant delay in diagnosis in those patients with hypertension on the basis of an aldosteronoma as compared with those with hypertension secondary to a pheochromocytoma (75.4 months versus 36.1 months, p = 0.02). 20560377: Hypertension due to pheochromocytoma can be masked by excessive reduction of intravascular volume by preoperative hemodialysis. 20662291: 0.1-0.2% of all cases of hypertension are caused by pheochromocytomas, or catecholamine-producing tumors derived from chromaffin tissue. 20939200: This is a case of a 38 year-old, male, with history of bilateral pheochromocyto-, ma, and hypertension secondary to pheochromocytoma, that was scheduled for open bilateral cortical-sparing adrenalectomy under general anesthesia combined with thoracic epidural anesthesia. 21189702: Pheochromocytoma is a curable, rare cause of hypertension, characterized by symptoms and signs related to increased catecholamine secretion. 21516925: Pheochromocytoma induced hypertension. 21752274: INTRODUCTION: Pheochromocytoma is a rare cause of hypertension but it could have severe consequences if not recognized and treated appropriately. 2195858: Pheochromocytoma is a rare, potentially lethal cause of hypertension that is surgically reversible. 2196128: Surgically confirmed pheochromocytoma was the cause of arterial hypertension in 6 out of 668 (0.8%) children with significant hypertension admitted to Child Health Centre in Warsaw. 22223909: Phaeochromocytoma is a rare cause of hypertension during pregnancy with potentially fatal consequences. 22679235: Pheochromocytoma is a rare cause of hypertension. 22736758: This report illustrates an uncommon presentation of pheochromocytoma in children and shows the importance of a careful investigation for pheochromocytoma as a cause of hypertension in children with cerebral ischaemic stroke. 22901822: Pheochromocytoma and renal artery stenosis are two common causes of surgically correctable childhood hypertension that may coexist. 2299787: The resected tumor was found to be a pheochromocytoma, which had provoked intraoperatively an intractable hypertension and ventricular arrhythmia. 23478505: Pheochromocytoma is a rare cause of hypertension in the general population. 24001749: CONCLUSIONS: NIPs differ from pheochromocytomas responsible for hypertension and display features of altered chromaffin differentiation. 24043985: Pheochromocytoma is a rare cause of hypertension in children. 24180171: The real challenge for clinicians is differentiating pheochromocytoma from other causes of hypertension (preeclampsia, gestational hypertension, and pre-existing or essential hypertension), from other cause of pulmonary edema (preeclampsia, peripartum cardiomyopathy, stress or Takotsubo cardiomyopathy, pre-existing cardiac disease [mitral stenosis], and high doses betamimetics), and from other causes of cardiovascular collapse (pulmonary embolism, and amniotic fluid embolism). 24288628: Phaeochromocytoma is a catecholamine producing tumour and an uncommon cause of hypertension. 24429046: Her young age and significant family history immediately prioritises secondary causes including phaeochromocytoma and familial syndromes causing hypertension. 24668034: Sleep apnea, pain, nocturnal hypoglycemia, drugs, excess aldosterone production, and pheochromocytoma should all be considered as causes of hypertension in older persons. 24784869: The patient was a 49-year old Iranian woman who presented with hypertension due to bilateral pheochromocytoma. 25546991: [Difficulty in diagnosis of primary hyperaldosteronism as the cause of resistant hypertension and severe hypokalemia--case report]. Renovascular hypertension, Cushing syndrome and pheochromocytoma were excluded as potential causes of drug-resistant hypertension in the presented case. 25759272: Acute airway obstruction due to retropharyngeal haematoma caused by a large fish bone in a patient with hypertension caused by a pheochromocytoma. We present the case of a 48-year-old man with formation of a RH after accidental ingestion of a large fish bone with hypertension as comorbidity caused by a so far undiagnosed pheochromocytoma. 26254120: Pheochromocytoma as a rare cause of arterial hypertension in a patient with autosomal dominant polycystic kidney disease: A diagnostic and therapeutic dilemma. DISCUSSION & CONCLUSION: Pheochromocytoma is a rare but treatable cause of hypertension in ADPKD; given the anatomical complexities these patients present, careful preoperative planning and surgical technique are essential to a favorable outcome. 26438407: Herein, we present the case of a pregnant woman who was found to have uncontrollable hypertension late in her pregnancy, secondary to a mediastinal pheochromocytoma, which was deemed unresectable at the time of exploration after her delivery. 2651458: Hypertension and tachyarrhythmias arising during an operative procedure are rarely caused by an unsuspected pheochromocytoma. 26595895: When carrying out an excision of cerebellar hemangioblastomas in patients with intracranial hypertension complicated by abnormal hypertension due to pheochromocytoma whose blood pressure is not sufficiently controlled, tumor resection of the pheochromocytoma prior to cerebellar hemangioblastoma excision in the same surgery may prevent increased ICP and reduce perioperative risk. We were not able to perform an craniotomy because abdominal compression in the prone or sitting position resulted in severe hypertension. INTRODUCTION: This report describes a patient with Von Hippel-Lindau (VHL) syndrome and uncontrolled hypertension due to pheochromocytoma who underwent craniotomy for the excision of a cerebellar hemangioblastoma combined with a laparoscopic adrenalectomy. Craniotomy for cerebellar hemangioblastoma excision in a patient with von Hippel-Lindau disease complicated by uncontrolled hypertension due to pheochromocytoma. 26648500: Pheochromocytoma is a catecholamine-producing adrenal tumor, being a rare cause of hypertension in pregnancy. 27158015: Although pheochromocytomas are the cause of hypertension in only a small number of patients, they can precipitate life-threatening hypertension or cardiac arrhythmias caused by excessive and episodic catecholamine secretion. 27275314: A rare finding is hypertension due to pheochromocytoma in patient with neurofibromatosis type 1. 27582850: Although phaeochromocytoma is a rare cause of hypertension in pregnancy, it can lead to potentially life-threatening cardiovascular complications for the mother and increased fetal mortality if left undiagnosed and untreated. 27603405: BACKGROUND: Pheochromocytoma is an endocrine tumor that causes hypertension, facial pallor, and headache. 27729064: Hypertension secondary to pheochromocytoma is often paroxysmal, and patients occasionally present with sudden attacks of alternating hypertension and hypotension. 27808580: The presence of pheochromocytoma is a rare cause of hypertension during pregnancy with an incidence of 0.007% of all pregnancies. 27908211: Pregnant women with neurofibromatosis type 1 (NF-1) have increased complications during gestation, including hypertensive disorders that are sometimes caused by pheochromocytoma. 28373587: Case of Chronic Indolent Pheochromocytoma That Caused Medically Controlled Hypertension but Treatment-Resistant Diabetes Mellitus. 28381449: As symptoms of pheochromocytoma are rather similar to those of other far more common causes of hypertension during pregnancy, timely diagnosis is a challenge. 29422732: Pheochromocytoma is a rare cause of hypertension, but it could have severe consequences if not recognized and treated appropriately. 29578356: Pheochromocytoma is a rare catecholamine-secreting neoplasm that is the cause of hypertension in <0.2% of patients with hypertension. 29747617: CONCLUSION: Our case and previous literatures suggest that hypertension caused by pheochromocytoma which is a rare but important and potentially lethal cause of hypertension in Turner syndrome. Clinicians should keep in mind that pheochromocytoma can be a cause of hypertension in patients with Turner syndrome. Here, we reported a pheochromocytoma as a rare cause of hypertension in Turner syndrome patient. Pheochromocytoma as a rare cause of hypertension in a 46 X, i(X)(q10) turner syndrome: a case report and literature review. 29800631: However, when the tumor arises near the renal hilum, hypertension may also be secondary to renal artery stenosis, which can occur via several purported mechanisms. Classically, pheochromocytomas and paragangliomas result in hypertension secondary to an excess release of catecholamines. 29923996: RATIONALE: Pheochromocytomas are rare catecholamine-secreting tumors arising from adrenomedullary chromaffin cells, usually causing hypertension, palpitation and headache. 30249813: A 74-year-old Chinese woman suffered from acute myocardial infarction on a background of 50 years of poorly controlled hypertension secondary to pheochromocytoma, which was surgically removed in June 2012 prior to the presentation. We conclude that multivessel coronary artery ectasia and severe calcification may be present in patients with a long-standing history of hypertension secondary to pheochromocytoma. 31929915: Uncontrolled hypertension precipitated by pheochromocytoma can cause microangiopathic hemolytic anemia and renal insufficiency. 32277359: Although renal artery stenosis and pheochromocytoma are well-known causes of HTN in NF1, this case demonstrates that HTN can be caused by AUK in patients with NF1. 33102719: Background: Pheochromocytoma is a rare cause of hypertension in pregnancy, which is often overlooked; especially in late pregnancy because of more prevalent pre-eclampsia. 33119816: The authors raised concerns regarding the lack of inclusion of obesity by several societies as a formal cause of hypertension considering not only the biologic plausibility but also the huge impact of weight loss therapies such as bariatric surgery on hypertension remission. In contrast, there is no discussion that a very rare condition-namely pheochromocytoma-is the most \typical\ cause of hypertension by promoting hypertension remission in the majority of patients after surgical procedure. If obesity becomes largely accepted by several societies as a secondary form of hypertension, this pandemic condition will be certainly the most common cause of hypertension. 33883999: Considering that she had marked hypertension (193/115 mmHg), we made a provisional diagnosis of left lateral pain due to a ruptured pheochromocytoma. 35716085: Pheochromocytoma is a rare cause of hypertension in pregnancy. 3598906: Our data suggest that both the sympathetic nervous system and circulating catecholamines are involved in the maintenance of hypertension due to pheochromocytoma. Hypertension due to pheochromocytoma is generally considered to be a straightforward, direct consequence of the elevated concentrations of circulating catecholamines. 36027141: Pheochromocytoma is the most typical cause of hypertension by promoting hypertension remission in the majority of patients after surgical procedure. 36789302: Pheochromocytoma is one of the rare causes of hypertension in pregnancy, occurring in one in every 50,000 pregnancies. 36856470: Pheochromocytoma and paraganglioma are rare causes of hypertension, estimated to explain 0.1-0.6% of all cases, but nonetheless an important diagnosis to make, due to serious side effects. 37148720: DISCUSSION: Pheochromocytoma is a rare but important cause of hypertension in pregnancy. 3725709: Pheochromocytoma, although rare, is a serious and potentially fatal cause of hypertension. 37260658: Pheochromocytoma in children is an exceptionally uncommon cause of hypertension in this age group. 37753024: Pheochromocytoma-Induced Hypertension After Traumatic Brain Injury. 3806123: The case of a 57 year old man with cognitive impairment, hypertension and insulin dependent diabetes mellitus caused by phaeochromocytoma is reported. 42512: Pheochromocytoma is an infrequent cause of hypertension. 4293946: [Arterial hypertension caused by pheochromocytoma. Apropos of 20 cases]. 4621553: Neurofibromatosis and hypertension due to pheochromocytoma or renal-artery stenosis. 5362413: [Hypertension due to pheochromocytoma (clinical aspects and results of the surgical treatment based on the analysis of 19 cases)]. 5370945: [Diagnosis and therapy of hypertension due to pheochromocytoma]. 5509552: [Arterial hypertension due to pheochromocytoma]. 5515708: [Fundus oculi in hypertension caused by pheochromocytoma]. 5606306: [Arterial hypertension due to pheochromocytoma]. 5742933: [Arterial hypertension due to pheochromocytoma]. 6121057: When is hypertension due to pheochromocytoma? 613594: [Catecholamine metabolism in arterial hypertension caused by pheochromocytoma]. 6146080: Effect of captopril on hypertension due to phaeochromocytoma. 6146900: Effect of saralasin on hypertension due to phaeochromocytoma. 6348590: [The renin-angiotensin-aldosterone system in pheochromocytoma-induced arterial hypertension. Description of a case with hyperreninemia and marked secondary aldosteronism]. 6367394: Despite the relative infrequency of pheochromocytomas, they remain a potentially curable yet lethal etiology of hypertension. 6413442: Vascular lesions in addition to pheochromocytoma are now recognized as causes of hypertension associated with neurofibromatosis. 6602433: Pheochromocytoma as cause of hypertension after coronary bypass. 6625515: Hypertension due to a phaeochromocytoma is a rare but curable disease. 6783201: Fifteen patients with hypertension due to phaeochromocytoma and 35 controls with essential hypertension were studied to assess the diagnostic value of urinary and plasma biochemical determinations in phaeochromocytoma. 6814376: Where pheochromocytoma is the cause of hypertension, its resection generally results in a better control of hypertension than that obtained in patients whose BPs were elevated from other unknown causes. 6956401: Hypertension secondary to pheochromocytoma. 7094503: The effectiveness of prazosin in controlling the hypertension induced by NE-secreting PHEO suggests that, in man, pressure responses to augmented levels of NE are mediated solely through alpha 1-receptors. 7103302: These two cases stress the problem of the respective responsibility of both pheochromocytoma and renovascular disease in hypertension genesis. 7231770: Since maternal and fetal prognosis of pheochromocytoma associated with pregnancy is strictly related to an antepartum diagnosis, the importance of suspecting pheochromocytoma as underlying cause of de novo appearing hypertension (or hypertension of unknown origin) during pregnancy is emphasized. 7375417: Pheochromocytoma, which triggers hypertension by producing excess catecholamines, can be identified by detecting metabolites of these substances in urine. 7783826: Phaeochromocytoma is one of the causes of hypertension. 8021480: CONCLUSIONS: The technique described enables the discrimination of patients with phaeochromocytoma as a cause of hypertension from other aetiologies of hypertension. 8064789: Hypertension in neurofibromatosis is mostly a consequence of a stenosis of the renal artery or is due to phaeochromocytoma. 8112909: Diagnostic use of metoclopramide in hypertension caused by pheochromocytoma. 8177442: The pheochromocytoma syndrome, constituted by arterial hypertension, headache and sweating, is due in 80% of cases to adrenal pheochromocytomas and only in 20% of cases is due to extra-adrenal secreting paragangliomas. 8403356: BACKGROUND: Pheochromocytoma is a catecholamine-secreting tumor of chromaffin cells that causes hypertension. 8527810: Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. 8655926: Pheo in hemodialyzed patients is a rare event and it may be hidden by other more common causes of hypertension. 8731321: This case has relevance for current practice reflecting similarity between mercury intoxication and hypertension secondary to pheochromocytoma. 8797958: We report a case of primary hepatic pheochromocytoma responsible for a severe hypertension in a 24-year-old man. Pheochromocytomas are uncommon tumors that represent a potentially curable cause of hypertension. 8804229: In general, these pheochromocytomas produce catecholamines that result in hypertension. Hypertension attributable to pheochromocytoma is a very attractive model for the elucidation of the pathogenesis of hypertension. 8935305: Pheochromocytoma is a rare cause of hypertension. 9119103: Pheochromocytoma is an unusual cause of hypertension during pregnancy. 9149678: Pheochromocytoma is a catecholamine-secreting tumor and a rare cause of hypertension that is usually curable. 9334112: Pheochromocytomas are active, catecholamine-producing tumours derived from chromaffine tissue, causing arterial hypertension. 9606283: Pheochromocytoma, a rare cause of hypertension: long-term follow-up of 55 surgically treated patients. 9820725: Pheochromocytomas are a rare cause of hypertension in pregnancy. 1476270: The hyperfibrinogenemia and concomitant hyperviscous plasma observed in the present study could either play a role in the pathogenesis of the hypertension or be the consequence of the hypertension itself, at least in some patients. 18541522: Plasma levels of catestatin are diminished not only in hypertensive patients but also in their still-normotensive offspring, indicating its role in the pathogenesis of hypertension. 2040091: Plasma factors have been implicated in causing increased calcium uptake and cytosolic (Ca++) in vascular tissue leading to hypertension. 21103027: Plasma levels of circulating a soluble fms like tyrosine kinase-1 (sFlt-1), an anti-angiogenic factor, vascular endothelial growth factor (VEGF) and placental growth factor (PIGF), both pro-angiogenic factors were analyzed in normal pregnant Malaysian women (control group, n = 34), women with pregnant induced hypertension (PIH, n = 34) and women with preeclampsia (PE, n = 34) all at three gestational ages, 24-28 weeks (early pregnancy: EP), 32-36 weeks (late pregnancy: LP) and 6 weeks after delivery (postpartum: PN). 28490531: In hypertensive animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated the hypertension caused by the high plasma level of ANG II. 31322515: The findings suggest the significant role of reducing of plasma levels of miR-133a in the pathogenesis of hypertension itself and in pathological remodeling of the heart. 3867126: Decreased plasma levels of antithrombin III (AT III) are observed in women with severe pregnancy-induced or aggravated hypertension. 6499237: Adrenaline was infused intravenously into conscious dogs to test whether chronically elevated plasma levels can produce arterial hypertension. These results are therefore not in accord with the hypothesis that increased plasma levels of adrenaline may cause hypertension by activation of pre-junctional beta-adrenoceptors. 6500673: These results, therefore, do not support the contention that the sympathetic nervous system mediates the hypertension produced by elevated plasma levels of ANG II. 6697562: The indices of overall sympathetic nervous tone which have been used, such as measurements of plasma noradrenaline concentration or total NA release to plasma, are seen to be not sufficiently specific, since the organs and regions thought to be central to hypertension pathogenesis (kidney, heart, splanchnic circulation) are responsible for no more than 35% of all noradrenaline released to plasma. 7562563: Infusion of endothelin-1 in humans to obtain pathophysiological plasma levels causes mild hypertension, strong sodium retention and renal vasoconstriction. 7721406: Endothelin-1 infusion into humans to obtain pathophysiological plasma levels causes mild hypertension, strong renal vasoconstriction, and sodium retention. 7807900: The amino acid pool of blood plasma, liver and bile was examined before and after operative elimination of biliary hypertension cause. 7872233: Activation of the plasma or tissue renin-angiotensin system may be one of the cause of hypertension. 32048973: An emerging concept is that microglia, the innate immune cells of the brain, are major players in AD pathogenesis. 32130931: Aging-related cellular and molecular processes including low-grade inflammation are major players in the pathogenesis of cardiovascular disease (CVD) and Alzheimer's disease (AD). 32197653: Because astrocytes are key players in the pathogenesis of AD, we studied here if and how ES affects astrocytes in wildtype (WT) and APP/PS1 mice and how these relate to the previously reported amyloid pathology and microglial profile. 32251633: Circular RNAs (circRNAs) function as crucial players in AD pathogenesis. 32739006: MAM and C99, key players in the pathogenesis of Alzheimer's disease. 33190798: Microglia, the resident immune cells of the brain, have recently emerged as key players in Alzheimer Disease (AD) pathogenesis, but their roles in AD remain largely elusive and require further investigation. 33573255: In the search for new, more reliable biomarkers and potential therapeutic options, epigenetic modifications have emerged as important players in the pathogenesis of AD. 33623128: Neuropeptides govern diverse pathophysiological processes and represent key players in AD pathogenesis, regulating synaptic plasticity, glial cell functions and amyloid pathology. 34211387: Amyloidogenicity and vascular dysfunction are the key players in the pathogenesis of Alzheimer's disease (AD), involving dysregulated cellular interactions. Overall, the current review informs about the interaction of neuronal and glial cell types in AD pathogenesis and its critical association with cerebrovascular dysfunction. 35247551: Microglia have been identified as key players in Alzheimer's disease pathogenesis, and other neurodegenerative diseases. 35348415: Microglia are critical players in the neuroimmune system, and their involvement in Alzheimer's disease (AD) pathogenesis is increasingly being recognized. 35527555: OBJECTIVE: The aim of this study was to use a differential co-expression analysis approach for analyzing a small RNA sequencing dataset from a well-established murine model in order to identify potentially new players in the etiology of AD. 35771435: Extensive researches suggest the probable role of mitochondrial complex II and III dysfunction as underlying players in the pathogenesis of AD, PD, and HD. 35893045: In the search for more reliable biomarkers, epigenetic mechanisms, able to mediate the interaction between the genome and the environment, are emerging as important players in AD pathogenesis. 36614325: Amyloid beta (Abeta) and protein Tau aggregates are disease hallmarks and key players in AD pathogenesis. 37587894: As amyloid b protein (Ab) is one of the key players responsible for the pathogenesis of AD, we sought to investigate the protective effects of fisetin in an Ab1-42-induced rat model of AD. 38219962: In conclusion, passive immunotherapy targeting key players in AD pathogenesis offers a promising strategy for effective AD treatment. Here, we review characteristics, clinical trial data, and mechanisms of action for monoclonal antibodies (mAbs) targeting key players in AD pathogenesis, including amyloid-beta (Abeta), tau and neuroinflammation modulators. 38260408: Genetic variations have emerged as crucial players in the etiology of AD, enabling hope for a better understanding of the disease mechanisms; yet the specific mechanism of action for those genetic variants remain uncertain. 38350636: This review explores the intricate interplay between two pivotal players in AD pathogenesis: beta-amyloid (Abeta) and tau protein. 11317203: Polymorphisms of the renin-angiotensin (RA) system have been implicated in the pathogenesis of hypertension and atherosclerotic vascular disease, and may play a role in the development of FMD. 11904385: The angiotensinogen M235T polymorphism in humans is linked to differential expression of the human angiotensinogen gene (AGT) gene and hypertension, but the homeostatic responses resulting from this polymorphism are not known. 12105131: Although the T594M polymorphism could increase renal sodium absorption through affected channels, it is not known whether this polymorphism causes hypertension. 12215464: A significant interaction between the polymorphism and aging in the pathogenesis of hypertension was also shown in nonheavy smokers. These analyses showed a significant interaction between the polymorphism and cigarette smoking in the pathogenesis of hypertension (P=0.0005). 15479618: Several studies have demonstrated the importance of angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphisms in the pathogenesis of hypertension. 15659047: We find that no correlation exists between the T102C genetic polymorphism and hypertension, which affords useful information on the pathogenesis of hypertension in the Chinese population. 15671602: CONCLUSION: The significance of the G(-930)A polymorphism of CYBA was confirmed in the present study with adequate statistical power, which strengthens the hypothesis that this polymorphism is important in the pathogenesis of hypertension and confers susceptibility. 16954165: Several genetic polymorphisms in the RAS have been identified and have been implicated as a cause of hypertension and cardiovascular disease. 19302427: The significance of these polymorphisms in the pathogenesis of hypertension in APIAs is unclear. 21440764: BACKGROUND: Genetic polymorphisms of the renin-angiotensin system (RAS) have been reported to play an important role in the pathogenesis of diabetes mellitus and hypertension. 23404385: Genetic polymorphism of genes involved in renal salt handling and arterial vessel tone is considered to be one of the causes of hypertension. 25054022: Polymorphisms of the aldosterone synthase gene, CYP11B2, have been suggested to be involved in the pathogenesis of diabetes mellitus (DM), hypertension and cardiovascular diseases. 25475696: CONCLUSIONS: Our findings support the contributory role of the II/I polymorphism in leptin gene in the pathogenesis of hypertension, and this role was more evident in Asians and for essential hypertension. 26416847: However, the biochemical function of this polymorphism in the mechanism responsible for hypertension is yet to be clarified. 30706833: Te review investigates the possible genetically determined mechanisms of the development of hypertension and endothelial dysfunction caused by polymorphism of the genes of endothelial nitric oxide synthase (eNOS) and enzymes of phases I and II of the xenobiotics detoxifcation system. 7358393: There was no convincing evidence for major loci causing hypertension in this population, and the polymorphism proposed by Platt was excluded as a principal cause of hypertension. 10027555: To investigate the further contribution of the polymorphism to the etiology of sporadic AD, we evaluated associations between Japanese AD and -491 A/T polymorphism of APOE. 10530514: Since reports about the relevance of these polymorphisms for the pathogenesis of AD have been contradictory, we performed an association study with some modifications. 12214130: These findings suggested that genetic polymorphisms of the neuronal nAChR genes might be related to the pathogenesis of sporadic AD. To identify the possible mutations and/or polymorphisms of neuronal nicotinic acetylcholine receptor (nAChR) genes related to the pathogenesis of sporadic AD, we have performed mutational analyses of the major neuronal nAChR genes (CHRNA3, 4, 7 and CHRNB2) expressed in central nervous system. 15200238: These results suggest that polymorphism in exon 11 of septin 3 may have a determinative role in the pathogenesis of AD. 15653174: In order to clarify the role of these polymorphisms in the complex pathogenesis of AD we examined genotype and haplotype frequencies of the two C-to-T SNPs at position -889 and -551 in the IL-1alpha and IL-1beta genes, respectively, and of the 86 bp VNTR intron-2 polymorphisms in the IL-1Ra gene. 16999857: The Multi Drug Resistance (ABCB1) gene, encoding for P-gp, is highly polymorphic and this may result in a changed function of P-gp and may possibly interfere with the pathogenesis of Alzheimer's disease. 18033638: BACKGROUND AND PURPOSE: The role of N-acetyltransferase gene (NAT2) polymorphism in the aetiology of Alzheimer's disease (AD) and Parkinson's disease (PD) is an interesting issue; it is suggested that the slow acetylator genotype favours the damage of central nervous system cells by environmental toxins. 18303265: Further investigations of polymorphisms in the gene encoding the NMDA receptor 2B subunit in AD patients with different genetic setting are needed to clarify their role in the pathogenesis of AD. 21176999: These findings suggest that polymorphisms within the IGF-I gene could infer greater risk for AD through their effect on IGF-I levels, and confirm the physiological role IGF-I in the pathogenesis of AD. 21840620: Finally, we discuss the possible impact of CR1 genetic polymorphisms in relation to the amyloid cascade hypothesis of AD and the way in which CR1 may lead to AD pathogenesis. 25538763: These results support the contribution of the polymorphisms of rs2227564 in the urokinase-type plasminogen gene to the pathogenesis of sporadic Alzheimer's disease in the Han Chinese population. 26809345: Since only ~30% of phenotypic diversity of AD can be explained by polymorphisms in risk genes, these and transgenic bioassay data argue that structurally distinct Abeta particles play a major role in the diverse pathogenesis of AD, and may behave as distinct prion-like strains encoding diverse phenotypes. 30026459: The odds ratios (ORs) and corresponding 95% confidence intervals (CI) were calculated to express the degree of risk of AD resulting from polymorphisms in the EGFR gene. 11894691: Sustained IAH leads to ACS which if left unrecognized or untreated is always fatal. 11972549: Multiple organ dysfunction attributable to intra-abdominal hypertension has been called the abdominal compartment syndrome. Intra-abdominal hypertension did not necessarily lead to abdominal compartment syndrome, and often resolved without clinical sequelae. 12467311: The observed association between ACS and ischemic bowel may result from decreased mucosal perfusion as a direct result of abdominal hypertension. ACS is the end result of uncontrolled intra-abdominal hypertension and results in systemic derangements. 12657976: PURPOSE OF REVIEW: Abdominal compartment syndrome (ACS) is the end result of sustained, uncorrected intraabdominal hypertension. 14768131: Abdominal compartment syndrome resulting from intra-abdominal hypertension can be prevented or treated with the formation of a laparostomy. 15897812: Intra-abdominal hypertension leading to abdominal compartment syndrome complicates trauma resuscitation. 15991559: The aim of the article is to present the definition and criteria of diagnosis of abdominal compartment syndrome (ACS) due to abdominal hypertension. 16333212: Rapid progression of intra-abdominal hypertension will lead to abdominal compartment syndrome, which is defined as an intra-abdominal pressure greater than 20 mmHg with at least one organ failure. 17375648: This suggested that Siriraj device catheter was useful, not invasive, and effective in reflection of actually IAP Siriraj burn unit suggested IAP measurement in all major burns > or = 40% TBSA to early recognize and treat intra-abdominal hypertension(IAH) that can lead to ACS. 18953663: Intra-abdominal hypertension (IAH), leading to abdominal compartment syndrome (ACS), is a frequent cause of acute kidney injury (AKI) in surgical and trauma intensive care units not commonly recognized by nephrologists. 19961614: INTRODUCTION: Critically ill surgical patients frequently develop intra-abdominal hypertension (IAH) leading to abdominal compartment syndrome (ACS) with subsequent high mortality. 20041295: An abdominal compartment syndrome secondary to intra-abdominal hypertension was suspected. 21912014: The fruitless effort at aggressive fluid resuscitation was at operation found not due to hypovolemia per se but due to IAH causing ACS. 22445990: [Effects of somatostatin in a rabbit model of abdominal compartment syndrome induced by prolonged intra-abdominal hypertension]. OBJECTIVE: To establish a rabbit model of abdominal compartment syndrome (ACS) induced by prolonged intra-abdominal hypertension (IAH) and evaluate the therapeutic effect of somatostatin on ACS. 22985571: CONCLUSION: IAB plus IAH may cause damage to the cardiovascular and respiratory functions and lead to ACS in rabbits. 24266989: Two porcine models of IAH that cause abdominal compartment syndrome [ACS] with organ dysfunction were created. Temporal differences in the development of organ dysfunction based on two different approaches to induce experimental intra-abdominal hypertension in swine. 25479905: BACKGROUND: Intra-abdominal hypertension (IAH) often leads to abdominal compartment syndrome, which is followed by intestinal ischemia and associated with a high mortality. 30983735: Intra-abdominal hypertension (IAH) leading to abdominal compartment syndrome (ACS) commonly occurs in major burns. 10981140: Excess weight gain is a major cause of essential hypertension, and abnormal kidney function appears to be a cause as well as a consequence of obesity hypertension. 12135327: Thus systolic heart failure in DS rats is mainly mediated by hypertension, while renal dysfunction of DS rats is due to both hypertension and the AT1 receptor itself. 12677190: These findings provide important insights into the action of adrenomedullin as an antioxidant in protecting cardiovascular and renal dysfunction induced by hypertension, salt loading, vascular injury, diabetes and ischemia-reperfusion injury. 15030297: Underlying the global rise in CKD is an increase in diabetes, hypertension and other cardiovascular risk factors leading to progressive renal dysfunction. 15180627: Hypertension might cause renal dysfunction, which leads to the development of renal cysts. 16352114: Obesity and hypertension both lead to cardiovascular complications. Endothelial, vascular and renal dysfunctions, all consequences of high blood pressure, further worsen hypertension. Multiple mechanisms involved in obesity-induced hypertension. 17469709: INTRODUCTION: Increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) is a cause of organ dysfunction in critically ill patients and is independently associated with mortality. The kidneys seem to be especially vulnerable to IAH induced dysfunction and renal failure is one of the most consistently described organ dysfunctions associated with IAH. CONCLUSION: IAH can cause renal dysfunction. 19615312: Hypertension in elderly patients is a common and frequent disease which could cause stroke, heart failure and renal dysfunction. 19693639: There is increasing evidence that obesity, independently from other comorbidities such as diabetes and hypertension, can cause renal dysfunction. 22449672: His renal dysfunction seemed to be mainly caused by hypertension and tubulointerstitial damage. 24881708: INTRODUCTION: Increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) is a cause of organ dysfunction in critically ill patients and is independently associated with mortality. The kidneys seem to be especially vulnerable to IAH induced dysfunction and renal failure is one of the most consistently described organ dysfunctions associated with IAH. CONCLUSION: IAH can cause renal dysfunction. 29866742: Hypertension often leads to cardiovascular disease and kidney dysfunction. 31045658: PURPOSE OF REVIEW: Renovascular disease (RVD) remains an important cause of hypertension and renal dysfunction. 33849006: Swimming Exercise Ameliorates Hypertension-Induced Kidney Dysfunction via Alleviating Renal Interstitial Fibrosis and Apoptosis. We sought to investigate whether periodic swimming could ameliorate hypertension-induced kidney dysfunction and its underlying mechanisms. CONCLUSION: Our results demonstrate beneficial effects of the periodic swimming on ameliorating hypertension-induced kidney dysfunction highlighting the potential of swimming exercise as a nonpathological therapy for early prevention of hypertension-caused kidney diseases. 8120668: These results suggested that in vivo platelet activation, an increase of lipid peroxides, and renal dysfunction occur in this order due to hypertension, and that the latter two are significantly prevented by vitamin E treatment. 9284425: ACE inhibitors have clinically beneficial effects not only for patients with either hypertension or congestive heart failure, but also can be used to prevent the progression of renal dysfunction induced by hypertension and diabetes mellitus. 17890266: This statistic is mainly attributable to the side effects of immunosuppression, with loss of allografts due to the chronic allograft nephropathy that is a consequence of calcineurin inhibitor toxicity or hypertension. 18469635: BACKGROUND: Raised intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) may induce many adverse effects including the abdominal compartment syndrome. 19091785: Cyclosporine A (CsA) is an efficient immunosuppressant used for reducing allograft rejection but with a severe side effect of causing hypertension. We hypothesize that the renal epithelial sodium channel (ENaC) may participate in CsA-induced hypertension. Since enhanced ENaC activity is known to cause hypertension, these data together suggest that CsA may cause hypertension by stimulating ENaC through a pathway associated with inhibition of ABCA1 and consequent elevation of cholesterol in the cells. 1910638: Chronic hypertension produces myriad adverse effects in the coronary circulation. 21742034: The impacts of DM and HTN in the brain differ, while their separate contributions can lead to some additive adverse effects within rodent brain grey matter. 22971247: These modifications may include precise glycemic control in diabetic men and the use of pharmacologic therapies for hypertension and depression, which are less likely to cause sexual side effects. 23195006: Immunosuppressive maintenance therapy after kidney transplantation leads to various undesired side effects such as calcineurin inhibitor (CNI)-associated nephrotoxicity or elevated cardiovascular risk due to posttransplantation diabetes and hypertension. 25371590: Orthodox drugs used for the treatment of hypertension and diabetes produce side effects such as headache, nausea, vomiting, stomach pain, constipation, diarrhea, weakness, fatigue and erectile dysfunction. 25392143: BACKGROUND: Poor adherence is thought to be one of the major common causes of uncontrolled high blood pressure over the world leading to useless drug dose or class changes which may lead to increased adverse effects and medical costs. 26400076: However, in clinical practice, overtreatment of hypertension in older adults may lead to side effects and an increased risk of falls. 29875965: Medicinal treatment of arterial hypertension (AH) may cause adverse effects which can be annoying and thus influence patient's compliance with treatment. 34048743: This earlier stage of hypertension may be a trigger BP range for adverse effects of air pollution in the development of hypertension and CVD, especially in young and middle-aged individuals. 343894: Although bethanidine and debrisoquine may produce these adverse effects, they are beneficial in severe hypertension and produce fewer side effects than guanethidine. 36456799: Most available pharmaceutical products used to treat hypertension lead to adverse effects on human health. 7102526: Administration of a once-daily dosage of pindolol seems to be a simple and effective way to treat mild to moderate hypertension and one that produces relatively few side effects. 8829047: Oral health care providers must remember that hypertension may produce adverse effects on various organ systems and management of the dental needs of these patients may require modification of routine treatment. 8914496: Chronic hypertension has been reported to produce adverse cognitive effects in elderly individuals, perhaps by altering central nervous system hemodynamics. 11268597: Obesity is associated with diabetes, hypertension, and hyperlipidemia, leading to arteriosclerosis. 11676285: The other is arteriosclerosis (AS), historically considered a consequence of chronic hypertension and also described as lipohyalinosis (LH), a clinicopathologic association that is increasingly questioned. 1234818: [Expermental contribution on the genesis of arteriosclerosis caused by hypertension]. 12395218: Hypertension is one of the important risk factors in the pathogenesis of arteriosclerosis. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 21435165: Critical ischemic disease is often caused by arteriosclerosis due to hypertension or diabetes. 25716000: Hypertension induces structural remodelling of arteries, which leads to arteriosclerosis and end-organ damage. 31390128: CONCLUSIONS AND CLINICAL IMPLICATIONS: The associations between arteriosclerosis and diseases other than hypertension were largely explained by the association with hypertension, indicating that hypertension could be the single most important factor that leads to arteriosclerosis. 32010328: Cardiovascular diseases are the main cause of death in the industrialized world, with the main risk factors being elevated blood pressure and blood lipid levels, leading to arterial stiffness and arteriosclerosis. 32201664: Atherosclerosis in mitochondrial disorders may result from a primary pathomechanism or a secondary one due to mitochondrial diabetes, arterial hypertension, or hyperlipidemia. 33858279: BACKGROUND: Arterial hypertension causes cardiovascular adverse events mainly through endothelial dysfunction, atherosclerosis, and inflammation. 34620585: BACKGROUND AND PURPOSE: Arterial sclerosis resulting from hypertension slows CSF transportation in the perivascular spaces, showing the intrinsic relationship between the CSF and the blood vasculature. 35307987: However, little is known about whether hypertension and diabetes mellitus had different correlations with the small artery occlusion (SAO) and LAA etiology of MCA disease. 35470476: Reactive oxygen species (ROS) have been shown to play key roles in the progression of diabetes, hypertension, and hypercholesterolemia which are independent risk factors that lead to atherosclerosis and the development of IHD. 35524670: Arterial hypertension (AH) is most often the cause of ICH, followed by atherosclerosis, blood diseases, inflammatory changes in cerebral vessels, intoxication and vitamin deficiencies. 36151345: Established risk factors for the metabolic syndrome as diabetes and arterial hypertension are believed to be the cause of arteriosclerosis and subsequently following diseases like coronary heart disease, apoplexy, or chronic renal failure. 36169279: Therefore, obesity may reduce the risk of arteriosclerosis caused by hypertension when hypertension and obesity coexist, especially in women and middle-aged people, which supports the obesity paradox. 36300739: Critical vascular disease background of atherosclerosis caused by diabetes mellitus or hypertension. 36359836: For example, hypertension causes systemic arteriosclerosis, and the kidney can be seriously affected by abundant blood vessels, which may lead to a decreased glomerular filtration rate (GFR) and proteinuria, resulting in hypertension-related kidney diseases. 36449232: CONCLUSIONS: This study demonstrated for the first time that circulating elabela declined in a higher stage of hypertension and hypertensive patients with increased carotid IMT, implicating that elabela may be involved in the pathogenesis of hypertension-associated subclinical atherosclerosis. 36613760: It is generally believed that exposure to air pollution in the long-term can accelerate atherosclerosis progression by promoting dyslipidemia, hypertension, and other metabolic disorders due to systemic inflammation and oxidative stress. 37401679: RESULTS AND DISCUSSION: In the course of natural aging, a structural remodeling of bladder vascular bed was observed, from the development of atherosclerosis of extra-organ arteries to restructuring of intra-organ arteries due to arterial hypertension. 37404379: However, aging is not the only deleterious factor of vascular problems; hypertension, hypercholesterolemia, diabetes mellitus, and kidney disease may induce atherosclerosis and arteriosclerosis (i.e., arterial stiffening), and the progression of these diseases ultimately leads to cardiovascular, cerebrovascular, chronic kidney, or peripheral artery disease. 37457142: Inflammation, oxidative stress, obesity, infection, hyperlipidemia, hypertension, and diabetes are the main causes of atherosclerosis, which in the long term lead to hardening of the arteries. 8090273: The cause of the neogenesis and enlargement of an intracranial aneurysm is important because of the changes in the arterial wall due to congenital factors, hypertension, arteriosclerosis, etc, or hemodynamic stress caused by hypertension. 10555182: Hypertension, in older female and male patients, with or without longstanding low blood estradiol levels, may cause atherosclerosis of the feeding vessels in the dura mater, resulting in the opening of a normal AV shunt to provide collateral circulation. 10581080: The interaction of polygenic hypertension and hyperlipidemia in the pathogenesis of atherosclerosis in Tg[hCETP]DS rats substantiates epidemiological observations in humans. 10690981: The cause of stroke is unknown but may be related either to atherosclerosis-like occlusive vasculopathy, caused possibly by hypertension or corticosteroid (CS) use, or to vasculitic arterial occlusion. 11705813: To test whether accelerated atherosclerosis and aortic aneurysms were due to hypertension, we administered hydralazine to male apoE/eNOS DKO mice to reduce blood pressure. 12183769: Several animal studies have shown the importance of established vascular risk factors such as hypercholesterolemia and hypertension in the pathogenesis of radiation-induced atherosclerosis. 12235451: OBJECTIVES: Lipoprotein oxidation, dyslipidemia, and hypertension are important underlying causes of accelerated atherosclerosis in patients with diabetes mellitus. 12480731: The consequences of hypertension include cerebrovascular disease, coronary heart disease, and general atherosclerosis. Hypertension and related factors in the etiology of Alzheimer's disease. 14723268: The fatal dissection may have resulted from atherosclerosis, hemodynamic stress caused by hypertension, or trauma due to surgical manipulation. 15510907: Aging, lipids (oxidized LDL), infective agents, inflammation, increased glucose level, hypertension, smoking, increased homocysteine level, oxidative stress etc. are recognized as factors which lead to endothelial dysfunction and cause atherosclerosis. 16033691: Atherosclerosis resulting from long-standing hypertension, and cerebral hypoperfusion secondary to severe atherosclerosis and to low blood pressure may be major biological pathways linking both high blood pressure in midlife and low blood pressure in late-life to cognitive decline and dementia. 16117998: While hypertension is thought to cause atherosclerosis, the two conditions may instead represent independent consequences of autonomic dysfunction. 16227775: The devastating long-term consequences of high blood pressure include stroke, heart disease, atherosclerosis, renal disease, and other end-organ damage. 17212195: Arterial hypertension is one of the leading causes of atherosclerosis. 17317436: Some studies suggest that LBP, neurocardiovascular instability, like the OH, and atherosclerosis resulting from long standing HBP, reduces cerebral blood flow, increasing the risk of cognitive impairment, morbidity and mortality. 18047429: OH is associated with several functional cardiovascular abnormalities and increased risk of atherosclerosis resulting from hypertension associated to atherogenic lipid profile. 18158357: Deoxycorticosterone acetate salt hypertension in apolipoprotein E-/- mice results in accelerated atherosclerosis: the role of angiotensin II. 18340679: Atherosclerosis, cause or consequence of hypertension in dialysed elderly patients, more and more old, lead to adapt treatment strategies in order to prevent hypotension, which is also, a major risk factor of morbidity-mortality in dialysed patients (reverse epidemiology). 18948435: Although commonly associated with risk factors such as dyslipidemia, diabetes and hypertension, the global etiology of atherosclerosis may be alternatively attributed to underlying anthropological pressures. 19063999: Long-standing hypertension may lead to severe atherosclerosis and impaired cerebrovascular autoregulation. 20029624: In the periphery, 5-HT(2A) receptors have been linked to vasoconstriction and hypertension, and to inflammatory processes that can lead to atherosclerosis. 20598675: Endothelial cell damage or injury is invariably associated with such clinical conditions as thrombosis, hypertension, renal failure and atherosclerosis and may be also responsible for accelerated atherosclerosis in patients with chronic renal failure. 20706956: Since impaired hemostasis and high blood pressure lead to atherosclerosis and to the development of aneurysm, in this study we tested and compared the concentration of extracellular purines (e-purines) in the blood in of patients having abdominal aortic aneurysm with that from healthy volunteers. 2258776: It is likely that prolonged stress-induced hypertension is the result of neurohormonal trophic factors which cause vascular hypertrophy or atherosclerosis. 22652826: Complications such as obesity, hypertension, diabetes, dyslipidemia, and hypercoagulability cause premature atherosclerosis and increase cardiovascular mortality. 22794155: Post-transplant, several preexisting risk factors like hypertension (HTN), dyslipidemia and hyperglycemia usually get exacerbated resulting in accelerated atherosclerosis causing cardiovascular disease which is the most common cause of death in transplant patients. 22906271: Hypertension-induced atherosclerosis was associated with significantly increased levels of MMP-9 mRNA, which may enhance both the deposition of types I and III collagen and atherosclerotic plaque formation. 23877852: BACKGROUND: Hypertension is one of the most common causes of atherosclerosis, morbidity and mortality in adults. 24372218: Inflammation plays a pivotal role in conjunction with obesity, hypertension and hypercholesterolemia in the etiology of atherosclerosis. 26587426: Cerebral hypoperfusion secondary to severe atherosclerosis resulting from long-standing hypertension may be a major biological pathway linking high blood pressure (BP) to cognitive decline and dementia. 26835195: Objective Hyperlipidemia (HL) and hypertension (HT) lead to systemic atherosclerosis. 2684477: Possible connections between stress, diabetes, obesity, hypertension and altered lipoprotein metabolism that may result in atherosclerosis. 26885242: BACKGROUND: Obesity is associated with many risk factors, such as hyperlipidemia, hyperinsulinemia, hypertension and leads to early atherosclerosis. 2830782: Diabetes mellitus in combination with hypertension results in more severe atherosclerosis of the aorta and coronary arteries but the effect of diabetes mellitus alone requires further study. 29063904: INTRODUCTION: Hypertension and atherosclerosis though separate entities, are interrelated as hypertension plays an important role in the pathogenesis of atherosclerosis. 29353881: Hypertension also induces atherosclerosis in diabetes. 30307448: Atherosclerosis and hypertension are the most common causes of CVD, and multiple factors confer the susceptibility. 30344302: High blood pressure is a major cause of atherosclerosis which leads to myocardial infarction and stroke. 3276133: Indeed, the synergistic impact of hypertension and hyperlipidemia in the pathogenesis of FGS may be analogous to the role of these factors in the pathogenesis of atherosclerosis. 3304637: A massive body of scientific evidence from clinical, experimental, pathological and epidemiological studies as well as from risk factor intervention trials and community studies has emerged until the 1980s; interpreted as a whole it leaves no more doubt about the major role of hyperlipidaemia, hypertension, cigarette smoking and some other modifiable factors in the aetiology of atherosclerosis and CHD, and about the great potential for primary prevention of CHD. 37893564: Background and objectives : Arterial hypertension (HTN) is the leading preventable cause of atherosclerotic cardiovascular diseases (ASCVD) and death from all causes. 3868711: The role of the nervous system in the pathogenesis of cardiovascular complications in hypertension has been clarified to a great extent in genetic rat models for hypertension, stroke and atherosclerosis, especially in the evolution of cardiovascular hypertrophy in hypertension, the most common process related to the pathogenesis and complications of hypertension, in the development of stroke, one of the most common sequelae of hypertension itself and in the pathogenesis of atherosclerotic vascular diseases, the most usual cause of myocardial infarction. 8131780: Recent studies have illustrated that in addition to the well known risk factors, such as lipoproteins, smoking, hypertension, there are others that cause atherosclerosis and myocardial infarction. 8322083: However, blacks were more likely than whites to identify renal failure as a consequence of hypertension, whereas whites were more likely to identify atherosclerosis. 8581231: Nevertheless, arterial hypertension is still a very important problem in diabetic patients with and without nephropathy and complications of atherosclerosis are common as a result of chronic hypertension and hyperlipidemia. 11558841: Hypertension is perhaps the most common cardiovascular antecedent cause of AF, and particularly a disproportionate cause of morbidity and mortality among blacks. 15913489: Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. 16157832: Hypertension (n = 48; 35%) was the most common primary cause of AF, followed by alcohol related (n = 23; 17%), coronary artery disease (n = 20; 15%), and valvular heart disease (n = 17; 12%). 16271942: Atrial fibrillation itself does not lead to structural remodeling, whereas this is frequently produced by hypertension or CHF, even in the absence of AF. 16607602: Cardiovascular diseases which are associated with an activation of the renin-angiotensin-system -- myocardial infarction, heart failure, hypertension -- often induce atrial fibrillation. 17664857: Arterial hypertension (HTN) represents one of the major causes of atrial fibrillation, a cardiac arrhythmia with high prevalence and comorbidity. 18765964: Hypertension was the most common cause of AF, followed by advanced age. 20185115: OBJECTIVE: The purpose of this study was to characterize the atrial substrate predisposing to AF due to short-duration hypertension. 20466075: BACKGROUND: Hypertension accounts for more atrial fibrillation (AF) than any other predisposing factor. 21097807: Such models should be relevant to and accurately reproduce the important substrates associated with ageing and with diseases such as hypertension, heart failure, and ischaemic heart disease which cause AF in the vast majority of patients. 22198902: This study was designed to compare the diagnostic accuracy of two widely diffused home BP monitoring devices in detecting AF in an unselected population of outpatients referred to a hypertension clinic because of high BP. 26259287: Obesity is associated with numerous comorbidities, including hypertension, lipid disorders and type II diabetes, and is also a major cause of cardiovascular disease, coronary disease, heart failure, atrial fibrillation, and sudden death. 28169950: RECENT FINDINGS: Diseases such as hypertension, valvular heart disease, and heart failure may induce atrial fibrillation, which increases the risk of stroke and sudden cardiac death. 28290877: Arterial hypertension (AH) occupies the first place among causes of atrial fibrillation (AF) in general population. 29049041: There is emerging evidence to suggest that the successful management of several cardiovascular risk factors [obesity, hypertension (HTN), diabetes mellitus, and obstructive sleep apnea (OSA)] can lead to fewer complications and atrial fibrillation prevention. 29670471: Purpose: to explore patients' characteristics associated with AF caused by hypertension. Methods: The sample of the study included 170 patients with AF caused by hypertension. 32196618: Correlation analysis between ADAMTS-13 gene polymorphism and hypertension-induced atrial fibrillation. Correlation analysis between ADAMTS-13 gene polymorphism and hypertension-induced atrial fibrillation.OBJECTIVE: The aim of this study was to explore the relationships between ADAMTS-13 gene polymorphisms and hypertension-induced atrial fibrillation (AF). CONCLUSIONS: ADAMTS-13 gene polymorphism is correlated with the susceptibility and procession of hypertension-induced AF. 32395776: Assessment of atrial conduction time by Doppler tissue imaging in hypertensive patients.BACKGROUND: Hypertension is the first cause of atrial fibrillation. 32613146: Highly Reactive Isolevuglandins Promote Atrial Fibrillation Caused by Hypertension. 32614933: Removing the Stress From Hypertension-Induced Atrial Fibrillation. 3285783: Hypertension, ischemic heart disease, and rheumatic valvular disease are the commonest causes of atrial fibrillation. 33390040: Aggressive blood pressure management in patients with known AF reduces overall arrhythmia burden, but it remains unclear whether hypertension is causative for AF. 33516406: Hypertension (HT) confers the highest population-attributable risk among factors leading to atrial fibrillation (AF). 35726314: Conclusion: In China, hypertension is the leading preventable cause of AF, and more than half of these cases can be prevented through improving those modifiable risk factors. 36026686: OBJECTIVE: It is known, that arterial hypertension (AH) is the main cause of atrial fibrillation (AF).The aim of our study was to assess the parameters of systemic hemodynamics as a predictor of AF development after coronavirus infection (CI). 37652577: Mediating effect of subclinical inflammation on the process of morning hypertension leading to atrial fibrillation in community-based older adults. 9809895: Because of its high prevalence in the population, hypertension was responsible for more AF in the population (14%) than any other risk factor. 9926906: Although rheumatic valvular diseases are still common in Saudi Arabia, ischemic heart disease and hypertension are emerging as important causes of AF in this developing nation, and therefore require prevention and control. 10652909: Measurement of blood pressure (BP) is problematic, mainly due to pseudo HT, postural hypotension and white-coat HT. 12697739: Treatment of mice with oral tetrahydrobiopterin reduces vascular ROS production, increases NO production as determined by electron spin resonance measurements of nitrosyl hemoglobin, and blunts the increase in blood pressure due to DOCA-salt hypertension. 1403229: BACKGROUND: In treating hypertension the optimal dose of angiotensin converting enzyme (ACE) inhibitor is derived from dose-response curves that relate the quantity of drug taken to the resulting fall in blood pressure; the blood pressure fall reflects a decrease in vascular resistance and hence, a degree of arteriolar vasodilation. 1694932: The complexity of pathophysiologic interrelationships and the fact that risk factors for atherosclerosis are increased in hypertension suggest that reduction of blood pressure cannot be expected to ameliorate all consequences of hypertension. 1715488: Although blood pressure (BP) may be effectively lowered by a variety of treatments, it is becoming clear that these structural adaptation, and the risks and consequences of hypertension, may persist long after BP has been restored to normal levels. 17161766: Thiazide diuretic/beta-blocker regimens lower BP, and clinical studies indicate that they reduce the risk for cardiovascular consequences of hypertension. 182009: Because of possible deleterious consequences of marked hypertension, blood pressures in these patients should be continuously monitored during the examinations and appropriate measures immediately instituted should the reaction occur. 19319498: Renal outcome is strictly dependent on blood pressure, no matter whether the kidneys are cause or consequence of hypertension. 19466524: Taken together, long-term control of BP alone is not sufficient to prevent aortic remodeling due to hypertension, but in myocardium it seems to be enough, except for cardiomyocyte hypertrophy. 20042448: The treatment of hypertension should cause blood pressure (BP) changes that reduce the long-term risks of cardiovascular morbidity and mortality. 2024278: Oxygen radicals are known to be produced by the cerebral vasculature during acute, pressor-induced hypertension and are also known to inactivate endothelium-derived relaxing factor. Superoxide dismutase decreases mortality, blood pressure, and cerebral blood flow responses induced by acute hypertension in rats. 20424941: Regardless of the mechanisms that initiate the rise of blood pressure, the development of structural changes in the systemic vasculature is the end result of established hypertension. 2053565: In animal models of hypertension it was shown that greater amounts of calcium must be given to cause a blood pressure change comparable with that in normal animals, suggesting that in high-risk human populations in which calcium metabolism may be disordered, calcium intake may have to be increased to amounts greater than 700-800 mg/d to demonstrate the blood-pressure-lowering effect. 21380549: Regardless of the mechanisms that initiate the increase in blood pressure, the development of structural changes in the systemic vasculature is the end result of established hypertension. 23523411: Failure to show benefit in some cardiovascular and renal outcome trials may be a consequence of masked hypertension, a blood pressure in the hypertensive range outside the office setting. 24398607: Regardless of the mechanisms that initiate the increase in blood pressure, functional and structural changes in the systemic vasculature are the final result of long-standing hypertension. 25099489: These data show that in a mouse model of hypertension and oxidative stress induced by AngII, exogenous H2S treatment in vivo reduces blood pressure, endothelial dysfunction and vascular oxidative stress, while inhibiting endogenous H2S production in vivo is deleterious. 25440573: ABPM revealed discordance between office BP and ambulatory BP in 61% of patients, with 3% caused by white-coat and 58% caused by masked hypertension (of which 33% were caused by isolated nocturnal hypertension). 25729324: RESULTS: This study found that, although there is good understanding of the causes and consequences of hypertension among Asian patients, there is a lack of urgency to control blood pressure. 25937175: The protective effects of GSP on blood pressure and cardiovascular remodeling in rats with DOCA-salt-induced hypertension were investigated. Our results indicated that DOCA-salt could induce hypertension, cardiovascular remodeling and dysfunction, oxidative stress and the release of endothelin-1 (ET-1) and could increase JNK1/2 and p38MAPK phosphorylation. These findings demonstrate that GSP has protective effects against increase of blood pressure induced by DOCA-salt hypertension and cardiovascular remodeling by inhibiting the reactive oxygen species/mitogen-activated protein kinase pathway via restraining the release of ET-1. 29803589: Effect of renal denervation on blood pressure in the presence of antihypertensive drugs: 6-month efficacy and safety results from the SPYRAL HTN-ON MED proof-of-concept randomised trial. 30485318: The effects of HR on the PPGF were influenced by BP, with a decreasing HR effect on the PPGF that resulted from a higher BP. 31218330: These results suggest that Ramipril can down-regulate the expression of Cx43 mRNA and protein in cerebral arterial cells of SHR, lower blood pressure, promote vasodilation, and improve arterial damage and vascular dysfunction caused by hypertension. 31644416: RESULTS: The use of telmisartan in complex treatment of high-risk patients with AH has led to decreasing blood pressure to the target level, increasing exercise tolerance (walking the distance from 315.5 m to 410.2 m in 6 minutes). 31838636: A re-evaluation at 12 months showed that although 9 out of 10 patients had normal in-office BP and BP loads improved, still 5 patients remained with MH due to nocturnal hypertension, and 7 remained with abnormal day-to-night dipping. 32008429: Recent trial results support catheter-based renal denervation (RDN) for treatment of hypertension, while the exact mechanisms causing blood pressure to fall remain incompletely understood. 32502426: The long-term cardiovascular consequences of elevated blood pressure during childhood are under investigation and it seems that the lower the childhood blood pressure the better and that the rate of change during childhood is predictive of adulthood disease. 33513094: METHODS: 10 subjects (38+/-10 years, 121+/-12 mmHg SBP) ranging from normotension to hypertension were repeatedly measured at rest and with induced changes in blood pressure (BP), and thus PWV. 33528509: The current study sheds light on older adults' beliefs about the consequences of hypertension and benefits of BP control by examining how their self-reports of hypertension diagnosis and BP control, as well as measured BP, contribute to subjective life expectancy (SLE), their perceived probability of surviving to a target age. 34084130: TDC effectively lowers blood pressure and protects against renal damage caused by hypertension in SHR. 34825245: Aims :To review peculiarities of HT in SSA, UBP causes, diagnostic modalities, AHD use, rationality and efficacy. 35965760: Hypertension is the main cause of blood pressure (BP), which further causes various cardiovascular diseases (CVDs). 36169064: Almost all (91.5%) were aware that hypertension could cause a stroke. INTRODUCTION: Achieving optimal control of blood pressure is easier when those affected understand the risks and consequences of hypertension and the principles of management. 36241705: Long-term reduction in morning and nighttime blood pressure after renal denervation: 36-month results from SPYRAL HTN-ON MED trial. 37189852: Central blood pressure (cBP) is known to be a better predictor of the damage caused by hypertension in comparison with peripheral blood pressure. 37255819: Volunteer healthcare staff interviewed the participants, measured their BP, and provided them with lifestyle advice and knowledge of the risks and consequences of high blood pressure. 37884820: Patients with systolic dysfunction without another cause, blood pressure > 95th percentile, and physician judgment that dysfunction was secondary to hypertension were included. 3891186: The antihypertensive effects of labetalol infusion (2 mg/min; maximal dose 150 mg) were evaluated in 22 subjects requiring rapid lowering of blood pressure because of severe hypertension, a hypertensive crisis after surgery, or before angiographic examination. 3900580: Over a 60 to 202 mmHg range of blood pressure induced pharmacologically or due to DOCA hypertension, the tail cuff SBP was within 4-10% of directly measured SBP. 8048614: The consequences of hypertension and aging on cardiovascular structure and function are reputed to be similar, suggesting that blood pressure plays a role in the aging process. 8539776: Because the blood pressures of SHR/y and SHR/a were also intermediate between SHR and WKY, the STS activity could be a secondary response to the hypertension. 8562273: These agents have been shown to have a beneficial influence on organ damage in hypertensive patients through an effective, continuous, smooth control of blood pressure and through specific effects on some of the functional and structural alterations induced by hypertension. 10210899: Visual hallucinations in a case of reversible hypertension-induced brain oedema. 14753396: Arterial hypertension combined with decompressive craniectomy produces extensive brain edema in the arterial boundary zone of the decompressive area. 21207238: Sever hypertension is a risk factor that exceeds the limits of brain autoregulation, leading to breakthrough brain edema. 24365441: Two opposing hypotheses are commonly cited, but the issue is controversial: (1) the current more popular theory suggests that severe hypertension exceeds the limits of autoregulation, leading to breakthrough brain edema; (2) the earlier original theory suggests that hypertension leads to cerebral autoregulatory vasoconstriction, ischemia, and subsequent brain edema. 24613735: According to the first theory, hypertension could cause a breakdown of the autoregulatory system in cerebral circulation, leading to brain edema. 29748058: Although the mechanisms underlying PRES remain unclear, research suggests that when the extent of hypertension exceeds the threshold of cerebral blood flow autoregulation, this induces blood-brain barrier disruption that leads to brain edema. 3950747: The data indicate that acute arterial hypertension may produce focal brain edema with increased permeability of the BBB in the cortex of normal brain, particularly in the arterial boundary zones. 5251121: The pathophysiology of brain swelling produced by mechanical trauma and hypertension. 5344362: Brain swelling caused by trauma and arterial hypertension. 56429: Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. 5718691: The pathophysiology of brain swelling produced by mechanical trauma and hypertension. 17498487: METHODS: A randomized controlled trial with single blind in various therapeutic centers was applied on the patients with the acute stage of hemorrhagic stroke due to hypertension, who were allocated to the trial group and the control group. 19080457: METHODS: Ninety-four patients with great hematoma as the result of brain hemorrhage due to hypertension, aged 70, were randomly divided into 2 equal groups: one point puncture group and multi-point puncture group. OBJECTIVE: To investigate the clinical effect of multi-point aspiration combined with continuous irrigation with urokinase in treating great hematoma as the result of brain hemorrhage due to hypertension. 19173202: Of the 15 haemorrhagic strokes, 40% due to arterial hypertension, six were lobar hemispheric, six were deep basal ganglia, and there were three cerebellar haemorrhages. 2047065: Chronic hypertension or preeclampsia was causative in three cases of hemorrhagic stroke. 24142453: Given that intracerebral inflammation and microglial activation play key roles in the mechanism of injury and brain damage in both ischaemic and haemorrhagic stroke, we have investigated the potential beneficial actions of Ang-(1-7) in stroke-prone spontaneously hypertensive rats (spSHRs), an established animal model of hypertension-induced haemorrhagic stroke. 24772593: One of the patients had a history of hemorrhagic stroke as a consequence of un-control hypertension. 2619442: We recommend that in patients with brain hematomas but without antecedents of arterial hypertension or with an atypically situated hematoma, a careful examination should be carried out to discard all possible causes of brain hemorrhage, together with the early performing of contrasted CT scans and posterior angiography. 26487610: Hypertension accounts for about one-third of intracerebral hemorrhage and is an important preventable cause of hemorrhagic stroke in young adults in Taiwan. 28151038: Hypertension was the major cause not only for hemorrhagic stroke but also for ischemic stroke and heart disease in the past, and the influence of hypertension has decreased with calendar years because of reduced salt intake and westernization of lifestyle, and also improved medical care. 31496339: One patient died of a hemorrhagic stroke at 27 months due to uncontrolled hypertension. 32860372: Screening for phaeochromocytoma in patients with acute cerebrovascular disease: Is it necessary?INTRODUCTION: Phaeochromocytoma may present with uncontrolled hypertension leading to haemorrhagic stroke (HS), ischaemic stroke (IS) and transient ischaemic attack (TIA). 7740564: CONCLUSIONS: Heavy drinking appeared to increase the risk of hemorrhagic stroke, in part due to hypertension, and to increase the risk of sudden death, which was probably due to drinking per se. 9432205: [Simultaneous supra- and infra-tentorial brain hemorrhage probably caused by hypertension]. 11016804: Endothelin-1 (ET-1), one of the endogenous pathological humoral factors of cardiovascular diseases such as hypertension and heart failure, has a strong vasoconstrictive action and could induce hypertension and cardiac hypertrophy. Benidipine could thus be a useful tool for preventing cardiac hypertrophy due to hypertension. 11026371: [Molecular mechanisms of cardiac hypertrophy induced by high blood pressure]. 11206683: Although many studies have examined the effects of antihypertensive therapies on hemodynamics, cardiac hypertrophy, and large vessel structure, the question of whether changes in microvascular density induced by hypertension can be restored by pharmacologic treatment has yet to be answered. 11705790: Pressure overload, such as hypertension, to the heart causes pathological cardiac hypertrophy, whereas chronic exercise causes physiological cardiac hypertrophy, which is defined as athletic heart. 12052842: Subcellular redistribution of GRK2 and GRK5 may be involved in cardiac hypertrophy resulting from chronic hypertension. 12190114: Cardiac hypertrophy refers to the abnormal growth of cardiomyocytes, and is often caused by valvular heart disease and hypertension. 12708758: The development of hypertension-induced cardiac hypertrophy is a complex process involving a number of biochemical pathways. 1283583: Several experimental and clinical studies have shown decreases of varying magnitudes in hypertension-induced cardiac hypertrophy after long term treatment. 12887125: Thus high night time blood pressure is associated with a greater morbidity and high salt intake causes cardiac hypertrophy and vascular stiffness independent of blood pressure levels. 129836: Selected groups of rats were made hypertensive by means of a surgical compression of the renal capsule which produced systemic hypertension. The purpose of this investigation was to determine whether growth hormone was an important element in the cardiac hypertrophy induced by systemic hypertension. Growth hormone in cardiac hypertrophy induced by nephrogenous hypertension. 1319958: Desensitization of adenylate cyclase and increase of Gi alpha in cardiac hypertrophy due to acquired hypertension. 1320072: This indicates that cardiac hypertrophy, at least in the early stages, is a protective adaptation allowing the heart to overcome the increased afterload resulting from hypertension. 132718: In almost all of the cases of cardiac hypertrophy due to sustained hypertension, left ventricular capacity is increased in proportion to increased left ventricular weight, even in the absence of manifest cardiac insufficiency. 1347256: Obtaining reversal of hypertension-induced cardiac hypertrophy seems to be a desirable objective of antihypertensive treatment. 14621187: Hypertension-induced pathological cardiac hypertrophy (hypertensive heart) and exercise training-induced physiological cardiac hypertrophy (athletic heart) have differences in cardiac properties. 15172670: Neuro-humoral and biomechanical processes, as seen in hypertension, produce cardiac hypertrophy, which predisposes to HF through apoptosis. 15563577: We hypothesized that the greater number of high-blood pressure episodes associated with enhanced blood pressure variability causes cardiac hypertrophy and dysfunction by activation of mechanosensitive and autocrine pathways. 15615841: Hypertension-induced cardiac hypertrophy alters the amplitude and time course of the systolic Ca2+ transient of subepicardial and subendocardial ventricular myocytes. 15792354: Chronic hypertension results in cardiac hypertrophy and may lead to congestive heart failure. 158962: However, coronary vascular resistance is greatly increased when hypertension is the cause of left ventricular hypertrophy. Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation. 15985699: In hypertension-induced cardiac hypertrophy, both PPARa and PPARg activation reveal cardio-protective effect. 16415074: Hypertension has been shown to cause cardiac hypertrophy and a shift in myosin heavy chain (MHC) gene expression from the faster alpha- to slower beta-MHC isoform. 16489410: It is suggested that autoimmune mechanisms are involved the pathogenesis of different types of hypertension and the AT(1A)-AAs may be one of the mechanisms leading to cardiac hypertrophy. 16535856: OBJECTIVE: To investigate the effect of trans-resveratrol on hypertension-induced cardiac hypertrophy and its potential mechanisms involving endothelin (ET), angiotensin II (AngII) and nitric oxide (NO). [Preventive effect of trans-resveratrol on hypertension-induced cardiac hypertrophy in partially nephrectomized rats]. 16628357: These data suggest that the activation of HO-1/CO pathway may be one of the important mechanisms by which statins inhibit cardiac hypertrophy caused by hypertension. 17085538: Our previous studies demonstrated that peripheral overexpression of angiotensin II (ANG II) type 2 receptors (AT(2)R) prevents hypertension-induced cardiac hypertrophy and remodeling without altering high blood pressure. 17210842: METHODS AND RESULTS: To explore the effect of an ameliorated mitochondrial ATP/ADP transportation on cardiac dysfunction, we generated transgenic rats overexpressing ANT1 in the heart (ANT rats) and crossed them with renin-overexpressing rats (REN rats) suffering from hypertension-induced cardiac insufficiency. Hypertension-induced cardiac hypertrophy in the REN rats was prevented by parallel ANT1 overexpression, however, and left ventricular function remarkably improved. 17386347: BACKGROUND: Chronic hypertension leads to cardiac hypertrophy, heart failure, and premature death. Little is known about the impact of dietary macronutrient composition on hypertension-induced cardiac hypertrophy and mortality. 17411275: We analyzed CMFM in patients with confirmed diagnosis of HCM (HCM, n=33, 43.8+/-13 years, 13 women, 20 men), a control group of healthy subjects (NORMAL, n=57, 39.6+/-8.9 years; 22 women and 35 men), and patients with confirmed cardiac hypertrophy due to arterial hypertension (HYP, n=42, 49.7+/-7.9 years, 15 women and 27 men). 17630346: As a critical step toward understanding the role of abnormal intracellular Ca(2+) release via the ryanodine receptor (RyR(2)) during the development of hypertension-induced cardiac hypertrophy and heart failure, this study examines two questions: 1) At what stage, if ever, in the development of hypertrophy and heart failure is RyR(2) hyperphosphorylated at Ser(2808)? 17874014: In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays an important role in cardiac tissue adaptations caused by aerobic exercise. CONCLUSION: Short term NO synthesis blockade in sedentary animals induced hypertension but did not cause cardiac hypertrophy. 18032575: Exercise training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. Severe hypertension increased systolic blood pressure to 202 +/- 9 mmHg and induced pathological hypertrophy (LV hypertrophy index was 0.34 +/- 0.02 vs. 0.44 +/- 0.02 in Ctl-Sed and HT-Sed groups, respectively) with LV relaxation alteration (early-to-atrial wave ratio = 2.02 +/- 0.11 vs. 1.63 +/- 0.12). 18070605: The altered combinatorial splicing profiles of Cav1.2 transcripts identified in SHR hearts provide a different and new perspective in understanding the possible role of molecular remodeling of Cav1.2 channels in cardiac hypertrophy as a consequence of hypertension. 18194601: OBJECTIVES: To investigate the role of focal adhesion kinase (FAK) in the pathogenesis of cardiac hypertrophy induced by hypertension. 1827058: Early after the onset of left ventricular hypertrophy secondary to hypertension, coronary vasodilator reserve is significantly impaired. During cardiac hypertrophy secondary to hypertension, the coronary arteries fail to enlarge in concert with ventricular enlargement. 1829565: [Validity of the Sokolow-Index in left heart hypertrophy caused by arterial hypertension]. 1833889: [Type of posture and RI + SIII index in Einthoven's bipolar limb ECG in left heart hypertrophy caused by arterial hypertension]. 1837967: [Assessment of the Sokolow-Lyon Index in left heart hypertrophy due to arterial hypertension. Discussion of the corresponding article by D. Naumann in the Zeitschrift fur die gesamte Innere Medizin 46 (1991) 214-216]. 1840461: The DOCA-salt model of hypertension was used to induce cardiac hypertrophy in the rat. 18703536: AIMS: Sustained hypertension leads to cardiac hypertrophy that can progress, through pathological remodelling, to heart failure. 18956652: OBJECTIVE: To investigate the role of focal adhesion kinase (FAK) in cardiac hypertrophy induced by hypertension. 19804115: Cardiac hypertrophy is caused by hypertension, myocardial infarction, endocrine disorders, and perturbations in sarcomeric function, and has become a major cause of human morbidity and mortality. 19911350: BACKGROUND: Increased salt intake may induce hypertension, lead to cardiac hypertrophy, and exacerbate heart failure. 20542874: AIMS: Innate and adaptive immune responses are associated with the development of hypertension-induced myocardial hypertrophy and fibrosis. As a result, we investigated whether heat shock protein (HSP) 70, which is a molecule of damage-associated molecular patterns, could induce inflammation in the myocardium and promote the development of hypertension-induced cardiac hypertrophy and fibrosis. 21248757: Hypertension causes cardiac hypertrophy characterized by low-grade inflammation. 2142126: Hypertension-induced cardiac hypertrophy. 21686210: Cardiac hypertrophy develops in response to increases in afterload, most commonly as the result of hypertension. 21866107: These results indicate that pirfenidone might be effective as an antifibrotic drug in the treatment of cardiac hypertrophy induced by hypertension. 22666483: BACKGROUND: Arterial hypertension (AH) induces cardiac hypertrophy and reactivation of \fetal\ gene expression. 23615214: Lowering profilin-1 expression in SHRs significantly attenuated hypertension-induced cardiac hypertrophy and fibrosis and displayed a significant preservation of myofibrils, sarcolemmal caveolae, abundance of caveolin-3 protein, activity of eNOS and production of nitric oxide (NO). 23956210: BACKGROUND: Cardiac hypertrophy and subsequent heart failure triggered by chronic hypertension represent major challenges for cardiovascular research. 2407153: Even cardiac hypertrophy, either idiopathic or as a consequence of hypertension, can be prevented by the action of Ca antagonists. 24388463: BACKGROUND: Hypertension leads to cardiac hypertrophy as an adaptive response to increased workload. 2467127: Experiments were undertaken to establish whether the chronic administration of amlodipine prevents the rise in blood pressure in spontaneously hypertensive rats (SHR), and whether it attenuates cardiac hypertrophy caused by hypertension. 24786827: Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure. 24790136: Correcting elevated blood pressure with losartan, an angiotensin II type 1 receptor antagonist, alleviated cardiac hypertrophy in Rap1b(-/-) mice, suggesting a possibility that cardiac hypertrophy develops secondary to hypertension. Defective endothelial release of dilatory nitric oxide in response to elevated blood flow leads to hypertension. 25093027: However, the underlying molecular mechanisms of AT on the hypertension-induced cardiac hypertrophy remain elusive. 2524290: These studies suggest that significant alterations in myocardial and coronary vascular structure and function occur in hypertension-induced cardiac hypertrophy. The purpose of these studies was to evaluate cardiovascular structural and functional changes in a model of hypertension-induced myocardial hypertrophy in which vasodilator therapy decreased blood pressure to normal levels. 25370512: RESULTS: Four weeks of hypertension (systolic BP 192 +/- 4 mm Hg) produced cardiac hypertrophy and thickened aortic arterial walls compared with controls (systolic BP 112 +/- 3 mm Hg). 25870195: Cardiac hypertrophy, which is commonly caused by hypertension, is a major risk factor for heart failure and sudden death. 25900768: CONCLUSION: CF6 protein was upregulated in cardiac hypertrophy induced by hypertension; further mechanisms involved in this process should be investigated. 25945137: This mechanical-chemical antagonism could lead to a potential therapeutic strategy of hypertension-induced cardiac hypertrophy. 25954323: CONCLUSION: Increased cardiac ALDH2 and proteasomal activities counteract the deleterious effect of excessive oxidative stress in hypertension-induced compensated cardiac hypertrophy in rats. Increased clearance of reactive aldehydes and damaged proteins in hypertension-induced compensated cardiac hypertrophy: impact of exercise training. 25992268: Pressure overload of the heart, such as seen with pulmonary hypertension and/or systemic hypertension, can result in cardiac hypertrophy and the eventual development of heart failure. 26458404: Importantly, this compound also prevented the development of cardiac hypertrophy induced by hypertension. 26708424: Hypertension causes cardiac hypertrophy, cardiac dysfunction and heart failure (HF). 26987380: Hypertension-induced cardiac hypertrophy is always accompanied by abnormal myocardial glucolipid metabolism due to an increase of HIF-1alpha. 27193439: L-NAME administration for 6 weeks elicited a significant increase in blood pressure which was corrected with MgO treatment; thereby cardiac hypertrophy developing secondary to hypertension was prevented. Hypertension significantly decreased the fractional shortening with slowing of shortening kinetics in left ventricular myocytes whereas magnesium treatment was capable of restoring hypertension-induced contractile dysfunction. 27268080: OBJECTIVE: We investigated the effect of polyphenol-rich CME on hypertension-induced cardiac hypertrophy in rats and its possible mechanism of action. However, the use of polyphenol-rich CME in the treatment of hypertension-induced cardiac hypertrophy has not been reported. Chrysanthemum morifolium extract improves hypertension-induced cardiac hypertrophy in rats by reduction of blood pressure and inhibition of myocardial hypoxia inducible factor-1alpha expression. 27281159: Dahl salt-sensitive hypertensive rats, a model of hypertension-induced cardiac hypertrophy, were fed a high-salt (8% NaCl) diet starting at 6 weeks. 28225023: In conclusion, BSJYD suppressed hypertension-induced cardiac hypertrophy by inhibiting the expression of ERK pathway. 28246204: However, a sustained increase in workload due to metabolic stress or uncontrolled high blood pressure induces pathological cardiac hypertrophy, which can contribute to heart failure. 28383811: HSF1 phosphorylation by ERK/GSK3 suppresses RNF126 to sustain IGF-IIR expression for hypertension-induced cardiomyocyte hypertrophy. Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure (HF). 28627693: In the present study, utilizing a model of hypertension-induced cardiac hypertrophy in spontaneous hypertensive rats, it was demonstrated that RD was significantly associated with a reduction in LV hypertrophy. In addition, RD in hypertension-induced LV hypertrophy rats was associated with the attenuation of cellular autophagic response over activation at a physiological level. 28796250: p53-mediated miR-18 repression activates HSF2 for IGF-IIR-dependent myocyte hypertrophy in hypertension-induced heart failure. Transgenic overexpression of miR-18 in cardiomyocytes is sufficient to protect against dilated cardiomyopathy during hypertension-induced heart failure. Hypertension-induced cardiac hypertrophy and attenuated cardiac function are the major characteristics of early stage heart failure. Our results demonstrated that the p53-miR-18-HSF2-IGF-IIR axis was a critical regulatory pathway of cardiomyocyte hypertrophy in vitro and in vivo, suggesting that miR-18 could be a therapeutic target for the control of cardiac functions and the alleviation of cardiomyopathy during hypertension-induced heart failure. 29180262: Thus, our study uncovered a novel MEL18-SUMO-1-HSF2-IGF-IIR pathway in the heart that profoundly influences cardiac hypertrophy for hypertension-induced heart failure. In this study, we found that heat shock transcription factor 2 (HSF2) activated IGF-IIR to induce cardiac hypertrophy for hypertension-induced heart failure. However, the detailed mechanism by which HSFs regulates IGF-IIR during hypertension-induced cardiac hypertrophy remains elusive. Inhibition of HSF2 SUMOylation via MEL18 upregulates IGF-IIR and leads to hypertension-induced cardiac hypertrophy. 29232407: Hypertension-induced cardiac hypertrophy was accompanied by acute plasma Ang II increase with amplified responses during the late phase of LV hypertrophy. 29266709: Hypertension causes cardiac hypertrophy and leads to heart failure. 29267303: Hypertension causes cardiac hypertrophy, one of the most important risk factors for heart failure (HF). 2935463: In conclusion, diltiazem can suppress hypertension induced cardiac hypertrophy. 29449707: Uncontrolled hypertension leads to cardiac hypertrophy, followed by cardiac failure. 29530793: Whether antioxidant effects induced by nitrite block critical signaling pathways involved in cardiac hypertrophy induced by hypertension has not been determined yet. While the lower nitrite dose (1 mg/kg) did not affect blood pressure, it exerted antioxidant effects and tended to attenuate mTOR pathway activation and cardiac hypertrophy induced by hypertension. Cardiac hypertrophy is a common consequence of chronic hypertension and leads to heart failure and premature death. This study may help to establish nitrite as an effective therapy in hypertension-induced cardiac hypertrophic remodeling. 29664809: MicroRNA-19a/b-3p protect the heart from hypertension-induced pathological cardiac hypertrophy through PDE5A. 2975341: These studies suggest that significant alterations in coronary vascular structure and function occur in hypertension-induced cardiac hypertrophy. The purpose of these studies was to evaluate structural and functional changes in a model of hypertension-induced cardiac hypertrophy in which vasodilator therapy prevented the increase in blood pressure. 30619368: Until recently, the role of STAT3 in hypertension-induced cardiac hypertrophy was unsettled. 30710427: Most importantly, we identify the efficacies of ATp300 inhibitors C646 and L002 in reversing hypertension-induced cardiac hypertrophy and fibrosis, and discover new anti-hypertrophic and anti-fibrotic candidates. Previously, we reported that acetyltransferase p300 (ATp300) inhibitor L002 prevents hypertension-induced cardiac hypertrophy and fibrosis in a murine model. Acetyltransferase p300 inhibitor reverses hypertension-induced cardiac fibrosis. In this short communication, we show that treatment of hypertensive mice with ATp300-specific small molecule inhibitor L002 or C646 reverses hypertension-induced left ventricular hypertrophy, cardiac fibrosis and diastolic dysfunction, without reducing elevated blood pressures. 30938418: Cardiac pressure overload (PO), such as caused by aortic stenosis and systemic hypertension, commonly results in cardiac hypertrophy and may lead to the development of heart failure. 31015570: Untreated pathological cardiac hypertrophy, which can be caused by sustained systemic hypertension, may lead to heart failure. In the present study, we investigated whether AS-1 had attenuating effects on hypertension-induced cardiac hypertrophy, and whether this process was mediated by the regulation of miRNA-143. AS-1 administration attenuated hypertension-induced cardiac hypertrophy by, at least in part, inhibin of MAPK signaling. 31285424: The aim of this study was to investigate the pharmacological effects of CTRP3 on pathological cardiac hypertrophy induced by hypertension. 31320543: Ventricular remodeling (VR) is a complex pathological process of cardiomyocyte apoptosis, cardiac hypertrophy, and myocardial fibrosis, which is often caused by various cardiovascular diseases (CVDs) such as hypertension, acute myocardial infarction, heart failure (HF), etc. 31660088: The objective of this study was to evaluate the efficacy of UTMC targeted delivery of antimiR-23a to the hearts of mice for suppression of hypertension-induced cardiac hypertrophy. AntimiR inhibition of miR-23a suppressed hypertension-induced cardiac hypertrophy in preclinical models, but clinical translation is limited by a lack of cardiac-targeted delivery systems. 31740371: CONCLUSIONS: Heart failure-related lung congestion was prevented when ACE-I was administered soon after LS impairment, accompanied by suppression of cardiac hypertrophy and fibrosis, thereby suggesting that the point of no return of myocardial remodeling due to hypertension was present after LS but before CS impairment. 32527992: Relationship Between Ubiquitin-Specific Peptidase 18 and Hypertension in Polish Adult Male Subjects: A Cross-Sectional Pilot Study.BACKGROUND Arterial hypertension (HT) is a leading cause of cardiac hypertrophy and heart failure. 32896627: Leech extract: a candidate cardioprotective against hypertension-induced cardiac hypertrophy and fibrosis. Leech extract: a candidate cardioprotective against hypertension-induced cardiac hypertrophy and fibrosis.ETHNOPHARMACOLOGICAL RELEVANCE: The prevalence of cardiovascular diseases (CVDs) has been increasing worldwide. Our findings imply that medicinal leach extract may be effective against hypertension-induced cardiac hypertrophy and fibrosis. 32903101: However, it suppressed hypertension-induced cardiac hypertrophy resulting from angiotensin II (0.8 mg/[kg.d], 7d), with inhibition of Nppa/Nppb mRNA upregulation, reduced cardiomyocyte hypertrophy and, notably, significant reductions in interstitial and perivascular fibrosis. 33093614: Pressure overload-induced cardiac hypertrophy, such as that caused by hypertension, is a key risk factor for heart failure. 33372534: In vivo, paroxetine treatment ameliorates hypertension-induced cardiac hypertrophy, dysfunction, and fibrosis in animal models. 33378940: This study aimed to investigate the effects of QDG on hypertension-induced cardiac hypertrophy and apoptosis, as well as explore its underlying mechanisms. 33390052: Moreover, SS- Clcn6 rats are protected from hypertension-induced cardiac hypertrophy and arterial stiffening; however, they have impaired vasodilation and dysregulated intracellular calcium handling. 34076830: Chronic, low-grade inflammation and oxidative stress are involved in both the initiation and progression of hypertension and hypertension-induced cardiac hypertrophy. 34357376: In this study, we revealed that liraglutide or alogliptin treatment ameliorated spontaneous hypertension-induced cardiac hypertrophy, as evidenced by decreased levels of cardiac hypertrophic markers (atrial natriuretic peptide, brain natriuretic peptide, and beta-myosin heavy chain), as well as systolic blood pressure, diastolic blood pressure, mean arterial pressure, and histological changes. However, the cardioprotective mechanism of GLP-1 on spontaneous hypertension-induced cardiac hypertrophy has not been fully elucidated. 34438076: Interestingly, the mast cell mediator, histamine, and its receptors profoundly impact the pathophysiology of the heart, resulting in hypertension-induced cardiac hypertrophy and other cardiac anomalies. 35026393: The purpose here is to survey the literature implicating Mef2 in hypertension induced cardiac hypertrophy, towards illuminating points of interest for understanding and potentially treating heart failure. 35124478: According to clinical experience, long-term hypertension will cause cardiac hypertrophy and other complications, and heart structure remodeling will significantly change the energy characteristics of the heart chambers, and impair heart function. 35730579: Cardiac hypertrophy resulting from hypertension induced by angiotensin II was reduced in these haploinsufficient PKN2 mice relative to wild-type littermates, with suppression of cardiomyocyte hypertrophy and cardiac fibrosis. 35832696: Introduction: The present study aimed to determine whether the presence of cardiac hypertrophy due to arterial hypertension is associated with a change in the activity of the oxytocinergic system in cardiomyocytes. 35964009: BACKGROUND: Hypertension-induced cardiac hypertrophy is one of the most common pre-conditions that accompanies heart failure. 36437833: In conclusion, GJD reduced the Ras/ERK1/2 pathway expression, which decreased hypertension-induced heart hypertrophy. 37888057: Pulmonary hypertension (PH) is a progressive and life-threatening disease characterized by increased pulmonary arterial pressure, which leads to right heart hypertrophy and eventually right heart failure [...]. 38334841: This study aimed to investigate the effects of ALM on hypertension-induced cardiac hypertrophy, as well as explore its underlying mechanisms. 38625371: Aerobic exercise training emerges as an effective approach to improve pathological cardiac hypertrophy and bioenergetics in hypertension-induced cardiac hypertrophy. 508010: Furthermore, propranolol mitigated hypertension induced cardiac hypertrophy, independently of its antihypertensive effect. 6214231: [Coronary flow in experimental cardiac hypertrophy caused by arterial hypertension]. 6456085: These findings indicate that the two antimyosins cross-react with a particular type of ventricular myosin heavy chain, whose distribution varies in different muscle cells and whose relative concentration changes during development and during cardiac hypertrophy induced by systemic hypertension. 7584822: Cardiac hypertrophy induced by exercise did not summate with that induced by arterial hypertension. 7590094: The ASR, which showed signs of overt heart failure, may be presented as a model for hypertension-induced end-stage cardiac hypertrophy. 7954588: METHODS: Cardiac hypertrophy induced by hypertension was produced in rats by giving saline drinking fluid and subcutaneous deoxycorticosterone acetate for four weeks. 8210751: To answer questions where and how cardiac hypertrophy occurs, secondary to hypertension and in what state the underlying hemodynamics in the heart is when it develops, various cardiac parameters were measured in 132 patients with hypertension, including cardiothoracic ratio (CTR) as calculated on a posteroanterior view and interval (Y) between the inferior vena cava and posterior outline of the heart 2 cm above their cross section on a lateral view of chest X-ray films, Wezler's parameters of vascular dynamics, Blumberger's systolic time intervals and thickness of the interventricular septum and posterior wall as measured by cardioechography. 8320834: It is well known that systemic hypertension induces cardiac hypertrophy, and it can be prevented by antihypertensive drugs. It is suggested that mechanism of left ventricular hypertrophy which is induced by systemic hypertension is related with cardiac angiotensinogen m-RNA expression. 8393491: Correlation of myosin heavy chain expression in the rat with cAMP in different models of hypertension-induced cardiac hypertrophy. Thus, our data suggest that the decreased alpha-MHC expression upon hypertension-induced cardiac hypertrophy could be mediated via decreased adenylate cyclase activity and thus decreased intracellular cAMP production. Both genetically determined and artificially-induced hypertension lead to cardiac hypertrophy and shift the myosin heavy chain (MHC) expression to the beta-MHC form. 8603509: To elucidate the regulation of very-low density-lipoprotein (VLDL) receptor, we have studied its gene expression in the heart of spontaneously hypertensive rats-stroke prone (SHR-SP, an animal model for hypertension-induced cardiac hypertrophy) compared with Wistar-Kyoto rats. 8843890: These findings have potential clinical significance in that regression of hypertension-induced cardiac hypertrophy by AT1 antagonists may be in part due to an unopposed antigrowth effect of Ang II mediated via AT2. 8964184: Moreover, in in vivo studies using spontaneously hypertensive rats, hypertension-induced cardiac hypertrophy was significantly reduced by treatment with subpressure doses of CV-11974. 9052886: Hypertension-induced cardiac hypertrophy is a predictor of the development of cardiac failure. 9072376: We studied the gene expression of the VLDL receptor in the heart of stroke-prone spontaneously hypertensive rats (SHRSP), an animal model for hypertension-induced cardiac hypertrophy. 9115206: Cardiac hypertrophy and heart failure caused by high blood pressure were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart failure. 9284412: We examined the signal transduction pathway for the development of cardiac hypertrophy induced by high blood pressure. 9293963: In this article, we summarize recent studies performed in our laboratory to investigate (1) the contribution of the renin-angiotensin system to the cardiac remodeling process, which is triggered by myocardial infarction (MI) or hypertension-induced cardiac hypertrophy; (2) the effects of angiotensin-converting enzyme (ACE) inhibition and angiotensin AT1 receptor antagonism on cardiac parameters, such as myocardial infarct size, cardiac hypertrophy, heart function, and myocardial metabolism; (3) the mechanism of an ACE inhibitor-induced increase in cardiac capillary density in spontaneously hypertensive rats (SHR) and stroke prone SHR (SHR-SP). 9314834: Hypertension-induced cardiac hypertrophy is associated with alterations in ventricular action potentials. 9650806: Thus, TG(mREN2)27 rats (TGR), a model with hypertension induced cardiac hypertrophy, was compared with age matched Sprague-Dawley rats (SPDR). 9740624: A functional consequence of hypertension-induced cardiac hypertrophy may be the inhibition of the cardioprotective action of ANP through cardiac vagal reflexes. 9865063: Localized hypertrophy in the basal part of the IVS in elderly patients could be a type of cardiac hypertrophy caused by hypertension. 9931137: A relatively new model of HF, the spontaneously hypertensive heart failure (SHHF) rat spontaneously and reproducibly develops left ventricular hypertrophy (LVH) and progresses to HF, thus enabling longitudinal studies to examine the cellular and molecular bases for hypertension-induced cardiac hypertrophy and subsequent HF. 15938091: Their determining risk factors are hypertensive disease and postoperative arterial hypertension, which, in combination with other risk factors, provokes cardiac complications in the postoperative period. 26864583: BACKGROUND: Hypertension is characterized by a maintained high blood pressure leading to cardiac complications such as left ventricular hypertrophy and fibrosis and an increased risk of heart failure and myocardial infarction. 30472885: Despite extensive research into the pathogenesis of hypertension and disease-related end organ damage, the mechanisms leading to cardiac complications of hypertensive patients are still not fully elucidated. 33611212: Small Molecule Compound Nerolidol attenuates Hypertension induced hypertrophy in spontaneously hypertensive rats through modulation of Mel-18-IGF-IIR signalling. However, their effects on hypertension induced cardiac complications are not completely understood. CONCLUSION: Collectively, the data reveals that the cardioprotective effect of nerolidol against hypertension induced hypertrophy involves reduction in blood pressure and regulation of the cardiac Mel-18-IGFIIR signalling cascade. 34102662: OBJECTIVE: Hypertension, diabetes mellitus and physical inactivity can cause cardiovascular complications or premature death. 35039140: STUDY AIM: Hypertension is a major public health concern worldwide and non-controlling it can lead to various cardiovascular complications. 35103095: As a serious cardiovascular complication, diabetic cardiomyopathy (DCM) refers to diabetes-related changes in myocardial structure and function, which is obviously different from those cardiomyopathy secondary to hypertension, coronary heart disease, and valvular disease. 36362997: Thus, this study provides a rationale for the medicinal use of CS and CL in hypertension and also against arsenic-induced cardiovascular complications. 36402827: Uncontrolled hypertension leads to cardiovascular complications and organ damage. 36409370: Hypertension remains the main cause of cardiovascular complications leading to increased mortality. Endothelial dysfunction as a factor leading to arterial hypertension. 36655145: Obesity, a chronic metabolic condition, is an increase in fat mass and blood lipid levels mainly causing atherosclerosis and hypertension, which further lead to cardiovascular complications. 38216731: Hypertension is the leading cause of cardiovascular complications. 38473800: Arterial hypertension is often the earliest onset symptom among ADPKD patients, leading to frequent cardiovascular complications. 38509942: Background: Hypertension has emerged as a chronic disease prevalent worldwide that may cause severe cardiovascular complications, particularly in older patients. 12898875: Left ventricular (LV) cardiomyopathy in hypertensive obese patients is a consequence of increased LV afterload due to systemic hypertension and increased LV pre-load subsequent to the augmentation of total blood volume in obese. 19653009: A 3-year-old girl with Alport syndrome presented with decompensated heart failure from hypertension-induced cardiomyopathy 6 months following renal biopsy. 19924547: We propose the two disorders of diabetes and hypertension have a similar etiology of cardiomyopathy resulting, in part, from an increase in the number of incomplete CRU's, due to a morphological change in the architecture and orientation of the t-tubules. 21450068: CONCLUSION: Our results indicate that the co-existence of diabetes and hypertension could induce cardiomyopathy which could further result in cardiac fibrosis, and that combination treatment with rosiglitazone and felodipine has a great protective role against the metabolic abnormalities, meanwhile, the treatment with rosiglitazone alone has a protective role with a minimal effect against these abnormalities and has no effect on decreasing BP in these cases which may lead to coronary artery diseases (CADs) in future. 21463333: METHODS: Heart samples were obtained from organ donors, including 22 high alcohol consumers, 22 with hypertension, 8 with other causes of CMP, and 10 healthy donors. 23192260: Hypertension remains the commonest cause of myocardial disease, followed by the cardiomyopathies. 23923748: We should keep in mind that obesity and diabetes also increase the risk of heart failure independent of coronary heart disease and hypertension and may cause a cardiomyopathy, a frequent, forgotten, and often fatal complication. 2688410: It is now clear that the co-existence of hypertension and diabetes mellitus produces a more severe cardiomyopathy than that produced by hypertension or diabetes alone. 30101852: These results make SGLT1 a potential candidate for the therapeutic target for hypertension-induced cardiomyopathy. 31584202: Both calcineurin and CaMKII could be valuable targets for developing treatment strategies against hypertension-induced cardiomyopathies. 31771489: Arterial hypertension is by far the most common cause of heart failure, followed by cardiomyopathies and rheumatic heart diseases. 32465006: The final prediction model included: (a) pre-implant variables (age >=62 years, hypertension, nonischemic etiology of cardiomyopathy, inotropic support); (b) post-implant laboratory variables (albumin <=3.8 mg/dL and glomerular filtration rate <=55 mL/min/1.73 m 2 at one year); and (c) post-implant adverse events (increasing rehospitalizations in the first year after LVAD implant). 32497582: Hypertension is an important and underrecognized cause of acquired cardiomyopathy in newborns. 33250480: Nephrectomy can be an effective treatment for a WT patient with hypertension causing hypertensive cardiomyopathy, and then cardiac function will be improved within several weeks. In this report, a pediatric case of WT with hypertension causing hypertensive cardiomyopathy and congestive heart failure is presented. The patient was diagnosed with cardiomyopathy caused by hypertension. 5608849: [On the protective effect of iproveratil in myocardial diseases due to hypertension in animal experiment]. 6742110: The authors propose that the additive effects of hypertension and diabetes mellitus on the myocardial microcirculation may be a primary cause of cardiomyopathy in this model of human disease. 10536660: Although they were studied in depth in relation to arterial hypertension and cardiovascular diseases, limited information on their interrelationships in causing hypertension and related target organ damage exists. 11304502: Furthermore, up to 75% of CVD in diabetes may be attributable to hypertension, leading to recommendations for more aggressive treatment (ie, reducing blood pressure to <130/85 mm Hg) in persons with coexistent diabetes and hypertension. 11391989: Blood pressure level, risk factor for cardiovascular disease and organ damage due to hypertension are essential in evaluating a patient with hypertension at outpatient clinic. 11821633: Hypertension is a major cause of cardiovascular disease in African Americans. 11927069: According to the third National Health and Nutrition Examination Survey (NHANES III), approximately 60% of the 50 million Americans with hypertension are at increased risk for cardiovascular disease resulting from uncontrolled hypertension. 11999140: In recent years, numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischaemia, myocardial infarction and left ventricular hypertrophy, have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental in the induction of cardiovascular-related diseases. 12432046: Cardiovascular diseases accounted for one third of this disparity, in large part because of hypertension (15.0 percent); HIV disease (11.2 percent) contributed almost as much as ischemic heart disease (5.5 percent), stroke (2.8 percent), and cancer (3.4 percent) combined; trauma and diabetes mellitus accounted for 10.7 percent and 8.5 percent, respectively. 12641483: In the general population, 27% of CVD in women and 37% in men is attributable to hypertension. 12693341: Education of both patients and physicians has to be conducted in order to minimize the incidence of other cardiovascular diseases that are directly or indirectly caused by hypertension. 12803737: BACKGROUND: Hypertension is one of the most important causes of cardiovascular disease, and treatment of hypertension leads to a significant reduction in cardiovascular mortality and morbidity. 12934569: Recently, it has been reported that hypertension causes not only cerebro-cardiovascular diseases, but also a decline of cognitive function in the elderly. 1446413: In order to clarify the predictive factors of cardiovascular diseases caused by hypertension and hypercholesterolaemia in adults, a longitudinal epidemiological study was started in 1978. 14551172: In recent years, numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction, and left ventricular hypertrophy have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular-related diseases. 15755466: The intricate and inextricable relationship between CKD and hypertension seems to cause cardiovascular disease that has assumed epidemic proportions. 15942455: This may be important, especially in developing countries, where poor control of hypertension is a major cause of cardiovascular diseases. 15983235: Limited information exists about the consequences of hypertension during adulthood on residual life expectancy with cardiovascular disease. 16288809: In this review, we describe damages related to hypertension in these target organs and the mechanisms involved in the pathogenesis of hypertension-induced cardiovascular diseases such as dementia, cardiac ischemia and remodeling, or nephropathy. 16513476: In recent years, numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction and left ventricular hypertrophy have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular-related diseases. 16533126: Hypertension is the leading cause of cardiovascular disease worldwide. 17000273: Although asymptomatic early on, untreated hypertension leads to cardiovascular disease, strokes, renal failure, and blindness. 17041806: BACKGROUND: Hypertension is a leading cause of cardiovascular diseases. 17643514: CONTEXT: Uncontrolled hypertension attributable to low medication adherence may cause such serious complications as cardiovascular disease and stroke. 1773499: The development of genetic rat models for research on hypertension, stroke and other cardiovascular diseases (CVD) such as spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) have contributed not only to the elucidation of the pathogenesis of hypertension-related CVD but also to their prediction and prevention. 17902522: Majority of the patients attending tertiary care OPD (80%) and 56% from PHC group believed that hypertension could lead to cardiovascular disease (CVD). 1827230: Arterial hypertension is a consistent and modifiable cause of cardiovascular disease. 18409527: Hypertension and hyperlipidemia, which are also responsible for cardiovascular diseases, are often associated with hyperuricemia. 18454246: In recent years, numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction, and left ventricular hypertrophy have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular-related diseases. 18678361: UNLABELLED: High blood pressure (BP) is a major cause of cardiovascular disease and primary hypertension is a frequent pathological condition. 18854020: BACKGROUND: The general practitioner (GP) can play an important role in promoting a healthy lifestyle, which is especially relevant in people with an elevated risk of cardiovascular diseases due to hypertension. 19202906: Metabolic syndrome, which is consisted of hypertension, dyslipidemia and impaired glucose tolerance, is one of the most significant lifestyle-related disorders that lead to cardiovascular diseases. 19403240: Hypertension is the leading cause of cardiovascular diseases, and an estimated 972 million people in the world are suffering from this problem. 19602331: Hypertension is largely responsible for premature cardiovascular disease in dialysis patients. 20380486: Inappropriate activation of the RAAS is important in hypertension-induced cardiovascular disease (CVD) and chronic kidney disease (CKD). 2039028: Hypertension and atherosclerosis make independent contributions to the pathogenesis of cardiovascular disease. 20439237: RESULTS: High blood pressure is the most common cause of cardiovascular disease and mortality globally. 20516270: OBJECTIVE: Matrix metalloproteinase (MMP)-9, also known as gelatinase B, is implicated in the development of hypertension and atherosclerotic plaque vulnerability to rupture, an important step in the etiology of cardiovascular diseases. 20805442: Cytochrome P450 1B1 contributes to angiotensin II-induced hypertension and associated pathophysiology. Hypertension is the leading cause of cardiovascular diseases, and angiotensin II is one of the major components of the mechanisms that contribute to the development of hypertension. Moreover, 2,3',4,5'-tetramethoxystilbene, which prevents both cytochrome P450 1B1-dependent and -independent components of angiotensin II-induced hypertension and inhibits associated pathophysiological changes could be clinically useful in the treatment of hypertension and associated cardiovascular and inflammatory diseases. These data suggest that cytochrome P450 1B1 contributes to angiotensin II-induced hypertension and associated pathophysiological changes. 21173343: This pathway may provide a new target for preventing cardiovascular disease resulting from hypertension. 21194777: CONCLUSION: Individuals with SD T2DM are at high risk of CVD as a result of untreated hyperglycaemia, hypertension and dyslipidaemia. 21738858: Hypertension can lead to cardiovascular diseases and other chronic conditions. 21872294: Hypertension is the leading cause of cardiovascular disease worldwide. 22111320: The objectives of treatment are to control hypertension and prevent the occurrence of cardiovascular diseases due to sustained high blood pressure, thereby reducing morbidity and mortality. 22183563: BACKGROUND: Hypertension is a leading cause of cardiovascular (CV) disease in the general population. 22527353: In recent years, numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction and left ventricular hypertrophy, have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular-related diseases. 22552991: PURPOSE: Hypertension is one of the main factors causing cardiovascular diseases. 22957211: The Pakistani population has higher incidence of cardiovascular (CV) diseases at younger ages, due to undiagnosed, uncontrolled hypertension (HTN). 22966894: BACKGROUND: Hypertension is one of the key factors causing cardiovascular diseases which make up the most frequent cause of death in industrialised nations. 23031143: Hypertension is a leading cause of cardiovascular disease and death worldwide. 23035939: Hypertension is the most prevalent, treatable cause of cardiovascular (CV) disease. 23425517: BACKGROUND: In Western societies, cardiovascular (CV) disease is the primary cause of mortality, and high blood pressure (BP) is the main reversible factor leading to CV disease. 23657109: Hypertension is a leading cause of cardiovascular disease and affects nearly one third of U.S. adults. 23662063: INTRODUCTION: Hypertension, hypercholesterolemia, and diabetes are the main causes of cardiovascular diseases in developed countries. 23671862: Patients with diabetes often develop hypertension and atherosclerosis leading to cardiovascular disease. 23913590: Pediatric cancer survivors have increased risk of obesity, hypertension, dyslipidemia, and type 2 diabetes, leading to premature cardiovascular disease (CVD). 23936809: OBJECTIVES: To examine the associations between cardiovascular disease (CVD) and hip fracture and to determine if these associations are attributable to hypertensive disease. 24024587: BACKGROUND: Hypertension is one of the key factors causing cardiovascular diseases. 24029670: Hypertension is the most common cause of cardiovascular diseases, accounting for at least half of haemorrhagic and ischaemic strokes, heart failure and renal failure in sub-Saharan Africa. 24520202: BACKGROUND: Hypertension is a leading cause of cardiovascular disease worldwide. 24533617: Hypertension is the most common non-communicable disease and the leading cause of cardiovascular disease in the world. 24594121: High blood pressure is the leading cause of cardiovascular diseases and deaths globally. 24658538: Hypertension is one of the major causes of cardiovascular-related diseases, which is highly associated with angiotensin-I-converting enzyme (ACE) activity and oxidative stress. 24672231: Hypertension is common in Asian populations and is a major cause of cardiovascular diseases. 24771883: Background: Arterial hypertension is one of the most important causes of cardiovascular diseases, and the latter are responsible for almost half of the deaths in the industrialised nations. 24910023: However, epidemiologic data are not so evident to sustain the causative association between NAFLD and hypertension, the major cause of CVD. 24915368: Hypertension is one of the main causes of cardiovascular diseases. 25174471: RESULTS: Among all the deaths due to cardiovascular diseases and DALYs, 64.0% of them were caused by high blood pressure. 25239071: Hypertension is one of the main factors causing cardiovascular diseases. 25296634: Hypertension leads to cardiovascular disease but, in specific groups, low blood pressure has been associated with a paradoxical increase in mortality. 25304106: Many studies have verified that risk factors, such as hypertension and obesity which are responsible for cardiovascular disease, start in early childhood. 25374046: BACKGROUND: Hypertension, homocysteine and renal resistive index are associated with atherosclerosis and lead to cardiovascular diseases. 25925498: Hypertension, the major cause of cardiovascular disease, is bidirectionally linked to arterial stiffness. 26039136: Hypertension is a leading cause of cardiovascular disease. 26125644: PURPOSE OF REVIEW: Hypertension, which is present in about one quarter of the world's population, is responsible for about 41% of the number one cause of death - cardiovascular disease. 26259287: Obesity is associated with numerous comorbidities, including hypertension, lipid disorders and type II diabetes, and is also a major cause of cardiovascular disease, coronary disease, heart failure, atrial fibrillation, and sudden death. 26619661: Abstract Hypertension is the major cause of cardiovascular disease. Persistent hypertension leads to cardiovascular remodeling and resulted in heart diseases such as coronary artery disease, heart failure, and arrhythmia. 26699542: Among them, almost half of T2D have hypertension, which is responsible for cardiovascular disease, morbidity, and mortality in these patients. 26812772: BACKGROUND: Hypertension is the leading cause of cardiovascular disease worldwide, and both high and low blood pressures are associated with various chronic diseases. 2694754: Early rise in blood pressure, sympathetic overresponsiveness, early development of cardiovascular hypertrophy, increased salt-sensitivity and membrane abnormalities detected in vascular smooth muscle cells (VSMC) from SHR and SHRSP, which are related to the pathogenesis of hypertension, have been examined for their applicability to the prediction of hypertension in man. The development of genetic models for research on hypertension and stroke, spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP), have contributed not only to the elucidation of the pathogenesis of hypertension-related cardiovascular diseases (CVD) but also to their prediction and prevention. 27102022: BACKGROUND: Hypertension is the leading cause of cardiovascular disease and premature death worldwide. 27168797: More importantly, it inhibited vascular and cardiovascular remodeling, which may reduce the risk of hypertension-induced cardiovascular diseases. 27688697: BACKGROUND: Hypervolemia is a major risk factor for hypertension leading to cardiovascular diseases and also a frequent problem in maintenance hemodialysis (MHD) patients. 27856040: BACKGROUND: Hypertension is a major cause of cardiovascular disease. 28058623: INTRODUCTION: Hypertension is the leading cause of cardiovascular disease worldwide. 28332303: Hypertension is the leading cause of cardiovascular disease in the United States and worldwide. 28482942: Impairment and disability associated with depression is significant and equal to that attributable to cardiovascular disease and greater than that due to other chronic physical disorders, such as hypertension, diabetes, and arthritis (Wells et al., 1989). 28554882: BACKGROUND: Hypertension holds a unique place in population health and health care because it is the leading cause of cardiovascular disease and the most common noncommunicable condition seen in primary care worldwide. 28618912: Hypertension is the leading cause of cardiovascular disease and death. 28656594: Metabolic syndrome is coexistence of abdominal obesity, hyperglycemia, hyperlipidemia and hypertension that causes cardiovascular diseases, diabetes and their complications, low quality and short lifespan. 28674682: Hypertension is a leading cause of cardiovascular disease worldwide; it contributes to stroke, heart disease, kidney failure, premature death, and disability. 2868658: However, hypertension is more likely to cause cardiovascular disease in those with additional risk factors, such as cigarette smoking, hyperlipidemia, diabetes mellitus, hypokalemia, loft ventricular hypertrophy, or electrocardiographic abnormalities. 28693458: BACKGROUND: Hypertension is a leading cause of cardiovascular diseases and a growing public health problem in many developed and developing countries. 28847045: In 2013, among the Chinese people aged 25 years old and above, deaths caused by cardiovascular disease and chronic kidney disease attributable to high blood pressure were 19.912 million and 0.966 million, accounting for 52.31% of the total deaths due to cardiovascular diseases and 62.11% to the total chronic kidney diseases. 28875847: Hypertension is the second leading cause of CKD after diabetes and is strongly related to morbidity and mortality. OBJECTIVE: Since there is a strong relation between hypertension and CKD, and hypertension seems to lead to cardiovascular diseases, which have epidemic proportions in CKD, this review article discusses the etiology of hypertension and the existing optimal therapies that contribute to the hypertension and heart rate management. Since this relation exists and hypertension leads to cardiovascular diseases, the management of hypertension and increased heart rate should be a main therapeutic target in these patients. 28936745: Circulating exosomes enriched with various types of biological molecules can be changed not only in the number but also in the composite cargos upon cardiac injury, such as myocardial infarction, myocardial ischemia reperfusion injury, atherosclerosis, hypertension, and sepsis cardiomyopathy, which may further influence cardiomyocyte function and contribute to the pathogenesis of cardiovascular diseases. 28943983: BACKGROUND: Hypertension is a major cause of cardiovascular diseases with a high prevalence in Jordan. 28978982: Hypertension and prehypertension may have important roles in the etiology of cardiovascular disease. 29150193: Medical histories of cardiovascular diseases were found, due mostly to hypertension (19.6%). 29220406: OBJECTIVE: A high salt intake causes hypertension and leads to cardiovascular disease. 29629296: Background: Hypertension is a major cause of cardiovascular disease and associated mortality, and postmenopausal women are at a high risk of hypertension. 29651953: BACKGROUND: Hypertension (HTN) is the main cause of cardiovascular diseases accounting for one-third of global mortality. 29866742: Hypertension often leads to cardiovascular disease and kidney dysfunction. 30058488: BACKGROUND: It is well documented in the scientific literature that high blood pressure can lead to cardiovascular disease. 30288097: Although there has been an observed progress in the treatment of hypertension, its prevalence remains elevated and constitutes a leading cause of cardiovascular disease development. 30307448: Atherosclerosis and hypertension are the most common causes of CVD, and multiple factors confer the susceptibility. 30310433: Hypertension is the most common preventable cause of cardiovascular disease. 30361193: BACKGROUND: Obesity and high blood pressure (HBP) pose high cardiovascular risks, and they are frequent causes of cardiovascular disease. 30646139: Importance: Hypertension is a leading cause of cardiovascular disease. 30723314: Hypertension is the most prevalent cause of cardiovascular disease and kidney failure, but only about 50% of patients achieve adequate blood pressure control, in part, due to inter-individual genetic variations in the response to antihypertensive medication. 30761199: Hypertension is a major health concern throughout the United States and is a major cause of cardiovascular disease. 30773269: The population attributable fraction of CVD due to hypertensive pregnancy disorder was 4.3% (95% CI 1.9-6.6) after multivariable adjustment. 30821170: OBJECTIVE: Hypertension is a major cause of cardiovascular disease. 30832344: Hypertension is the leading cause of cardiovascular disease in the United States, affecting up to one-third of adults. 30875817: Hypertension, a major cause of CVD progression, is widely attributable to genetic, behavioral, and environmental risk factors. Among the genetic reasons, angiotensin II enzyme, produced as a result of abnormal functioning of the renin-angiotensin system, is reported as the foremost cause of hypertension. 30997940: High blood pressure can lead to cardiovascular diseases. 31034450: : High blood pressure (BP) is a highly prevalent modifiable cause of cardiovascular disease, stroke, and death. 31044374: Hypertension is the leading risk factor for global mortality and morbidity and remains the major preventable cause of cardiovascular diseases. 31119677: The metabolic and physiologic responses to healthy dietary habits and physical exercise have become an increasingly interesting research area, since equilibrated diet and regular physical activity are commonly recommended for their antioxidant capacity and for the prevention and treatment of several disorders as insulin resistance, dyslipidemia, obesity, and hypertension that may result in cardiovascular disease and type II diabetes. 31156832: Objectives: Hypertension is among the leading causes of cardiovascular disease worldwide. 31170095: PURPOSE OF REVIEW: Arterial hypertension is the leading preventable cause of cardiovascular disease worldwide. 31228169: AIM: To determine the avoidable burden of cardiovascular diseases (CVDs) due to hypertension, diabetes, smoking, overweight, and obesity in countries of EMRO of the WHO. 31309069: Objective: Hypertension is an important cause of cardiovascular disorders. 31485348: Hypertension is a global public health issue and the most important preventable cause of cardiovascular diseases. 31488369: BACKGROUND: Hypertension is the leading cause of cardiovascular disease globally. 31518242: BACKGROUND: Hypertension is a major cause of cardiovascular disease in older individuals. 31743794: Hypertension is one of the main risks causing cardiovascular diseases. 31781382: Background: Hypertension is the leading cause of cardiovascular disease. 31792659: In an attempt to standardize diagnostic and therapeutic strategies and, ultimately, to increase the rate of patients with controlled blood pressure and to decrease the burden of cardiovascular disease, 13 Austrian medical societies reviewed the evidence regarding prevention, detection, workup, treatment and consequences of high blood pressure in general and in various clinical scenarios. 31908841: Background: Hypertension is a leading cause of cardiovascular disease, stroke, and death. 31948464: Uncontrolled hypertension among patients with comorbidities in sub-Saharan Africa: protocol for a systematic review and meta-analysis.BACKGROUND: Uncontrolled hypertension is the most important risk factor and leading cause of cardiovascular diseases. 31956599: Background: Hypertension is the leading cause of cardiovascular disease and death in the world. 32000777: Barriers and facilitators to the implementation of a community-based hypertension improvement project in Ghana: a qualitative study of ComHIP.BACKGROUND: Globally, hypertension is a leading cause of cardiovascular disease and mortality, with the majority of deaths occurring in low- and middle-income countries. 32024986: Hypertension is the leading cause of cardiovascular disease and premature death worldwide. 32141245: Effect Modification of Acetaldehyde Dehydrogenase 2 rs671 Polymorphism on the Association between Alcohol Intake and Blood Pressure: the Dong-gu Study.BACKGROUND: Elevated blood pressure is a major preventable cause of cardiovascular diseases. 32185742: CONCLUSIONS: These results indicate that African American breast cancer survivors have a significantly higher risk of CVD due to hypertension even after controlling for other comorbid conditions such as diabetes and obesity. 32447003: The efficacy and safety of low dialysate sodium levels for patients with maintenance haemodialysis: A systematic review and meta-analysis.BACKGROUND & AIM: Fluid overload and hypertension frequently results in cardiovascular disease, which is one of the leading causes of death in dialysis patients. 32684918: High blood pressure (BP) is a highly prevalent modifiable cause of cardiovascular disease, stroke, and death. 32715126: Introduction: Hypertension is a major and preventable risk factor that can lead to cardiovascular disease. 32740722: Role of FTO and MC4R Polymorphisms in Escalating Obesity and Their Indirect Association With Risk of T2D in Indian Population.INTRODUCTION: Obesity plays a pivotal role in the development of metabolic syndrome-excessive body fat, spikes in blood glucose levels and hypertension-and ultimately leads to cardiovascular diseases and type 2 diabetes (T2D), if left unattended. 32852643: Recent human gene sequencing efforts have identified thousands of variants among the genes encoding ENaC, and research efforts to determine if these variants and their expression in extra-renal tissue play a role in hypertension will advance our understanding of the pathogenesis of ENaC-mediated cardiovascular disease and lead to novel therapeutic targets. 33031171: OBJECTIVE: Hypertension remains the leading cause of cardiovascular disease and premature mortality globally. 33048789: Hypertension (HTN) and metabolic syndrome (MS) are important causes of CVD. 33074161: BACKGROUND: Hypertension is a major cause of cardiovascular disease, which is the leading cause of premature death. 33186318: OBJECTIVE: Hypertension is the leading cause of cardiovascular disease and premature death. 33191808: Hypertension makes up the leading cause of stroke, kidney disease, arterial disease, eye disease, and cardiovascular disease (CVD) growth. 33300570: Hypertension is one of the most important modifiable risk factor causing cardiovascular disease. 33364773: Background: Hypertension is a global health concern that can lead to cardiovascular disease and death. 33607192: BACKGROUND: Heart failure (HF), the dominant form of cardiovascular disease in Africans, is mainly due to hypertension, rheumatic heart disease and cardiomyopathy. 33620445: Importance: Hypertension is a leading cause of cardiovascular disease in adults; preclinical associations between hypertension and cardiovascular disease are seen in childhood. 33668219: However, apart from their ergogenic effects, the regular consumption of energy drinks also increases blood pressure and consequently incites problems such as hypertension, tachycardia, and nervousness, all of which can lead to cardiovascular disorders. 33749553: Hypertension is a common chronic disease that particularly affects the elderly and can trigger several cardiovascular conditions. 33808872: Among these, gasotransmitters such as nitric oxide (NO) and hydrogen sulfide (H 2 S) are very active molecules constitutively produced by endotheliocytes for the maintenance and control of vascular physiological functions, while their impairment is responsible for endothelial dysfunction and cardiovascular disorders such as hypertension, atherosclerosis, and impaired wound healing and vascularization due to diabetes, infections, and ischemia. 33840430: OBJECTIVES: Uncontrolled hypertension is a common cause of cardiovascular disease, which is the deadliest and costliest chronic disease in the United States. 34006116: COVID-19 mitigation strategies have unintended consequences on managing chronic conditions such as hypertension, a leading cause of cardiovascular disease and health disparities in the United States. 34072304: Arterial hypertension (HT) is a chronic condition of elevated blood pressure (BP), which may cause increased incidence of cardiovascular disease, stroke, kidney failure and mortality. 34161417: BACKGROUND: Hypertension is a serious and persistent public health problem and is one of the main causes of cardiovascular diseases and general mortality. 34242327: Hypertension remains the leading cause of cardiovascular disease worldwide and disproportionately impacts patients living in low- and middle-income countries (LMICs). 34269332: Global burden of cardiovascular diseases attributable to hypertension in young adults from 1990 to 2019. Young adults are not well represented in current knowledge about the CVDs burden attributable to hypertension. 34327014: Background: Hypertension is the leading cause of cardiovascular disease and premature death worldwide. 34340611: OBJECTIVE: Hypertension (HT) is the most important preventable cause of cardiovascular disease and mortality. 34359440: Hypertension, causing cardiovascular disease, stroke, and heart failure, has been a rising health issue worldwide. 34449507: ABSTRACT: The prevalence of hypertension has increased with the rise in the elderly population, and high blood pressure is a major cause of cardiovascular disease. 34464291: Hypertension is the major preventable cause of cardiovascular disease and all-cause death. 34631164: Background: Hypertension is the leading cause of cardiovascular disease, particularly in low- and middle-income countries. 34671490: Introduction: Hypertension is a major global cause of cardiovascular disease and death with rising worldwide prevalence, particularly in low-income countries. 34736077: Hypertension is one of the important causes of cardiovascular diseases, and the imbalance of vascular homeostasis caused by oxidative stress and endothelial inflammation occurs throughout hypertension pathogenesis. 34775787: Hypertension is a major cause of cardiovascular disease and deaths worldwide especially in low- and middle-income countries. 34848164: BACKGROUND: Hypertension is a leading cause of cardiovascular disease in the United States and is costing the health care system billions of dollars annually. 34889118: OBJECTIVES: Cardiovascular diseases (CVD) exert a heavy toll on health of women, mainly due to hypertension said to cluster around the period of transition to menopause. 35048969: AIMS: Hypertension is the major cause of cardiovascular diseases and global mortality. 35164833: BACKGROUND: High blood pressure is the leading cause of cardiovascular disease worldwide. 35187200: Hypertension is the major cause of cardiovascular diseases. 35325078: For CVD, largest PAFs were due to hypertension (18.7%), abdominal obesity (15.4%), tobacco use (13.5%), low strength (5.6%), and diabetes (5.3%). 35384578: RECENT FINDINGS: Hypertension is increasingly common in Sub-Saharan Africa and a leading cause of cardiovascular disease for PLWH. 35546745: INTRODUCTION: Hypertension is a leading cause of cardiovascular disease and chronic kidney disease resulting in premature death and disability. 35597366: CVDs are the number one cause of death globally, coronary artery disease (CAD) was the leading cause of death in the US in 2019, and hypertension is one of the most potent causes of CVDs. 35633212: Long risk factors like age, overweight, high dietary salt intake, smoking, sedentary lifestyle, and term hypertension might lead to various cardiovascular diseases. 35673334: Hypertension is the most important modifiable cause of cardiovascular (CV) disease and all-cause mortality worldwide. 35731159: Largest PAFs for CVD were attributable to hypertension (13.1%), high non-HDL cholesterol (11.1%), diabetes (8.9%), low education (7.7%), abdominal obesity (6.9%), and household air pollution (6.1%). 35756330: Background: Hypertension is a major cause of cardiovascular disease, chronic kidney disease (CKD), and death. 35768805: BACKGROUND: Hypertension (HTN) is a leading cause of cardiovascular diseases and deaths globally. 35805864: Hypertension is a leading cause of cardiovascular disease and premature death worldwide. 35859023: Hypertension is a leading cause of cardiovascular disease and despite established strategies to lower blood pressure, the control of hypertension remains poor. 35860751: Background and Objectives: Hypertension (HTN) is a major health concern that leads to cardiovascular disease and premature death. 35887089: Cardiovascular diseases (CVDs) are the top cause of death worldwide, and arterial hypertension per se remains the major preventable cause of CVDs [...]. 35965760: Hypertension is the main cause of blood pressure (BP), which further causes various cardiovascular diseases (CVDs). 35969164: OBJECTIVE: Hypertension is one of the most important causes of cardiovascular disease. 36000198: Hypertension is a major cause of cardiovascular disease and related mortality worldwide. 36017016: Background: Although calcium channel blockers (CCBs) are recognized as clinical first-line agents for the treatment of hypertension, their use in combination with diuretics in cardiovascular disease caused by hypertension remains controversial. 36027554: OBJECTIVE: Objective: Hypertension remains the leading cause of cardiovascular diseases worldwide. 36102254: Metabolic syndrome (MetS) is a common feature in obesity, comprising a cluster of abnormalities including abdominal fat accumulation, hyperglycemia, hyperinsulinemia, dyslipidemia, and hypertension, leading to diabetes and cardiovascular diseases (CVD). 36128474: Hypertension remains the leading cause of cardiovascular disease globally despite the availability of safe and effective treatments. 36279858: Insulin resistance, hyperglycaemia, hypertension and the metabolic abnormalities of type-2 diabetes are all involved in the pathogenesis of CVD. 36301471: They are mostly associated with cardiovascular disease as a result of concurrent hypertension, accelerated atherosclerosis, and volume overload. 36505231: Angiotensin-converting enzyme I (ACE I) is a zinc-containing metallopeptidase involved in the renin-angiotensin system (RAAS) that helps in the regulation of hypertension and maintains fluid balance otherwise, which results in cardiovascular diseases (CVDs). 36528409: For CVD, the main PAFs were due to hypertension (18.7%), abdominal obesity (15.4%), smoking (13.5%), low muscle strength (5.6%), and diabetes (5.3%). 36537265: Hypertension is the main cause of cardiovascular disease, especially in women. 36547528: Angiotensin converting enzyme (ACE) overactivation is one of the primary causes of hypertension, which leads to cardiovascular disorders all over the world. 36591357: Hypertension is the leading cause of cardiovascular disease and the primary risk factor for mortality worldwide. 36604473: Hypertension is a leading cause of heart failure and other cardiovascular diseases. 36613430: Hypertension is the leading cause of cardiovascular disease and premature death worldwide. 36728933: OBJECTIVE: Hypertension is a critical cause of cardiovascular disease, and women with HIV have a higher prevalence of hypertension compared to women without HIV. 36861733: Cardiovascular diseases are the leading cause of death worldwide (18 million deaths per year) and hypertension remains the largest preventable cause of cardiovascular disease globally. 36970367: Hypertension is the primary cause of cardiovascular disease, which is a leading killer worldwide. 37047458: Metabolic syndrome (Mets) is the major contributor to the onset of metabolic complications, such as hypertension, type 2 diabetes mellitus (DM), dyslipidemia, and non-alcoholic fatty liver disease, resulting in cardiovascular diseases. 37068598: INTRODUCTION: Hypertension is a leading cause of cardiovascular disease and premature death worldwide. 37147438: On the other hand, hypertension is a leading cause of cardiovascular disease. 37185978: Elevated blood pressure is the leading cause of cardiovascular diseases related mortality and a major contributor to non-communicable diseases globally, especially in sub-Saharan Africa where about 74.7 million people live with hypertension. 37224164: Hypertension (HTN) is the leading cause of cardiovascular diseases. 37252082: Background: Hypertension is one of the most important causes of cardiovascular diseases. 37272379: BACKGROUND: Hypertension is the leading global cause of cardiovascular disease and premature mortality in women. 37292774: Background: Hypertension is a major cause of cardiovascular disease. 37324400: The renin-angiotensin-aldosterone system (RAAS) regulates body hypertension and fluid balance which causes CVD. 37458378: Hypertension is a world-leading cause of cardiovascular disease and premature deaths. 37481950: Hypertension is a major cause of cardiovascular diseases. 37530942: Although hypertension is the leading cause of cardiovascular disease and premature death worldwide, it remains difficult to control. 37558452: INTRODUCTION: Hypertension is the major cause of cardiovascular disease and mortality in the world. 37616271: BACKGROUND AND OBJECTIVES: Hypertension (HTN), a major global health concern, is a leading cause of cardiovascular disease, premature death and disability, worldwide. 37633897: BACKGROUND & OBJECTIVES: Hypertension is a major cause of cardiovascular disease and premature death worldwide. 37694241: Background: Hypertension (HTN) is a leading cause of cardiovascular diseases and its control is poor. 37706295: Hypertension remains the leading cause of cardiovascular disease and premature death globally, affecting half of US adults. 37808381: Hypertension occupies a unique position in public health care, because it is the major cause of cardiovascular disease and the most frequent non-communicable disorder seen in primary care globally. 37892623: Erroneously, HTN, which is the leading cause of cardiovascular disease and premature death worldwide and is present in more than 90% of HF patients, is tightly linked with SNS overactivity. In contrast, it has been undermined in HF with preserved LVEF (HFpEF), which is due to hypertension (HTN) in the vast majority of the cases. 37900092: Hypertension continues to be a leading cause of cardiovascular diseases and premature death globally. 37917063: Importance: Hypertension is a major cause of cardiovascular disease, and although the Dietary Approaches to Stop Hypertension (DASH) diet lowers blood pressure (BP), adherence is typically low. 37928782: Background: Uncontrolled hypertension can cause cardiovascular disease and is an important public health issue. 38015048: The metabolic syndrome (MetS) refers to the co-occurrence of risk factors, including hyperglycaemia, increased body weight, hypertension and dyslipidemia, which eventually lead to diabetes and cardiovascular disease, a common health problem worldwide. 38083055: Hypertension is a leading cause of cardiovascular disease and premature death worldwide and it puts a heavy burden on the healthcare system. 38155990: Introduction: Hypertension (HTN) among adolescents is common in high-income countries, and leads to increased premature cardiovascular diseases (CVD). 38238381: Hypertension is one critical health issue causing cardiovascular diseases. 38270742: Hypertension is a global health problem and leads to cardiovascular disease and renal injury. 38291114: Hypertension is a major cause of cardiovascular diseases. 38359096: Hypertension is the leading cause of cardiovascular disease in women, and sub-Saharan African (SSA) countries have some of the highest rates of hypertension in the world. 38380541: Hypertension, a leading cause of cardiovascular disease and premature death, remains incompletely understood despite extensive research. 38395029: Hypertension is a major cause of cardiovascular diseases such as myocardial infarction and stroke. 38400845: The consumption of processed food is on the rise leading to huge intake of excess dietary salt, which strongly correlates with development of hypertension, often leading to cardiovascular diseases such as stroke and heart attack, as well as activation of the immune system. 38433856: Hypertension, also known as high blood pressure (BP), is a critical health issue that can cause cardiovascular disease. 38455904: Background: Undiagnosed hypertension is a major public health problem causing severe cardiovascular disorders that are responsible for a high proportion of morbidities and mortalities, especially among adults living in low-income countries. 38624058: BACKGROUND: Hypertension is a leading cause of cardiovascular disease. 7660418: BACKGROUND: Arterial hypertension is the leading cause of cardiovascular disease and is associated with an increased risk of stroke and heart attack. 7857756: Moreover the importance of left ventricular hypertrophy and structural vascular abnormalities in the developing of cardiovascular disease induced by hypertension were evaluated. 7857757: Arterial hypertension is the leading cause of cardiovascular disease in Western countries. 8754362: Congestive heart failure (CHF) continues to be a lethal end stage of cardiovascular diseases caused by hypertension, coronary heart disease, valve deformity, diabetes and cardiomyopathy. 8772576: Syndrome X, or the syndrome of insulin resistance, is a cluster of related metabolic abnormalities of hyperinsulinemia, glucose intolerance, increased very low density lipoprotein (VLDL), decreased high density lipoprotein (HDL), and hypertension in nonobese adults and plays an important role in the genesis of cardiovascular disease. 10348950: Hypertension remains a major cause of cardiovascular morbidity and mortality in the United States. 10743369: BACKGROUND: Hypertension is one of the most important causes of cardiovascular morbidity and mortality in the elderly. 10999642: In the treatment of arterial hypertension, the optimal reduction in blood pressure is obviously the one that causes the maximum achievable prevention of hypertension-associated cardiovascular morbidity and mortality. 11434450: Whether increased use of fixed low dose combination therapies would translate to better control of arterial hypertension in the population and thereby further reduction of cardiovascular/cerebrovascular morbidity and mortality caused by hypertension remains to be assessed. 11840229: Hypertension remains a major cause of cardiovascular morbidity in Belgium. 11933703: AIMS: Hypertension remains as a major cause of cardiovascular morbidity in Mexico. 12556667: Hypertension is a major cause of cardiovascular-renal morbidity and mortality and all-cause mortality. 1305808: Growth hormone (GH) hypersecretion is associated with an increased incidence of hypertension and cardiac hypertrophy, resulting in excess cardiovascular morbidity and mortality. 14560934: BACKGROUND: Hypertension is an important cause of cardiovascular morbidity and mortality. 15029220: These results suggest that the efficacy of the management of hypertension in Hungary cannot be solely responsible for the high cardiovascular morbidity and mortality. 15803895: INTRODUCTION: Arterial hypertension is one of the leading causes of cardiovascular morbidity and mortality. 16116057: BACKGROUND: Hypertension, a major cause of cardiovascular morbidity and mortality, can result from chronic hypoxia; however, the pathogenesis of this disorder is unknown. 1674840: Despite the demonstrated efficacy of traditional antihypertensive therapy in reducing blood pressure, hypertension continues to be a major cause of cardiovascular disease morbidity and mortality. 17023668: Hypertension is a prominent underlying factor in the genesis of cardiovascular-related morbidity and mortality. 18984927: BACKGROUND, Hypertension is one of the major causes of cardiovascular morbidity and mortality. 19212031: Hypertension is one of the major causes of cardiovascular morbidity. 19506447: Hypertension is one of the most important causes of cardiovascular morbidity and mortality and its treatment is a major focus of primary and secondary disease prevention strategies. 19806828: Hypertension is one of the major causes of cardiovascular morbidity and mortality. 20053965: Alterations in the circadian blood pressure pattern are frequently observed in hypertension and lead to increased cardiovascular morbidity. 20499748: BACKGROUND: Hypertension remains the commonest non-communicable disease in Nigeria and a leading cause of cardiovascular morbidity and mortality. 20590485: IMPORTANCE OF THE FIELD: Hypertension is the most common preventable cause of cardiovascular morbidity and mortality. 21286758: Epidemiologic studies in adults show that uncontrolled hypertension results in cardiovascular morbidity, but reveal increased mortality risk at low blood pressure, so that it remains unclear what the target blood pressure should be. 22816211: Hypertension is an important public health problem and the major causes of cardiovascular morbidity and mortality among aged and elderly population in India. 22981547: CONCLUSIONS: The model suggests that catheter-based renal denervation, over a wide range of assumptions, is a cost-effective strategy for resistant hypertension that might result in lower cardiovascular morbidity and mortality. 23067322: INTRODUCTION: Hypertension is a leading cause of cardiovascular morbidity and mortality, and uncontrolled hypertension remains common despite the availability of several classes of effective antihypertensive medications. 23124953: Sympathetic hyperactivity has long been recognized as a major contributor to resistant hypertension, but radical sympathectomy was abandoned several decades ago due to its significant side effects. Hypertension is a leading cause of cardiovascular morbidity and mortality. 23575708: BACKGROUND: Arterial hypertension is one of the main causes of cardiovascular disease morbidity and overall mortality. 24602391: BACKGROUND: Hypertension (HTN) is one of the major causes of cardiovascular morbidity and mortality. 24685592: Obesity plays a central role in the development of a number of risk factors and chronic diseases like hypertension, dyslipidaemia and type 2 diabetes mellitus inducing cardiovascular morbidity and mortality. 25227395: OBJECTIVES: Hypertension (HTN) is an important cause of cardiovascular related morbidity and mortality. 25300359: Hypertension is common and leads to significant cardiovascular morbidity and mortality. 25332797: High blood pressure (HBP) or hypertension (HTN) is one of the leading causes of cardiovascular (CV) morbidity and mortality throughout the world. 25526235: INTRODUCTION: Hypertension (HTN) is a preventable cause of cardiovascular morbidity and mortality. 26105249: Because hypertension is one of the leading causes of cardiovascular morbidity and mortality, the simple and accurate measurement of BP can be life saving. 26198558: Hypertension remains a leading cause of cardiovascular morbidity and mortality worldwide. 26827149: Hypertension is a leading cause of cardiovascular morbidity and mortality worldwide, yet the molecular mechanisms underpinning the development of high blood pressure remain incompletely understood. 27453854: INTRODUCTION: Hypertension is a major cause of cardiovascular morbidity and mortality in Kerala. 27498444: BACKGROUND/AIM: Hypertension is one of the leading causes of cardiovascular morbidity and mortality and more than a half of all health insurance expenditures for reimbursed medicines are allocated to antihypertensive drugs in Serbia. 27779208: Systemic arterial hypertension is an important cause of cardiovascular disease morbidity and mortality. 27855717: BACKGROUND: Hypertension is as prevalent in many developing countries, as in the developed world and is the leading cause of cardiovascular morbidity and mortality in Africa. 28069557: Hypertension is the most common cause of cardiovascular morbidities and mortalities, and a major risk factor for renal dysfunction. 28259219: Hypertension, a leading cause of cardiovascular morbidity and mortality worldwide, continues to challenge health professionals. 28306674: PURPOSE OF REVIEW: Hypertension is a leading cause of cardiovascular morbidity and mortality, affecting nearly 80 million individuals in the United States alone. 28439398: Hypertension is the leading cause of cardiovascular (CV) morbidity and mortality in adults over the age of 65. 29086364: Despite the improvements in the management of hypertension during the last three decades, it continues to be one of the leading causes of cardiovascular morbidity and mortality worldwide. 30229358: PURPOSE OF REVIEW: Obesity is a major risk factor for the development of hypertension (HTN), a leading cause of cardiovascular morbidity and mortality. 30358363: In the case of energetic elderly people without vascular disease, one should start with cholesterol-lowering drugs only if they have a high risk of cardiovascular morbidity, for example, because of diabetes mellitus or very high blood pressure. 30403686: Hypertension is a major cause of cardiovascular disease morbidity and mortality in Ghana. 30430478: INTRODUCTION: Hypertension is a major cause of cardiovascular morbidity and mortality. 30474909: Hypertension, the leading cause of cardiovascular morbidity and mortality, affects more than 1 billion people globally. 3063791: Hypertension is a cardinal risk factor in the genesis of cardiovascular morbidity and mortality. 30898362: Uncontrolled hypertension can lead to significant cardiovascular morbidity and mortality and accelerate progression to end-stage kidney disease. 31239534: The occurrence of HT is one of the leading causes of cardiovascular morbidity and mortality in adults. 31508915: HT can aggravate their prognosis and then lead to a very high cardiovascular morbidity and mortality. 32362222: * Patients were better than physicians in estimating actual average cardiovascular morbidity due to hypertension during a follow-up of 10 years. 32696080: Growing evidence indicates that patients with NAFLD are at substantial risk for the development of hypertension, coronary heart disease, cardiomyopathy, and cardiac arrhythmias, which clinically result in increased cardiovascular morbidity and mortality. 32929131: Hypertension (HTN) is an important cause of cardiovascular-related morbidity and mortality. 32964302: The increasing prevalence of hypertension is one of the leading causes of cardiovascular morbidity and mortality. 3300234: Thus, there is still room for improvement of antihypertensive drugs both in this respect and, more importantly, in achieving a further lowering of hypertension-induced cardiovascular morbidity and mortality. 33266465: Background and Objectives: Arterial hypertension remains an important cause of cardiovascular morbidity and mortality, despite all the progress made in the methods of diagnosis, monitoring of target organs' damage and treatment. 33390048: Hypertension continues to account for significant cardiovascular morbidity and mortality, with increasing prevalence anticipated. 33836171: Hypertension is a major cause of cardiovascular morbidity and mortality, despite the availability of antihypertensive drugs with different targets and mechanisms of action. 33880188: Background: Hypertension is the leading cause of cardiovascular disease morbidity and mortality worldwide. 33898117: Metabolic syndrome is a constellation of disorders including insulin resistance, hypertension, dyslipidemia, and obesity, and is considered a leading cause of cardiovascular morbidity. 33910363: High blood pressure (BP) is the leading cause of worldwide cardiovascular disease morbidity and mortality. 34046436: Background: Hypertension is a leading cause of cardiovascular-related morbidity and mortality. 34886968: Hypertension is the leading cause of cardiovascular morbidity and mortality globally. 35227430: Hypertension is a major cause of cardiovascular morbidity and mortality globally. 35380749: BACKGROUND: Globally, hypertension is a leading cause of cardiovascular morbidity and mortality. 35803634: OBJECTIVES: Hypertension is a common cause of cardiovascular morbidity and mortality. 36084087: Non-adherence to antihypertensive medications is a major cause of uncontrolled hypertension, leading to cardiovascular morbidity and mortality. 37619947: Arterial hypertension is a major cause of cardiovascular morbidity and mortality and the most common cause of and comorbidity in heart failure (HF) with preserved ejection fraction (HFpEF). 38159830: BACKGROUND: Hypertension is highly prevalent and remains one of the most frequent and preventable causes of cardiovascular morbidity and mortality. 3951141: Hypertension, or high blood pressure, is a clinical disorder, which if left untreated, results in premature cardiovascular morbidity and mortality. 7609513: Hypertension and atherosclerosis are the two leading causes of cardiovascular morbidity and mortality. 8622247: These findings argue against the hypothesis that current lead exposure levels are associated with excess cardiovascular morbidity and mortality caused by hypertension. 8845083: The main reason for treating arterial hypertension is obviously to reduce hypertension-induced cardiovascular morbidity and mortality. 8934379: OPTIMAL BLOOD PRESSURE REDUCTION: The optimal blood pressure reduction when treating arterial hypertension is obviously the one which causes the maximum achievable prevention of hypertension-associated cardiovascular morbidity and mortality. 9820439: Failure by the world dialysis community to understand and use the dry-weight method of blood pressure (BP) control has resulted in an increasing incidence of treatment-resistant hypertension, which remains the principal cause of cardiovascular morbidity and mortality. 9928746: Hypertension has become a major cause of cardiovascular morbidity and mortality in both the developed and the developing nations. 9989130: Systemic hypertension is present world-wide and it is a leading cause of cardiovascular morbidity and mortality. 1033698: An 18-year-old primipara developed acute hypertension leading to cerebral edema and convulsions following the IV injection of a bolus of 10 units of oxytocin with 0.2 mg methylergonovine maleate. 12942802: Rarely, however, the disease may be complicated by oliguria and/or severe hypertension which can cause cardiac congestion or cerebral edema. 20340827: Meningo-cerebral oedema caused by arterial hypertension. 23789896: This case suggests that, in the context of an overnight blunted blood pressure profile, even a mild or moderate hypertension can result in cerebral vasogenic oedema, underlining the diagnostic importance of 24-h blood pressure monitoring in patients with PRES without severe hypertension or other commonly recognized causes of posterior reversible encephalopathy. 28959467: With the loss of normal cerebral autoregulation, theoretical concerns are twofold: high BP can lead to cerebral oedema, haematoma expansion or haemorrhagic transformation; and low BP can lead to increased cerebral infarction or perihaematomal ischaemia. 35046075: Although the aetiology of PRES remains to be fully elucidated, hypertension with failed autoregulation results in brain oedema. 37691242: The study included 184 cases of pregnancy-related cerebrovascular disorders; 39 cases of cerebral hemorrhage, 18 of subarachnoid hemorrhage, 25 of cerebral infarction, 5 of cerebral venous sinus thrombosis, and 2 cases of eclampsia and hypertensive encephalopathy. vascular disease, resulting in venous stasis, focal cerebral edema, and eventually hemorrhagic venous infarction. 4024178: The present studies were performed to determine whether cerebral edema will develop as a consequence of arterial hypertension and/or craniectomy. 56429: Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. 8605807: Acute hypertension (rapid increase in perfusion pressure above the autoregulatory limit) may result in cerebral edema, persistent vasodilation, and brain injury. 31883791: Absence of Microbleeds Reduces the Risk for Recurrent Intracerebral Hemorrhage.BACKGROUND: Many known risk factors, including hypertension and hyperlipidemia cause intracerebral hemorrhage (ICH). 32122779: Aggressive management of hypertension is essential to halt the recent increased trends of ICH due to hypertension. 32742502: Arterial hypertension was the most common etiologic factor leading to intracerebral hemorrhage. 32953191: We describe a patient suffering from bilateral intracerebral hemorrhage after severe olanzapine intoxication without underlying thrombocytopenia, arterial hypertension, or vascular malformation as cause of intracerebral hemorrhage. 34326486: Hypertension and cerebral amyloid angiopathy (CAA) are the most common causes of primary ICH, but the mechanism of hemorrhage in both conditions is unclear. 34415518: Clinical and experimental studies show that hypertension induces intracerebral hemorrhages (ICH), including cerebral microhemorrhages in the aged brain, which contribute to the pathogenesis of vascular cognitive impairment (VCI). 34513463: Due to the patient's history of hypertension, it was believed to be a case of primary ICH caused by high blood pressure, but because of the odd positioning of the hemorrhaging, it was recommended for magnetic resonance imaging (MRI) and angiography (MRA) to be taken. 35447508: Hypertension is a common cause of intracerebral hemorrhage (ICH). 35524670: Arterial hypertension (AH) is most often the cause of ICH, followed by atherosclerosis, blood diseases, inflammatory changes in cerebral vessels, intoxication and vitamin deficiencies. 35677981: CAA had high odds of recurrent ICH (aOR, 3.38; 95% CI, 1.48 to 7.69; P=0.004) while the odds was lower in ICH due to hypertension (aOR, 0.42; 95% CI, 0.19 to 0.93; P=0.031). ICH due to hypertension had a higher odds of functional independence (adjusted odds ratio [aOR], 1.33; 95% confidence interval [CI], 1.00 to 1.77; P=0.05) and lower mortality (aOR, 0.64; 95% CI, 0.47 to 0.86; P=0.003). CONCLUSIONS: Although hypertension is the leading etiology of ICH, other etiologies are frequent. 36276494: Although the patient in case 2 succumbed to an intracerebral hemorrhage due to hypertension, aumolertinib remained effective as a treatment in cases 1 and 3. 38308370: Hypertension is most often the cause of ICH. 38520890: ICH is a type of stroke where a blood vessel in the brain ruptures due to high blood pressure, causing bleeding. 10436114: BACKGROUND AND PURPOSE: It has been speculated that the same type of hypertensive small-artery disease can cause either intracerebral hemorrhages or ischemic lesions, depending on the circumstances. 10436115: CONCLUSIONS: Our findings suggest that antiplatelet or anticoagulant medication, hypertension, or minor head trauma are most likely to precipitate cerebral hemorrhage in patients with CAA who are also epsilon2 carriers. 108061: Preliminary experience in surgical treatment of 22 cases of cerebral hemorrhage due to hypertension. 11059669: OBJECT: For the past 130 years, it has been believed that hypertension-induced cerebral hemorrhages are the result of ruptures of microaneurysms or ruptures of arteries that have degenerative changes. In this study, the authors attempted to verify the cause of hypertension-induced cerebral hemorrhage by using surgical specimens of the penetrating arteries responsible for the hemorrhages. 1132858: Intracerebral haemorrhage is most commonly due to hypertension but, as in the case of other haematomas, bleeding disorders may also be a cause. 11988589: We estimate that a third of all cases of lobar ICH are attributable to possession of an apolipoprotein E4 or E2 allele and that half of all cases of nonlobar ICH are attributable to hypertension. 12136995: The causes of death included 42 acute intoxications, 5 intestinal obstructions/bowel perforations, 1 gunshot wound, 1 intracerebral hemorrhage due to hypertensive disease, and 1 undetermined. 12621685: In practical day-to-day terms, most patients have one of the common causes of stroke: ischemic stroke caused by the complications of atherothrombosis, intracranial small Vessel disease, embolism from the heart, primary intracerebral hemorrhage caused by hypertension, or subarachnoid hemorrhage as a result of a ruptured saccular aneurysm. 1343384: Hypertension appears to be the most important cause of cerebral hemorrhage. 14648349: Arterial hypertension (AHT) is the most common cause of primary ICH, causing changes in the wall of small vessels, leading to its rupture. 15384858: All patients had supratentorial intracerebral hemorrhage caused by hypertension, with IVH, moreover clinically worsening course due to the obstructive hydrocephalus confirmed by CT. 15832987: [Complications of intracerebral hemorrhage caused by arterial hypertension]. 15948067: Arterial hypertension was the principal cause of ICH in 76%. 16269890: Intracerebral hemorrhage occurs from rupture of cerebral vessels often as the result of hypertension. 16450803: We here review the pathophysiology of primary intracerebral hemorrhage to compare and contrast bleeds due to hypertension and congophilic angiopathy. 16909699: Hypertension is the commonest cause of intracerebral hemorrhage (ICH) but non-hypertensive intracerebral hemorrhages (NHICH) are not rare. 17685130: This may implicate hypertension as the main cause of ICH. 18024696: Deep intracerebral haemorrhage, even in those over the age of 50 years, can still be due to underlying, treatable structural abnormalities, and should not be dismissed as being a result of hypertension. 18941943: These arteries were easily ruptured by hypertension, resulting in intracerebral haemorrhage. 19724290: We speculate that acute hypertension, especially when induced by AngII, may be critical in spontaneous ICH during chronic hypertension, possibly through oxidative stress and MMP-9. Incidence of ICH and levels of oxidative stress and MMP-9 were greater in mice with acute hypertension produced by AngII than by norepinephrine. The goal of this study was to develop a new model of spontaneous ICH, based on the hypothesis that acute, superimposed on chronic, hypertension produces ICH. 21294617: CONCLUSIONS: Moderate chronic hypertension resulted in more severe ICH-induced neuronal death and neurological deficits, but did not exaggerate hematoma enlargement and perihematomal brain edema in the rat ICH models. OBJECT: Hypertension is the main cause of spontaneous intracerebral hemorrhages (ICHs), but the effects of hypertension on ICH-induced brain injury have not been well studied. 21306832: Primary intracerebral hemorrhage (ICH) is caused by hypertensive disease of small penetrating blood vessels in the basal ganglia, brain stem and cerebellum. 23126354: Recurrent cerebral hemorrhages caused by hypertension secondary to reninoma are extremely rare in children. 2330079: Recurrent intracerebral hemorrhage due to hypertension. We report a series of 14 patients who had recurrent intracerebral hemorrhage due to hypertension. 23390648: Authors studied the influence of the psychoemotional stress preceding the stroke on the dynamics of neurological symptoms (Glasgo coma scale, Scandinavian stroke scale and Barthel index) and on the conformational changes of albumin in 59 patients with intracerebral hemorrhage due to arterial hypertension. 24066936: In the cerebral circulation an impaired myogenic response results in impaired cerebral autoregulation and susceptibility hypertension-induced cerebral haemorrhage. 24128695: CONCLUSION: Hypertension is the commonest cause of ICH in young Indian adults and its outcome is related to volume of ICH, GCS score and admission leukocyte count. 24276837: Intracerebral hemorrhage was probably caused by severe hypertension due to paraganglioma. 24336586: This 14 kg 3-year-old girl presented following an intracerebral haemorrhage secondary to severe systemic hypertension. 24365295: Hypertension causes pathologic changes in the walls of small (diameter<300 microns) arteries and arterioles usually at short branches of major arteries, which may result in either ischemic stroke or intracerebral hemorrhage. 24790308: In this patient, CH was suspected to have occurred due to hypertension. 26487610: Hypertension accounts for about one-third of intracerebral hemorrhage and is an important preventable cause of hemorrhagic stroke in young adults in Taiwan. 26661173: Cerebral deposition of amyloid beta promotes the hypertension-induced ICH, thus supporting the notion that hypertension is a risk factor for ICH among patients with CAA. 26738811: BACKGROUND: Intracerebral hemorrhage (ICH) is a devastating form of stroke and depending on the underlying cause, primary ICH is mainly caused by hypertension (HTN-ICH) or cerebral amyloid angiopathy (CAA-ICH). 27596750: BACKGROUND: Hypertension is the most common cause of intracerebral haemorrhages (ICHs), yet the short-term impact factors associated with hypertensive intracerebral haemorrhages (HICHs) in patients who undergo different surgical treatments are still unknown. 27799045: ICH can be spontaneous or caused by hypertension, coagulopathy, angiopathy, head trauma, bleeding disorders, tumors, or drug usage. 29412114: HS is caused by intra-cerebral hemorrhage mainly due to high blood pressure, while IS is caused by either embolic or thrombotic stroke. 29521335: Risk factors for ICH are surprisingly common in young adults, in whom ICH is often caused by structural lesions or hypertension, and only rarely by anticoagulation therapy and cerebral amyloid angiopathy (which are common predisposing factors in elderly patients). 29571760: BACKGROUND AND PURPOSE: Hypertension is an important etiology of intracerebral hemorrhage (ICH) in neurosurgical practice. 29998426: Primary ICH is due to arterial hypertension or cerebral amyloid angiopathy, and secondary ICH is due to cerebral vascular malformations, coagulopathies, infectious complications, brain tumors, and illicit stimulant drug use. 30169999: BACKGROUND: Hypertension is the main cause of intracerebral hemorrhage with a thalamic location frequency that varies from 6% to 26.5%. 30258397: ICH due to hypertension (AUC 0.81). 30915485: The location of the intracerebral hemorrhage alone should not be used to determine the cause because atypically located hemorrhages can be caused by long-standing arterial hypertension and typically located hemorrhages can occur due to non-hypertensive causes. 31375404: CONCLUSIONS: Hypertension was the most common cause of intracerebral hemorrhage in a young urban population. 31621130: Although Alzheimer's disease (AD) is associated with an increased risk of intracerebral hemorrhage (ICH) caused by hypertension and cerebral amyloid angiopathy, the precise clinical course after hypertensive ICH in AD patients is still unknown. 3265616: Arterial hypertension was the most common cause of cerebral hemorrhage and the cause in the great majority of the cerebral infarction cases was atherosclerosis. 4852815: Letter: Hypertension as the cause of cerebral hemorrhage. 6471321: The most important toxic effect of the alpha-adrenergic agonist phenylpropanolamine is hypertension, which may result in hypertensive encephalopathy or intracerebral hemorrhage. 6646340: Published information regarding the anatomy of intracerebral hemorrhages due to hypertension is inconclusive, but the bilateral basal ganglias are believed to be most frequently involved. 7233893: (2) Severe hypertension and advanced age are the two most important predisposing factors leading to intracerebral hemorrhage; the deceased patient had neither. The plaintiff alleged that failure of the attending physician to manage her husband's hypertension properly resulted in his death from intracerebral hemorrhage. 7519755: Postoperatively, uncontrollable hypertension resulted in huge intracerebral hematoma formation and increased intracranial pressure. 8085429: Hypertension (25.5%) and arteriovenous malformations (20.5%) were the main causes of cerebral hemorrhage; all subarachnoid hemorrhages except one were due to berry aneurysms. 8125619: We report a patient who developed a fatal intracerebral hemorrhage resulting from severe hypertension following embolization of a branch of the left renal artery. 8443976: All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth. 9104737: Uncontrolled high blood pressure may cause cerebral hemorrhage. 9158633: ICH secondary to hypertension (n = 311) and of undetermined etiology (n = 73) were the most common subtypes in blacks. 9622133: These findings provide evidence for a greater increase in risk of ICH due to hypertension among younger persons, current smokers, and those discontinuing antihypertensive therapy. However, those dying from ICH displayed a greater risk of ICH due to hypertension than survivors, with the ratio of the two ORs being 5.47 (95% CI, 1.23 to 24.44). 12480731: The consequences of hypertension include cerebrovascular disease, coronary heart disease, and general atherosclerosis. Hypertension and related factors in the etiology of Alzheimer's disease. 14503023: Hypertension may cause cerebrovascular disease that may increase the likelihood that individuals with AD encephalopathy will express a dementia syndrome, but hypertension may also accelerate the AD process, subclinical AD may lead to increased blood pressure, and similar biological mechanisms may be involved in the pathogenesis of both disorders. 15257371: RESULTS: In regard to total deaths in the elderly, the proportional mortality due to cerebrovascular disease and ischemic heart disease decreased 42.5% and 34.4%, respectively, while that due to hypertension increased 119%, increasing from 2.1% to 4.6%. 15830073: PURPOSE: To determine the association of homocysteine with ischemic stroke, considering age, gender, cigarette smoking, hypertension, diabetes and etiology of cerebrovascular disease. 16191231: Hypertension may cause cerebrovascular disease that may increase the likelihood that individuals with AD encephalopathy will express a dementia syndrome, this may accelerate the AD process, subclinical AD may lead to increased blood pressure, and similar biological mechanisms may be involved in the pathogenesis of both disorders. 16945211: Hypertension may thus cause cerebrovascular disease that may increase the possibility for individuals with AD encephalopathy to express a dementia syndrome. 19021021: In terms of pathophysiology of hypertensive brain damage, several hypotheses were developed, such as that vascular alterations induced by hypertension can induce lacunar or cortical infarcts and leucoaraiosis, that hypertension is responsible for cerebrovascular disease and acts into the contest of a pre-existing subclinic Alzheimer's disease (AD), that hypertension determines neurobiologic alterations (such as beta-amyloid accumulation) resulting in neuropathologic damage, and that aging and cerebrovascular risk factors act together to cause cerebral capillary degeneration, mitochondrial disruption, reduced glucose oxidation, and reduced ATP synthesis. 21861837: Isolated hypertension plays significantly major action to cause cerebrovascular disease including stroke, recurrent stoke and transient ischaemic attack. 22279736: Complex evaluation neurotrophic protein S100b, differentiation factor HLDF, idio-and antiidiotypic antibodies against these proteins in patient sera with hypertension-induced cerebrovascular disorders was performed by ELISA. These findings may be useful in further diagnostic and prognostic studies of hypertension-induced cerebrovascular disorders. 2495547: Similarly, cerebrovascular disease results largely from uncontrolled high blood pressure, much of which is attributable to unhealthy lifestyle behaviors. 26587454: However, the risks for cerebrovascular disease and coronary artery disease which are attributable to hypertension were the highest in Korea. 28353077: PURPOSE OF REVIEW: Hypertension is one of the most challenging health problems inducing cerebrovascular disease and high percentage of death when associated with diabetes, dyslipidemias, and obesity. 28757483: BACKGROUND: Left ventricular (LV) hypertrophy and subclinical cerebrovascular disease are early manifestations of cardiac and brain target organ damage caused by hypertension. 2928822: Concurrently, SMR for myocardial infarctions and cerebrovascular diseases due to hypertension has declined. 33222546: The intracranial arteries play a major role in cerebrovascular disease, but arterial remodeling due to hypertension has not been well described in humans. 3542138: [Respective roles of atheroma and hypertension in the etiology of cerebrovascular disorders]. 5715271: [The differential significance of atherosclerosis and hypertension in the pathogenesis of acute cerebrovascular disorders]. 7971936: Approximately 50 million Americans are at risk for cardiovascular and cerebrovascular disease as a result of hypertension (HTN). 10405790: Hypertension mechanisms causing stroke. Hypertension can cause stroke through many mechanisms. 10461046: Hypertension is a major cause of stroke in the African-American community, and lack of control of hypertension appears to be common. 10522259: Morbidity and mortality in hypertension are mainly determined by arterial lesions which may occur in different regional circulations: kidney, cerebral, coronary ..., causing respectively nephroangiosclerosis, stroke or myocardial infarction... 10645696: Cerebrovascular disease (CVD) is the third leading cause of death in United States and hypertension is a leading cause of both stroke and heart disease. 10731625: Its abuse can, however, be associated with massive hypertension resulting in strokes, ruptured aneurysms, or myocardial infarction. 10859502: We determined the population attributable fraction (PAF) of stroke due to hypertension (HT), atrial fibrillation (Af) and smoking in a Japanese community. 11337009: Hypertension is the main cause of stroke that represents the second most common cause of death in the industrialized world and a leading cause of inability of the elderly. 11790921: In the United States, cardiovascular disease, e.g., atherosclerosis and hypertension, that lead to heart failure and stroke, is the leading cause of mortality, accounting for over 40 percent of deaths in those aged 65 years and above. 11991910: People generally mentioned stress, diet, high blood pressure, age, and smoking as causes of stroke. 12022207: Hypertension is a major public health problem both in the developing and developed countries of the world and if untreated, can lead to various fatal complications like cerebral stroke, encephalopathy, ischaemic heart disease (IHD), renal failure and sudden cardiac death, etc. 12417834: Long-term hypertension has been implicated as one of the greatest risk factors for the cause of stroke, but yet it is a very controllable one. 12735271: Seventy-one percent and 62% of patients were aware that stroke and heart attack respectively are possible consequences of high blood pressure. Forty-five percent attributed a variety of symptoms to their high blood pressure while 55% believed that stress was a cause of their high blood pressure. 12782643: The rationale for their study in hypertension follows the observation that the major consequences of hypertension are stroke and myocardial infarction. 13770532: [Pathomorphological changes in the hypophysis in apoplexy and encephalomalacia caused by hypertension]. 14627591: Blood pressure response to renal artery stenting or enhanced medical therapy varied according to blood pressure, as did the incidence of myocardial infarction and stroke resulting from hypertension. 14681960: Twenty patients with stroke of hemisphere localization developed as a result of arterial hypertension were treated with eprosartan mesilat. 15015340: CONCLUSION: Zhenzhu Qishi Wan had significant hypotensive effect, and some protective effect on the stroke caused by hypertension. 15073389: BACKGROUND AND PURPOSE: Arterial hypertension constitutes a central factor in the pathogenesis of stroke. 15191701: Although it is clear that hypertension is a primary cause of stroke, there has been recent controversy about blood pressure management after stroke. 1524504: White matter of the brain in 25 autopsy cases with the stroke and chronic cerebro-vascular pathology produced by arterial hypertension (AH) was studied morphologically. 15559224: The data on examination of 83 patients in acute period of cerebral stroke caused by arterial hypertension and 30 healthy controls are presented. 15619477: BACKGROUND: Three medical conditions--cervical carotid artery disease, atrial fibrillation, and hypertension--cause the majority of strokes. 15683590: Although it is clear that hypertension is a primary cause of stroke, there has been controversy concerning blood pressure management after stroke. 15700394: If left unchecked and untreated, uncontrolled high blood pressure can lead to heart failure, kidney failure, heart attack and stroke. 15883684: The purpose of this article is to review the pathophysiological relevance of hypertension as a leading cause of stroke. 16132238: In contrast to men, hypertension and diabetes represent the major risk factors for development of HF in women and hypertension is also the major cause of left ventricular hypertrophy and stroke. 16198941: In Latin America, uncontrolled hypertension is one of the major causes of stroke, but other modifiable risk factors also play a role, such as heavy alcohol consumption and smoking. 16227775: The devastating long-term consequences of high blood pressure include stroke, heart disease, atherosclerosis, renal disease, and other end-organ damage. 16356365: INTRODUCTION: Hypertension is a leading cause of stroke, coronary artery disease, heart attack, and heart and kidney failure in the United States, all of which contribute to the rising costs of health care. 16392277: In obese patients with type 2 DM (T2DM) there can be associated complications of hyperinsulinaemia, dyslipidaemia, and hypertension, which can lead to coronary artery disease and stroke. 16408568: BACKGROUND: Hypertension is the most important modifiable cause of stroke. 16429165: Hypertension is a leading cause of stroke, heart disease, and kidney failure. 16614018: BACKGROUND AND PURPOSE: This retrospective study investigated the dependence of N-acetyl aspartate (NAA) ratios on risk factors for cerebral vasculopathy such as sex, age, hypertension, diabetes mellitus, carotid stenosis, and dyslipidaemia, which may have affected brain vessels and induced metabolic brain abnormalities prior to stroke. 17000273: Although asymptomatic early on, untreated hypertension leads to cardiovascular disease, strokes, renal failure, and blindness. 17317470: Measurements of carotid wall thickness via Doppler were considered to be valuable in prediction of risk of brain damage and future stroke due to hypertension in diabetic and non-diabetic patients. 17643514: CONTEXT: Uncontrolled hypertension attributable to low medication adherence may cause such serious complications as cardiovascular disease and stroke. 17885259: METHODS: Pioglitazone (1 mg x kg(-1) x d(-1)) was orally administered to stroke-prone spontaneously hypertensive rats (SHRSP) to examine the effect on incidental stroke, cerebrovascular injury, brain inflammation, oxidative stress, and vascular endothelial dysfunction induced by hypertension. 18311087: AIM: Smoking and hypertension are known causes of stroke and dementia. 18669192: In chronic situations, arterial hypertension is a frequent cause of stroke, either ischemic or hemorragic, both in patients free and those who have already suffered from brain damage. 1899938: The strong discrepancy in stroke mortality relative to prevalence of hypertension and salt intake raises the issue of the etiology of stroke in Tianjin. 19245692: BACKGROUND: Hypertension affects 29% of the adult U.S. population and is a leading cause of heart disease, stroke, and kidney failure. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 19486134: Hypertension (88.6%) was the commonest risk factor identified; 13.8% identified evil spirit/witchcraft as a cause of stroke, whilst one-sided body weakness (61.9%) was most commonly identified as warning symptom. 19615312: Hypertension in elderly patients is a common and frequent disease which could cause stroke, heart failure and renal dysfunction. 19763921: Hypertension is a leading cause of heart attack, stroke, and kidney failure and represents a serious medical issue worldwide. 19766467: It has been demonstrated that hypertension can lead to coronary heart disease, heart failure, stroke, and memory loss. 2013169: Although controversial, uncontrolled hypertension in certain population groups (e.g., northern Japanese) and high dietary saturated fat in others (e.g, Pacific-Islanders) are believed to be responsible for the high stroke incidence rates. 2021360: Hypertension, a major cause of stroke in the black population, is just one example of the impact of accessibility to intervention in central nervous system disease. 20578563: An unhealthy lifestyle may lead to hypertension which can cause strokes and cardiovascular disease. 20729727: Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. 20730072: Global health care resources and economies in general will be stressed to breaking point if this condition is not dealt with in an aggressive and timely manner because the consequences of untreated hypertension such as stroke, myocardial infarction, and dementia are exceedingly costly in the long term. 21331710: As a consequence of the sustained high BP, there is an increased risk of mortality and morbidity that is characterized by myocardial infarction, congestive heart failure, stroke, end-stage renal failure, and peripheral vascular disease (1-3). 21371277: Untreated hypertension results in stroke, dementia, and damage to major organs. 21676859: RESULTS: Direct risk reduction for stroke caused by hypertension, heart attack, kidney disease, and heart disease was calculated for a 100% compliant strategy. 21951373: This review summarizes the factors involved in the hypertension-induced stroke, such as oxidative stress, inflammation, and arterial baroreflex dysfunction, and potential strategies for its prevention, therefore, provides clues for clinicians. Fully understanding the factors involved in the hypertension-induced stroke helps to develop new strategies for stroke prevention. 22165077: INTRODUCTION: The aim of this paper is to compare the cost of secondary prevention and treatment of CVA caused by untreated arterial hypertension. 22627064: It is estimated that almost 50% of strokes may be attributable to hypertension. 22801431: Conditions such as hypertension, diabetes, atrial fibrillation, ischemic heart disease, dyslipidaemia and obesity have propensity to induce strokes, which increase risk of dementia up to five-fold in the elderly. 22941155: Approximately 54 % of stroke and 47 % of ischemic heart disease events worldwide were attributable to high blood pressure in the year 2001. 23064369: In this issue of the JCI, Young et al. show that endoplasmic reticulum (ER) stress is an essential signaling event for angiotensin II-induced hypertension in cells of the central nervous system. Hypertension occurs in approximately 30% of individuals in Western populations and is known to be a major cause of stroke, heart failure, and myocardial infarction. 23510543: This led to the initial misdiagnosis of uncontrolled hypertension as the cause of the stroke. 23680888: Stroke caused predominantly by hypertension is now a major cause of disability and premature death. 23785797: Recent advances in research into salt-sensitive hypertension revealed that mineralocorticoid receptor activities independent of aldosterone induce both salt-sensitive hypertension and organ damage, which is closely related to oxidative stress. Although novel therapeutic agents have become available and blood pressure tends to be lowered, the morbidity and mortality rates of hypertension-induced renal failure or stroke in Japan have not decreased in recent decades. 24600247: More than 60% reported that untreated hypertension may cause heart disease or stroke. 25211544: BACKGROUND: A national health objective is to reduce average U.S. sodium intake to 2,300 mg daily to help prevent high blood pressure, a major cause of heart disease and stroke. 2570426: Chronic beta-blockade inhibits atheroma formation (in animals) and beneficially modifies the incidence of stroke and myocardial infarction, which in man are the long-term consequences of hypertension. 25767287: Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke. 25932893: Hypertension is a chronic condition that can lead to heart disease, stroke, and other diseases that can result in premature death. 26060838: INTRODUCTION: Hypertension is an important cause of stroke, heart and kidney disease and these diseases are the cause for about two-thirds of all mortalities around the world. 26204337: Up to 50% of all strokes may be attributable to hypertension. 26869067: Our aim was to estimate the burden of stroke in rural SA that is attributable to high blood pressure, excess weight and high blood glucose using World Health Organization's comparative risk assessment (CRA) framework. 26913199: For example, there is an association between disrupted circadian rhythms and abnormal vital parameters such as anomalous blood pressure, irregular pulse rate, aberrant endothelial function, myocardial infarction, stroke, sleep-disordered breathing and its long-term consequences of hypertension, heart failure and cognitive impairment. 27072344: BACKGROUND: Hypertension is the leading cause for heart disease and stroke, for mortality and morbidity worldwide, and a high sodium-to-potassium intake ratio is considered a stronger risk factor for hypertension than sodium alone. 27214144: BACKGROUND: Blood pressure (BP) variability has been shown to be an independent risk factor of stroke and target organ damage because of hypertension, but so far, there have been very few studies investigating the impact of BP variability on cerebrovascular atherosclerosis. 27491737: Hazard ratios for the risk of total stroke resulting from high central systolic blood pressure (CSBP) and high PI were calculated with Cox proportional hazard models. 27722964: Hypertension is a common but complex human disease, which can lead to a heart attack, stroke, kidney disease or other complications. 27960152: BACKGROUND/AIMS: Hypertension is a major cause of stroke, and diabetes can increase incidence of this disease. 28292514: The highest PAF for CHD was caused by smoking in men and by hypertension in women; that for stroke was caused by hypertension in both sexes. 28426127: Because severe hypertension is known to cause maternal stroke, women with severe hypertension sustained over 15 minutes during pregnancy or in the postpartum period should be treated with fast-acting antihypertension medication. 28507654: BACKGROUND: More than half of all heart disease and stroke are attributable to hypertension, which is associated with approximately 10% of direct medical costs globally. 28906541: CONCLUSIONS: Hypertension affects millions of people in SSA and if left untreated, is a major cause of heart disease and stroke. 29042191: CONCLUSIONS: Hypertension affects millions of people in SSA and if left untreated, is a major cause of heart disease and stroke. 29187935: Endothelial dysfunction, alteration of brain self-regulation and severe hypertension are, probably, the cause of many strokes in pregnant women and during postpartum period. 29649151: Systemic hypertension, which eventually results in heart failure, renal failure or stroke, is a common chronic human disorder that particularly affects elders. 29702856: OBJECTIVE: Uncontrolled hypertension (HTN) results in strokes, myocardial infarction (MI), and other complications, which are the leading cause of disability, death, and severe economic consequence. 29755915: She was diagnosed with type 2 diabetes mellitus at the age of 40 years and had a cerebrovascular accident due to hypertension at the age of 42. 30022799: Resistant hypertension (failure to achieve target blood pressures with three or more antihypertensive drugs including a diuretic) is an important and preventable cause of stroke. 30209282: Autosomal-dominant hypertension and brachydactyly syndrome (HTNB; Bilginturan syndrome) is known to cause stroke before age 50 when untreated. 30281618: Hypertension, which leads to heart attacks and strokes, already affects one billion people worldwide, making it a global public health issue. Log-binomial regression was used to estimate predictors of hypertension at ART initiation, while competing risks regression was used to evaluate the relationship between predictors of incident hypertension, accounting for death as a competing risk. 30395142: CONCLUSIONS: Hypertension affects millions of people in Africa and if left untreated is a major cause of heart disease, kidney disease and stroke. 31034450: : High blood pressure (BP) is a highly prevalent modifiable cause of cardiovascular disease, stroke, and death. 31123838: PURPOSE OF REVIEW: Despite enhanced screening and therapeutic management, hypertension remains the most prevalent chronic disease in the United States and the leading cause of heart disease, chronic kidney disease, and stroke in both men and women. 31156217: MATERIAL AND METHODS: A randomized, double-blind, placebo-controlled study of the efficacy and safety of the 5-hydroxy-3-carboxypyridine-L-glutamine acid monocalcium salt (ampasse) was performed in 80 patients, aged from 50 to 75 years, with chronic cerebrovascular accident due to arterial hypertension and/or atherosclerosis of the main arteries of the head. 3120215: Hypertension, when severe, damages small blood vessels, causing kidney failure, hemorrhage, strokes, and heart failure; when the condition is mild to moderate, it produces atherosclerosis. 31700925: Background: Hypertension is a leading cause of stroke and the significance of blood pressure lowering treatment strategies for prevention of stroke has been well established. 31969096: Systematic Understanding of the Mechanisms of Flos Chrysanthemi Indici-mediated Eeffects on Hypertension via Computational Target Fishing.AIM AND OBJECTIVE: Hypertension-induced stroke and coronary artery disease are significant causes of global morbidity and mortality. 32270083: Conclusion: While hypertension does not result in as long leaves and costs, it should be prevented for being a significant cause of stroke and HF, both of which account for longer sick leaves and higher social security costs. 32317757: Among them, hypertension is a leading cause for stroke, heart disease and kidney failure. 32464941: Relationships between higher flow PI and Ao pulsatility with lower Ao compliance may partly explain the increased risk of stroke due to HTN. 32654560: Hypertension is a leading cause of stroke and dementia, effects attributed to disrupting delivery of blood flow to the brain. 32848742: Hypertension is a major cause of heart attack and stroke. 32922929: SR-B1 likely has an impact on stroke through its interaction with smoking, diabetes mellitus, diet, physical inactivity, obesity, hypercholesterolemia, atherosclerosis, coronary heart disease, hypertension, and sickle cell disease, all of which are critical risk factors in the pathogenesis of stroke. 33191808: Hypertension makes up the leading cause of stroke, kidney disease, arterial disease, eye disease, and cardiovascular disease (CVD) growth. 33238806: Cerebral hemorrhage, a devastating subtype of stroke, is often caused by hypertension and cerebral amyloid angiopathy (CAA). 33423734: Hypertension plays an important role in the pathogenesis of stroke,which,however,is only known at the blood pressure level.The relationship between circadian rhythm of blood pressure(especially the circadian rhythm disorder of blood pressure)and stroke has been a hot research topic. 34091009: The present study aims to understand the underlying vasoprotective effects of nutritional NO 2 - and NO 3 - co-therapy in mice with angiotensin-II (AT-II)-induced arterial hypertension. High-dose AT-II (1 mg/kg/d, 1w, s. c.) was used to induce arterial hypertension in male C57BL/6 mice. Arterial hypertension is one of the major health risk factors leading to coronary artery disease, stroke or peripheral artery disease. 34111216: In Brazil, the prevalence of SAH is 23.7%, which caused 203,000 deaths and 3.9 million DALYs in 2015. Stroke accounted for the highest cost attributable to SAH and the third highest PAR, representing 47% of the total cost of circulatory diseases attributable to SAH. 34359440: Hypertension, causing cardiovascular disease, stroke, and heart failure, has been a rising health issue worldwide. 34468630: The time of brain injury was from three to 10 years, caused predominantly by Stroke caused by Systemic Arterial Hypertension. 34548653: Therapy-resistant hypertension is a serious medical problem, causing end-organ damage, stroke, and heart failure if untreated. 34719512: PD patients were more often admitted with falls/fractures, infections, gastrointestinal complications, PD, dementia, psychosis/hallucinations, postural hypotension, electrolyte disturbances, stroke and surgical procedures and slightly less often due to hypertension. 34812747: SUMMARY: Hypertensive disorders of pregnancy are a continuum of failure of autoregulation mechanisms that may lead to eclampsia, posterior reversible encephalopathy syndrome, reversible cerebral vasoconstriction syndrome and stroke. 34825310: Small-vessel disease is a progressive condition, often related to common vascular risk factors such as arterial hypertension and is an important cause of stroke, vascular cognitive impairment, and dementia. 35409698: Most importantly, uncontrolled HPT can lead to severe complications (stroke, heart attack, kidney disease, and heart failure), mainly ignoring the signs in nascent stages. 35903432: Objective: Measurement and monitoring of blood pressure are of great importance for preventing diseases such as cardiovascular and stroke caused by hypertension. 35998558: OBJECTIVE: Arterial stiffness, cerebral pulsatility, and beat-to-beat blood pressure variability partly mediate the relationship between hypertension and stroke, but it is unknown if these intermediate phenotypes of vascular ageing differ between stroke aetiologies. 36169064: Almost all (91.5%) were aware that hypertension could cause a stroke. INTRODUCTION: Achieving optimal control of blood pressure is easier when those affected understand the risks and consequences of hypertension and the principles of management. 36882886: With respect to the cause of stroke, this is multifactorial, due to atherosclerotic heart disease, inflammation , atrial fibrillation, and hypertension with the latter being the most important cause. 37344814: BACKGROUND: Cardiovascular diseases, such as stroke and ischemic heart disease attributable to hypertension, are major causes of premature death in Japan and worldwide. 5448328: [Cerebrovascular accidents caused by arterial hypertension in an urban environmental]. 6000201: [Apropos of hypothalamic neurosecretion in apoplexy and softening of the brain caused by atherosclerosis and hypertensive diseases]. 6095720: This paper reports a case of a patient who suffered a cerebral vascular accident due to hypertension resulting from a catecholamine-secreting infratemporal fossa paraganglioma. 7491641: On the basis of data from the 1990 PRC population census, vital statistics, and the 1991 PRC National Hypertension Survey, the excess annual mortality from stroke due to hypertension was estimated to be at least 545,000 deaths, with a population attributable risk of 49.5%. To quantify the effect of hypertension on stroke in the PRC, we conducted a meta-analysis and estimated the population attributable risk of stroke due to hypertension. The overall relative risk of stroke in hypertensive persons and the population attributable risk of stroke due to hypertension were calculated by pooling the risk estimates from individual studies. 7738547: Presumed hypertensive small artery disease was not always found, but was still the leading cause of stroke, being present in 59% of the patients and in 62% of those with small deep infarcts. 7758051: Hypertension is a potentially life-threatening condition that can lead to heart failure, stroke, and kidney disease. 7842274: Untreated essential hypertension leads to cardiovascular and renal disease and stroke, but antihypertensive drug therapy effectively reduces these consequences of hypertension. 7974575: Men who had an elevated risk of stroke due to hypertension, diabetes, and other risk factors were excluded from the analysis. 8443976: All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth. 8623099: The age-related increase in risk of thromboembolic stroke among normotensive men resulted in a decrease in the percentage of strokes attributable to hypertension (50% in those aged 45 to 54 years to 18% in those > or = 65 years; P < .05). 8784118: CONCLUSIONS: Although factors such as hypertension and smoking are of major importance in the etiology of stroke, there is a link between a history of parental death from cardiovascular disease (stroke or heart trouble) and the risk of stroke that appears to be independent of the established risk factors. 8996484: BACKGROUND AND PURPOSE: Ambulatory blood pressure monitoring (ABPM) devices are increasingly used in the assessment of hypertension, but their value in patients after a stroke is unknown, despite the fact that hypertension is an important cause of stroke and many patients have relatively high blood pressure (BP) levels at presentation. 9154032: Consequently, hypertension remains the commonest cause of strokes in Britain and of renal failure in the United States. 9233121: The consequences of untreated hypertension include myocardial infarction, stroke, congestive heart failure, peripheral vascular disease and renal disease. 9324122: Hypertension accelerates the development of diabetic retinopathy; hypertensive/diabetic cerebral disease leads to vascular dementia, transient ischemic attacks, and strokes. 9453014: The hypertension was defined as severe, resulting in stroke before age 50 years, featuring normal renin, aldosterone, and catecholamine responses, and did not appear to be salt-sensitive. 9594990: Only 20% of the total group understood that hypertension had probably caused their stroke, although 76% of the older group and 56% of the younger group had been told at some stage that they were hypertensive. Do stroke patients realise that a consequence of hypertension is stroke? 973515: The main diseases which led to the brain stroke were hypertensive disease and general atherosclerosis. 9926911: Although mortality from hypertension as the main cause of death accounts for 1% to 4% of all deaths, mortality from stroke, mainly caused by hypertension, accounts for 10% of all deaths, indicating a failure in the treatment of hypertension. 10333847: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10333848: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10333849: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10333850: VALUES: A high value was placed on avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10333851: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10333852: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10333853: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by uncontrolled hypertension. 10426261: Hypertensive disorders and haemorrhage were the main causes of death. 10487483: The object of this study was to clarify whether or not the acute muscle cell death of the aortic media observed in normal rabbits treated with Russell's viper venom (RVV) and angiotensin II (Ang) is a result of either acute hypertension or the apoptotic effect of angiotensin II. 10624417: VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. 10856280: African Americans not only have a higher prevalence of hypertension, but the disease strikes earlier, with greater severity, and often results in death at an earlier age compared with whites in the United States. 10952370: BACKGROUND: Hypertension was the eighth leading cause of death in Taiwan in 1996, and the prevalence of hypertension has increased recently. 11173796: Presence on parental death certificates of cerebrovascular disease, other vascular disease, bronchial carcinoma, hypertension, diabetes mellitus and other causes of death was recorded. 11194313: Analyses of cause-specific mortality revealed that, overall, ectopic pregnancy, embolism, and hypertension were the leading causes of death. 11721101: Presence on parental death certificates of cerebrovascular disease, other vascular disease, bronchial carcinoma, hypertension, diabetes mellitus and other causes of death was recorded. 11812403: Hypertension was mentioned as a leading cause of death among African Americans in none of the 4 focus groups of 18-year-old to 29-year-old participants, in 2 of the 4 focus groups of 30-year-old to 49-year-old participants, and in 3 of the 4 focus groups of 50-year-old to 74-year-old participants. 11887868: And finally, the impaired ultrafiltration present in the high transporter leads to fluid overload, which is one of the driving forces for ventricular hypertrophy, hypertension, and increased cardiovascular risk--cardiovascular events being most prevalent cause of death in dialysis patients. 1189673: Persons with arteriosclerotic and hypertensive diseases as a cause of death are more often of pyknic constitution. 1196533: Arterial hypertension (68%) was the main cause of death, while renal disease, leukaemia, angioma of the pons, and embolism due to bacterial endocarditis were also observed. 12409667: SUMMARY BACKGROUND DATA: Chronic pancreatitis is generally associated with continued pain, parenchymal and ductal hypertension. and progressive pancreatic dysfunction, and it is a cause of premature death in patients who receive conservative treatment. 12554249: Haemorrhage, sepsis and Hypertensive diseases in pregnancy were the leading causes of death. 12589160: Univariate analysis of risk factors showed a significant reduction of graft survival in recipients transplanted with kidneys coming from donors older than 60 years, donors with a history of hypertension, a cerebrovascular cause of death, and a preharvesting serum creatinine greater than 150 micromol/L. 12780563: A scoring system was developed from five donor variables (age, 0-25 points; history of hypertension, 0-4; creatinine clearance before procurement, 0-4; cause of death, 0-3; HLA mismatch, 0-3) that showed a significant correlation with renal function and long-term graft survival. 12916385: CONCLUSION: Intrapartum asphyxia, birth trauma, antepartum haemorrhage, complications of hypertension in pregnancy and spontaneous preterm labour account for more than 80% of the primary obstetric causes of death. 12959913: The hypertension is severe and results in death at about age 50 years from stroke. 1326383: Hypertension and diabetes were the 5th and 6th leading causes of death in 1985 and ranked 12th and 13th, respectively, in 1966. 13342055: [Renin content in kidneys of men after death caused by hypertensive disease and in rabbits with experimental hypertension induced by coarctation and with cholesterin-induced atherosclerosis]. 14614: Hypertension is a common disease and plays an important role as a potentially remediable contributor to cardiovascular causes of death in the community. 14692137: Clinical significance of portopulmonary hypertension follows from the fact that the failure of the right heart is most commonly the direct cause of death in these patients. 14723755: MAIN OUTCOME MEASURES: We test the hypothesis that countries with higher MMR would have proportionally more cases of direct obstetric death due to thromboembolism, hypertension, haemorrhage or infection compared with other countries in the study. 15230037: The authors' findings indicate that in the study cohort, there is a paradoxical epidemiological situation with a high risk of death due to arterial hypertension whereas the prevalence of this disease in the watch-and-expeditionary workers do not differ from that in the country's population. 15233809: When Nyberg variables (cold ischemia time, donor diabetes and hypertension status, incremental donor age >55 yr and cause of death) in conjunction with the dCrCl were considered, they were no better than dCrCl alone. 15599115: National multiple-cause mortality files for 1980-1998 were analyzed for adult decedents with hypertension listed as one of 20 conditions causing death. 15715924: The processes of induction of hypertension, possible pathogenesis, characteristics, advantages, and limitations of these animal models are reviewed. Hypertension and related cardiovascular diseases are the leading causes of death in many countries. These models are classified as genetically-induced, environmentally-induced, pharmacologically-induced, and renal-induced hypertension according to the way of induction; the typical representatives of each of these major types of experimental hypertension are spontaneous hypertension, cold-induced hypertension, DOCA-salt-induced hypertension, and renal-induced hypertension, respectively. 15747907: Hypertension is the most common cause of death. 157830: Replacement of clonidine by water induced hypertension and lability which led to death in hypertensive but not in normotensive rats. 15959806: This sample included 2,195 subjects in 87 Utah pedigrees ascertained for early death due to coronary heart disease (CHD), early strokes, or early onset hypertension. 16260449: BACKGROUND: Hypertension is one of the major causes of death in developed and underdeveloped nations. 16333008: CONTEXT: Transplantation using kidneys from deceased donors who meet the expanded criteria donor (ECD) definition (age > or =60 years or 50 to 59 years with at least 2 of the following: history of hypertension, serum creatinine level >1.5 mg/dL [132.6 micromol/L], and cerebrovascular cause of death) is associated with 70% higher risk of graft failure compared with non-ECD transplants. 16585410: Hypertension incidence (n=647) was determined by physician diagnosis, hospital record, or cause of death over the 8- to 10-year follow-up period between 1982 and 1992. 16649458: Infection and hypertensive disorders remained the leading causes of death but the contribution of haemorrhage declined due to improved blood transfusion services. 16840082: This paper reviews the epidemiological evidence on the association of alcohol consumption with the major cardiovascular diseases (hypertension, stroke and coronary heart disease), and all causes of death. 16936922: The degree of arterial lesions, arteriolar lesions and the degree of interstitial fibrosis closely correlate to the donor's age, hypertension and nontraumatic cerebrovascular accident as the cause of death. 17059790: Hypertension is one of the leading causes of death and disability in developing countries. 17143129: BACKGROUND: In sub-Saharan Africa, hypertension and stroke are emerging as an important cause of death and disability, whereas coronary heart disease appears still to be uncommon. 17351163: Hypertension is one of the leading causes of death in developed countries, and the number of prehypertensive patients is increasing. 17521076: Hypertension is a major disease, being one of the top ten causes of death in Taiwan. 17703633: High blood pressure (BP) is the major cardiovascular risk factor and the main cause of death around the world. 17985494: SUBJECTS: Mexican American (MA), Puerto Rican (PR), Cuban (CA) and NHW female decedents ages > or =45 years with hypertension listed as one of up to 20 conditions resulting in death. 18001617: Arterial hypertension is one of the most important preventable causes of death worldwide; therefore, adequate treatment of high blood pressure should be mandatory in each hypertensive patient. 18072449: INTRODUCTION: Hypertension is one of the cardiovascular diseases which has been reported as one of the common causes of death worldwide. 18295159: Deaths from cardiovascular disease increased by 2% annually from 1990 to 1994, with hypertension being the leading cause of death for persons aged 60 years or more. 18308869: Stroke and high blood pressure are major causes of death and disability worldwide. 18380058: Hypertension is still the leading cause of death worldwide. 1843977: Cases of death caused directly by hypertension were found more frequently in the group with systolic-diastolic hypertension (56%) than in the group with isolated systolic hypertension (36%). 18443234: Hypertension is a leading cause of death because of cardiovascular disease and predominantly affects total mortality. 18515919: BACKGROUND: Hypertension is a leading cause of death worldwide, and a major public health problem in Canada. 18551103: BACKGROUND: In South Africa (SA) cardiovascular disease (CVD) is the second leading cause of death, with hypertension (HTN) being the predominant contributor to morbidity and mortality associated with this disease. 18587717: Fluid status and volume homeostasis are extremely important in patients with CKD stage 5, as cardiovascular disease, including congestive heart failure and hypertension, is one of the leading causes of death in this patient group. 19142386: The hypertension is one of the main causes of death all over the world and may result in the reduction or absence of the skeletal muscular tone. 19303588: Arterial hypertension, diabetes mellitus and cancer were significant causes of death. 19357029: As right ventricular function is impaired in patients with moderate and severe PPH, any dramatic hemodynamic changes in liver transplantation or other procedures may result in death from pulmonary and cardiac events. 19887503: BACKGROUND: Hypertension is a risk factor for the two leading causes of death in renal transplant recipients: cardiovascular disease (CVD) and graft failure. 19962803: Hypertension is a major public health problem and a leading cause of death and disability in developing countries. 20409957: Hypertension (HTN) and cardiovascular disease are the most common causes of death in developed countries. 20517296: While pulmonary fibrosis and hypertension are currently the most frequent causes of death, there is evidence that cardiovascular disease will have an important role in the long-term prognosis of SSc in the future. 20528389: Hypertension is a major public health problem, being one of the leading causes of death and disability worldwide and a major risk factor for cardiovascular disease. 20678065: Cardiovascular diseases (CVDs) such as atherosclerosis, hypertension and diabetes, are major global health problems and one of the leading causes of death. 20865852: BACKGROUND: Cardiovascular diseases, including hypertension, are a leading cause of death in developing and developed countries. 20879053: RESULTS: A scoring system was derived from six donor variables [age, 0-25; renal function, 0-4; history of hypertension, 0-4; Human Leukocyte Antigen (HLA) mismatch, 0-3; body weight, 0- 1; cause of death, 0-3 points]. 21164494: BACKGROUND: Hypertension (HTN) is a major cause of death in Chinese farmers. 21294617: CONCLUSIONS: Moderate chronic hypertension resulted in more severe ICH-induced neuronal death and neurological deficits, but did not exaggerate hematoma enlargement and perihematomal brain edema in the rat ICH models. OBJECT: Hypertension is the main cause of spontaneous intracerebral hemorrhages (ICHs), but the effects of hypertension on ICH-induced brain injury have not been well studied. 21320198: BACKGROUND: Hypertension is the third most common cause of death worldwide. 21326793: Untreated thoracic aortic coarctation leads to early death predominantly because of hypertension and its cardiovascular sequelae. 21403089: Although diabetes mellitus is associated with increased risks of death and cardiovascular events in Framingham subjects, much of this excess risk is attributable to coexistent hypertension. 21468495: Hypertensive disorders were the main cause of death. 21529315: Hypertension is an important risk factor for the commonest cause of death among men, namely, cardiovascular diseases. 21767645: Hypertension is a disorder affecting millions worldwide, and is a leading cause of death and debilitation in the United States. 21894804: Death due to coronary disease, stroke, hypertension, diabetes and obesity were significantly more common among higher social classes 1-3 and among victims with higher body mass index (BMI) compared to social class 4 and 5 who had lower BMI. 22058026: Hypertension is the leading cause of death worldwide and is responsible for a significantly increased burden of cardiovascular events and progression to end-stage kidney disease in patients with chronic kidney disease (CKD). 22143601: Population aging, smoking, unhealthy diet and physical inactivity, in the context of globalization and unregulated urbanization, explain the high prevalences of hypertension, hypercholesterolemia and diabetes in the Americas, making cardiovascular diseases the main cause of death. 22318471: Hypertension is a major contributor to cardiovascular diseases, which are a leading cause of death, disability, and health-care costs in the United States. 22825083: Hypertensive disorders, hemorrhage, and embolism were the most important causes of pregnancy-related death for all other groups of women. 22906468: Gender, age, stage of hypertension and risk stratification is associated with the constituent ratios of the causes of death. 2296213: Because of the large numbers of patients in whom hypertension is a major risk factor for cardiovascular disease, a leading cause of death in the United States and other industrialized nations, an approach was devised in which, with physician supervision, specially trained nurses managed many aspects of the acute and long-term outpatient care of hypertensive patients. 23149074: BACKGROUND AND AIM: Hypertension is a major public health problem and a leading cause of death and disability in both developed and developing countries, affecting one-quarter of the world's adult population. 23172306: Hypertensive cardiac disease is a major cause of death worldwide. 23258458: Envenomed victims can show symptoms ranging from headaches, severe pain, nausea and vomiting to pulmonary oedema, cardiac failure and severe hypertension resulting in death. 2338680: A family history of heart disease occurred in 7 of 41 (17%), of high blood pressure in first degree relatives in 17 of 29 (60%), of death due to high blood pressure in 12 of 41 (29%). 2357402: However, arterial hypertension and anemia accompanying prolonged work of the AHV and resulting from the interaction of the last named with the cardiovascular system sharply aggravate homeostasis and the course of LVB and lead to early death of the animals. 23700822: UNLABELLED: The hypertension is a civilization disease, slowly destroying the cardio-vascular system and leading to serious complications, which may result in patient death. 23777761: Hypertension was the second most common cause of death overall and the leading cause of death in patients more than 50 years old. Hypertension was the leading cause of death in patients over the age of 50 years and 57% of hypertension-related deaths occurred in patients less than 65 years old. 23877918: Hypertension is a leading cause of death and disability globally, and its prevalence continues to accelerate. 23900565: Leading causes of death were due to heart disease, diabetes, cancer, and hypertension. 23978544: Hypertension is a leading cause of death, and lowering blood pressure prevents mortality and morbidity in women and men. 23991561: According to the WHO, arterial hypertension is a major cause of death in adult populations all over the world, regardless of the socio-economic level of a specific population. 24147251: In most severe cases of untreated progressive early-onset spinal deformities, respiratory insufficiency and pulmonary and cardiac hypertension (cor pulmonale), which characterize thoracic insufficiency syndrome (TIS), can develop, sometimes leading to death. 24400884: Yet, paradoxically, this virtual blank slate could be an opportunity to develop an innovative pragmatic approach to the equally devastating problem of hypertension as the most common contributing cause of death in Haiti. 24461311: Cardiovascular disease remains the leading cause of death worldwide with hypertension being a major contributing factor to cardiovascular disease-associated mortality. 24591795: BACKGROUND: Hypertension is the leading cause of death in the world and is the commonest cause for outpatient visits to physicians. 24616621: Hypertension and diabetes, the most common causes of chronic kidney disease, are particularly common in southeast Asian Countries. Chronic noncommunicable diseases (NCDs) such as hypertension, atherosclerosis, acute myocardial infarction, stroke, diabetes, obesity, and chronic kidney disease are the major cause of death not only in high income, but also in medium and low income countries. 24741981: The stage and risk stratification of hypertension are associated with constituent ratios of the causes of death. 24954126: Consequences are major, leading quickly to death secondary to intracerebral hypertension and later to neuropsychic sequelae. 24976848: Hypertensive cardiac disease remains a major cause of death worldwide because its typically complex etiology renders current treatments ineffective. 25070209: Patients with cardiovascular risk factors, including obesity, hypertension, and diabetes, may incur medical expenditures through treatment of the risk factors themselves and through procedures for associated diseases that usually require hospitalization and sometimes result in death. 25461379: Cardiovascular diseases, including hypertension are the leading cause of death in the developed countries. 25509556: Hypertension, worldwide considered the most frequent disease, is one of the major contributors to the leading cause of death in women: cardiovascular diseases. 25604204: Hypertension, which is pointed to be the most frequent cause of death in the World and in Turkey and defined by the World Health Organization as global health crisis and the prominent risk factor for cardiovascular diseases, is a problem threatening public health. 2565199: An estimated 58 million Americans are at increased risk of morbidity and premature death due to high blood pressure (BP) and require some type of therapy or systematic monitoring. 2565688: Conventional stepped-care approaches for the control of high blood pressure based on the use of diuretics and beta-blockers have had a disappointing impact on coronary heart disease, the major cause of death in hypertension. 25796827: OBJECTIVE: To examine the reliability of accounting causes of death of the population of hypertension in the centers of primary health care at the regional level and to detect defects that affect the quality of coding of causes of death. 25853242: BACKGROUND: Hypertension is the leading cause of death in developed countries and reduction of salt intake is recommended as a key preventive measure. 25884380: Tuberculosis (10.4%) was the leading single indirect cause of maternal deaths while hypertensive disorders (9.1%) were the leading direct cause of death. 25909595: Hypertension is a leading cause of premature death worldwide and the most important modifiable risk factor for cardiovascular disease. 25961942: Cardiovascular disease is the most common cause of death worldwide, and hypertension is the major risk factor. 26005357: BACKGROUND: Hypertension is one of the most common causes of premature death and morbidity and has a major impact on health care costs. 26113481: Hypertension is the leading cause of death in developed countries; its management is the subject of guidelines that are regularly reviewed and updated. 26188454: Cardiovascular conditions such as hypertension are a growing concern in developing countries, where they are now the leading cause of death. 26204671: Hypertension is one of the most common causes of death, a complex and incompletely controlled disease for millions of patients. 2628954: Among insulin treated diabetics the hypertension was a death-risk of most importance in men usually due to the vascular brain disease and other diseases of the cardiovascular system but to a lesser degree to the circulatory diseases, as a whole. 26330373: This finding is particularly important because it suggests that religiosity and not just lifestyle is related to lower risk of hypertension, a leading cause of death in the USA. 26407222: In sub-Saharan Africa (SSA) in 2010, hypertension (defined as systolic blood pressure >= 115 mmHg) was the leading cause of death, increasing 67% since 1990. 26471319: Cardiovascular diseases (CVDs), primarily myocardial infarction (MI), atherosclerosis, hypertension and congestive heart failure symbolize the foremost cause of death in almost all parts of the world. 2650749: Death may be caused by severe uncontrollable hypertension or by concomitant problems. 26550488: Hypertension, once a rare problem in Sub-Saharan Africa (SSA), is predicted to be a major cause of death by 2020 with mortality rates as high as 75%. 26619652: In Japan, hypertension (HT) is the second greatest cause of death from non-communicable diseases next to tobacco. 26677425: Hypertension is one of the most common causes of death across the globe. 26711315: BACKGROUND: High blood pressure (BP) is the leading cause of death and disability in the world. 26738624: Once confirmed, it may help to produce new method for control of hypertension, which is the leading cause of death in the world. 26751802: BACKGROUND/AIMS: Hypertension or persistent high blood pressure (BP) is a leading cause of death worldwide. 26831225: BACKGROUND: Cardiovascular diseases, including dilated cardiomyopathy (DCM) and hypertension, are the leading cause of death worldwide. 26862126: RESULTS: We found that the sharp decrease in registered cerebrovascular mortality was by a half due to an increased selection of hypertension as the underlying cause of death. 26933708: Hypertension is the leading cause of death worldwide. 26975032: OBJECTIVES: To examine the prevalence, diagnosis, treatment, and control of hypertension and to assess the CVD mortality attributable to hypertension in China. Uncontrolled hypertension was associated with relative risks for CVD mortality of 4.1 (95% CI, 3.7-4.6), 2.6 (95% CI, 2.4-2.9) and 1.9 (95% CI, 1.8-2.0) at ages 35 to 59, 60 to 69, and 70 to 79 years, respectively, and accounted for about one-third of deaths due to CVD (approximately 750 000) at 35 to 79 years of age in 2010. IMPORTANCE: Hypertension is a leading cause of premature death in China, but limited evidence is available on the prevalence and management of hypertension and its effect on mortality from cardiovascular disease (CVD). 26990765: CONCLUSION: suboptimal diet, high SBP, and high BMI are major causes of cardiometabolic death in Brazil, informing priorities for policy initiatives. 27067719: A significant proportion of true hypertensive subjects therefore remains undetected based on office BP, which is particularly relevant in sub-Saharan Africa, where hypertension is now a major cause of death. 27096524: In 2010, SAH was the cause of death of about 9.4 million people worldwide. 27187006: Cardiovascular diseases are major contributors to global deaths and disability-adjusted life years, with hypertension a significant risk factor for all causes of death. 27355586: BACKGROUND: Cerebrovascular and hypertensive diseases are among the main causes of death worldwide. 27357953: They were also awareness that severely high blood pressure could result in death. It was widely believed that stress and weakness caused high blood pressure in pregnancy and it caused symptoms of headache. 27363822: WHAT IS KNOWN AND OBJECTIVE: Hypertension is a leading cause of death and major contributor to heart attacks, strokes, heart and kidney failure. 27379932: However, from data obtained during the last few years, we know that surgical causes of hypertension are unusual: less than 10% of the patients in a reference centre. Arterial hypertension is a very common disease, and one of the main causes of death in our countries. The first step of treatment must be the research for curable causes of hypertension. 27502908: BACKGROUND: Hypertension is the leading preventable cause of premature death worldwide. 27548652: We are focusing on systemic sclerosis (SSc)-associated pulmonary hypertension, which remains a leading cause of death with only a 50-60% of 2-year survival rate. 27565218: Myocardial infarction (MI) and hypertension are the leading cause of death worldwide so protection of heart is focus of intense research. 2763000: The causes of death are the same ones that have afflicted women through the ages: excessive blood loss, difficult delivery, infections, eclampsia due to hypertension, and complications of abortion. 27713283: Hypertension is still one of the major causes of death from cardiovascular failure. 27776558: BACKGROUND AND AIMS: Arterial hypertension is a major cause of death worldwide. Characterization and history of arterial hypertension leading to inpatient treatment. 27795991: We investigated the variation of donor characteristics of sex, age, body mass index, smoking status, blood group, multiple organ donation, cytomegalovirus status, terminal creatinine, hypertension, and cause of death for pancreas transplantation over time. 27826399: BACKGROUND: Worldwide, systemic arterial hypertension is a leading cause of death and non-communicable cardiovascular disease. 27906837: OBJECTIVES: Although the prevalence rates of hypertension (HTN) and diabetes mellitus are slowing in some high-income countries, HTN and diabetes mellitus remain as the two major risk factors for atherosclerotic cardiovascular disease (CVD), the leading cause of death in the United States and worldwide. 28104166: Data collected from donor medical records included age, height, weight, hypertension or diabetes history, cause of death, serum creatinine (sCr), and donation after cardiac death. 28216386: In dextran sulfate sodium-induced colitis mice (an IBD disease model), in which colonic 5-HT levels were markedly elevated, BW administration induced death in along with large amount of BW invasion into colon submucosa, and time to death was negatively related to the amount of BW injected. 28358015: Hypertension is a leading cause of death worldwide; data on hypertension among ethnic minorities in China are sparse. 28404590: Hypertension is growing in epidemic proportions worldwide and is now the leading preventable cause of premature death. 28511722: Hemorrhage (27.0%) and hypertensive disorders (18.0%) were the most common categories of suspected causes of death, and deaths after termination of pregnancy were statistically significantly more common than deaths during pregnancy or delivery. 28530211: According to the WHO, hypertension is one of the major causes of death worldwide. 28535761: BACKGROUND: Arterial hypertension is the commonest cause of cardiovascular death. 28597404: The prevalence of HTN is increasing in developing countries and is one of the leading causes of death in older individuals. 28600028: Compared with other lifestyle and metabolic risk factors, hypertension is the leading cause of death in women. 2861880: The main aim of the trial was to determine whether drug treatment of mild hypertension (phase V diastolic pressure 90-109 mm Hg) reduced the rates of stroke, of death due to hypertension, and of coronary events in men and women aged 35-64 years. 28628970: Hypertension and cardiovascular complications are the leading causes of death worldwide.? 28809621: Severe hypertension and intracranial bleeding were the most common causes of death. 28822828: BACKGROUND: High blood pressure (BP) is the most common modifiable cause of death from cardiovascular disease. 28969113: INTRODUCTION: High Blood Pressure (HBP), Diabetes Mellitus (DM), Metabolic Syndrome (MS) and Cardiovascular Diseases (CVD) are among the main causes of death worldwide and HBP is one of the most common chronic health problem representing an important and modifiable risk factor for vascular events and mortality. 28985247: BACKGROUND: Hypertension is the leading risk factor responsible for premature death worldwide, but its burden has shifted to low- and middle-income countries. 29098616: Also, hypertension is the main cause of the two most frequent causes of death worldwide: myocardial infarction and stroke. 29164016: Hypertension is one of the leading causes of death and disability worldwide. 29173650: Hypertension is one of the most important preventable causes of premature death. 29417224: Hypertension is a major public health problem leading to death. 29450979: Hypertension is an important modifiable cardiovascular risk factor and a leading cause of death throughout Asia. 29473870: Hypertension has become the leading cause of death worldwide; data on hypertension among Nanchang adults are sparse. 29478153: PURPOSE OF REVIEW: Hypertension still represents a huge health problem, causing death and disability and rising at epidemic levels worldwide. 29545075: Untreatable right heart failure (RHF) from PAH eventually ensues and remains a significant cause of death in these patients. 29574470: INTRODUCTION: Systemic hypertension (SH) is a major long-term health condition and is the leading cause of premature death among adults throughout the world, including developed, developing, and lesser developed countries.In recent years there has been a progressive increase in SH among children and adolescents. 29794095: INTRODUCTION: In recent times, hypertension has become one of the major public health concerns in both the developed and the developing world and is responsible for death due to heart diseases and stroke. 29803603: BACKGROUND: Smoking and hypertension are 2 leading causes of death worldwide, and it has been claimed that smoking is a cause of hypertension despite inconsistent results in the literature. 29843153: Chronic high blood pressure induces inflammation. BACKGROUND/AIMS: Hypertension is the leading cause of death worldwide. 29870833: Cerebrovascular and hypertensive diseases as multiple causes of death in Brazil from 2004 to 2013. CBVDs and HYPDs were evaluated according to their mentions as the underlying cause of death or entry in any line of the death certificates (DCs), according to their International Statistical Classification of Diseases and Related Health Problems, 10th Revision codes. When HYPDs were the underlying causes of death, CBVDs were mentioned in only 5.0%. This article aims to evaluate mortality related to HYPDs and CBVDs as multiple causes of death, in Brazil from 2004 to 2013. 29908661: Hypertension (HT) is the first cause of death and disability worldwide. 29983819: Septic abortion (13, 21.3%) and hypertensive diseases of pregnancy (10, 16.4%) were the leading causes of death. 30056881: BACKGROUND: Despite an increasing utilization of kidneys procured from expanded-criteria donors, little is known about the effects of particular expanded-criteria donors definition components, that is, hypertension, increased creatinine prior to procurement, and cerebrovascular cause of death on the kidney graft Doppler parameters measured shortly after transplantation, whose increased values are associated with unfavorable outcomes. 30115106: BACKGROUND: Systemic sclerosis-associated pulmonary arterial hypertension (SSc-PAH) is one of the leading causes of death in SSc. 30135711: Background: Hypertension (HT) has been one of the leading global risk factors for health and the leading cause of death in Thailand for decades. 30147302: Purpose: Hypertension is an increasing threat to global public health, a leading cause of premature death, and an important modifiable risk factor for cardiovascular and cerebrovascular disease. Results: Overall, most patients reported hypertension awareness prior to diagnosis and were conscious about consequences of hypertension. 30281618: Hypertension, which leads to heart attacks and strokes, already affects one billion people worldwide, making it a global public health issue. Log-binomial regression was used to estimate predictors of hypertension at ART initiation, while competing risks regression was used to evaluate the relationship between predictors of incident hypertension, accounting for death as a competing risk. 30299518: While it has been known since the 1940s that men have greater increases in blood pressure (BP) compared with women, there have been intense efforts more recently to increase awareness that women are also at risk for developing hypertension and that cardiovascular diseases (CVDs) are the leading causes of death among both men and women in the United States. 30645210: BACKGROUND: In sub-Saharan Africa, cardiovascular disease is becoming a leading cause of death, with high blood pressure as number one risk factor. 31023080: BACKGROUND: Hypertension is a major cause of death and morbidity worldwide and is increasing in prevalence. 31028527: Hypertension is one of the most important risk factors and a leading cause of death from cardiovascular and cerebrovascular diseases. 31078374: Hypertension is the most prevalent cardiovascular risk factor worldwide and the leading cause of death and premature morbidity. 31166537: Hypertension is the underlying cause of death assessed at the autopsy of individuals. CONCLUSION: The prevalence of hypertension was high, and it was the second most common underlying cause of death. RESULTS: The prevalence of hypertension was 66.2% and it was the second leading cause of death (25.6%) identified by autopsy, preceded by atherosclerosis (37.8%). OBJECTIVE: To analyze hypertension and its relationship with the causes of death identified by the autopsy. 31180254: In our study, the major cause of death was heart disease, but previous study found hypertensive disorder to be the leading cause of death in adolescents. 31196079: BACKGROUND: Hypertension remains one of the leading causes of death in Nigeria. 31238747: Maternal risks include hypertensive disorders of pregnancy, rejection, and failure of the cardiac allograft that may lead to death. 31266254: Conclusions: Risk factors most significantly associated with stillbirth include maternal history of chronic hypertension and abruptio placenta which is a common cause of death in stillbirth. 31271020: Even hypertensive diseases during pregnancy have an influence on pregnancy possibly leading to the death of the untreated mother. 31343491: Sarcoidosis-associated pulmonary hypertension (SAPH) is an independent cause of death in advanced pulmonary sarcoidosis. 31365384: Sarcoidosis-associated pulmonary hypertension (SAPH) is an independent cause of death in advanced pulmonary sarcoidosis. 31427898: Background: Hypertension is a major risk factor related to leading causes of death among older adults. 31438239: Cerebrovascular and hypertensive diseases are among the leading causes of death in the world. 31508051: It is estimated to be responsible for 4% of the global disease burden, and is third only to tobacco and hypertension as a leading cause of death in high-income countries. 31540146: High blood pressure is a leading cause of death in Costa Rica, with an estimated mortality rate of 30%. 31544349: High blood pressure is the world's leading cause of death, but despite treatment for hypertension being safe, effective, and low cost, most people with hypertension worldwide do not have it controlled. 31587339: Hypertension is a common type of cardiovascular disease that remains a major cause of death in the world. 31596365: OBJECTIVES: Hypertension is one of the main causes of premature death in the world; also, it is associated with several bone alterations. 31625597: BACKGROUND AND PURPOSE: Hypertension has been the leading preventable cause of premature death worldwide. 31734688: Hypertension and high total cholesterol are the main NCD drivers (adult prevalence of 20.5% (5.3 million) and 9.0% (2.3 million)), with CVD and cancers the main causes of death. 31865779: Obesity-related hypertension is one of the world's leading causes of death and yet little is understood as to how it develops. 31918428: The Impact of CYP24A1 Polymorphisms on Hypertension Susceptibility.BACKGROUND: Hypertension is one of the leading causes of human death and disability. 31926088: Background Hypertension is one of the major health problems of the world and one of the most important causes of death in Indonesia. Complication due to hypertension leads to myocardial infarction, stroke, and renal failure. 32035519: Hypertension is a leading cause of death in India. 32036911: Elevated blood pressure causes approximately 7.6 million deaths, which account for ~13.5% of the total deaths and will continue to rise. 32037893: Consequently, hypertension is the leading cause of cardiovascular death in Japan. 32110437: Arterial hypertension is the leading cause of death worldwide and is one of the most important public health problems. 32238889: Hypertension (HTN) is a leading cause of death and disability throughout the world. 32299635: Worsening Hypertension Awareness, Treatment, and Control Rates in Canadian Women Between 2007 and 2017.BACKGROUND: Hypertension continues to be the leading cause of preventable death and disability. 32307147: The variables analyzed were age, weight, height, sex, race and/or ethnicity, history of hypertension or diabetes, cause of death, serum creatinine, KDPI, KDRI, and biopsy result from each graft prior to transplant. 32317817: Data extracted from the records included age, gender, knowledge of hypertension status, systolic and diastolic blood pressure at time of diagnosis, reported adherence to medications, complications of systemic hypertension, duration of survival from diagnosis to demise, cause of death, body length, and heart weight at autopsy. 32331360: Therefore, noninvasive and continuous BP measurement methods are needed to ensure appropriate diagnosis and early management before hypertension leads to irreversible complications. Elevated blood pressure (BP) is a major cause of death, yet hypertension commonly goes undetected. 32335621: INTRODUCTION: Hypertension is one of the leading causes of death and disability in both developed and developing countries. 32404470: Progress on sodium reduction in South Korea.INTRODUCTION: High dietary sodium is a leading contributor to hypertension, and hypertension is the leading underlying cause of death globally. 32525916: Prevalence and risk factors of hypertension among civil servants in Sidama Zone, south Ethiopia.INTRODUCTION: Hypertension is the leading cause of death and disability in adult populations globally. 32569417: Patients with high insulin persistence had significantly lower risks than did those with low insulin persistence of death due to hypertension, diabetes, cardiovascular disease, liver disease, kidney disease, respiratory disease, sepsis, and cancer. 32748331: Some recently reported studies revealed that individuals of elderly age group and with pre-existing medical conditions such as hypertension, diabetes mellitus had severe consequences, even may lead to death. 32776866: A Systematic Review.CONTEXT: High blood pressure is one of the leading preventable causes of cardiovascular death worldwide. 32884457: Hypertension continues to be the leading cause of death and disability in the industrialized world, with a high level of unawareness and unacceptably poor control. 32884467: High blood pressure (BP) is the leading global preventable cause of death and the most common risk factor for cardiovascular disease (CVD). 33027066: Systemic hypertension is the leading cause of death and disability worldwide. 33027067: Systemic hypertension is the leading cause of death and disability worldwide. 33029293: Effect of nutrition education in reducing sodium intake and increasing potassium intake in hypertensive adults.BACKGROUND/OBJECTIVES: Hypertension is the major risk factor for cardiovascular disease, a leading cause of deaths in Korea. 33072318: BACKGROUND: Hypertension is among the growing non-communicable diseases (NCDs) in developing countries and the leading cause of death worldwide. 33082518: Seventy-five percent of global deaths due to HTN occur in low- and middle-income countries where HTN prevalence is higher, and HTN control and population awareness are lower, than in high-income countries. 33113094: Prevalence and Risk Factors of Hypertension Among Young Adults in Albania.INTRODUCTION: Hypertension is one of the major risk factors for cardiovascular disease and the leading cause of death worldwide. 33150452: BACKGROUND: In autosomal dominant polycystic kidney disease (ADPKD), hypertension is prevalent and cardiovascular events are the main cause of death. 33168561: Hypertension, cardiovascular disease and cause of death in Danish living kidney donors: matched cohort study. 33170835: Hypertension is the most important cause of death and disability in the elderly. 33208066: BACKGROUND: Cardiovascular diseases (CVDs) such as stroke, high blood pressure, peripheral vascular disease, ischemic heart disease and acute myocardial infarction are some of the leading causes of death. 3326701: The main aim of the trial was to determine whether drug treatment of mild hypertension (phase V diastolic pressure 90-109 mm Hg) reduced the rates of stroke, of death due to hypertension, and of coronary events, in men and women aged 35-64 years. 33299773: Background: Elevated blood pressure is the leading cause of death worldwide; however, treatment and control rates remain very low. 33327460: Obesity and its comorbidities like diabetes, hypertension and other cardiovascular disorders are the leading causes of death and disability worldwide. 33382819: INTRODUCTION: Hypertension is a major public health problem globally and it is a leading cause of death and disability in developing countries. 3341784: Most of malignant pheochromocytomas are endocrinologically active and they often cause hypertension leading to death. 33446309: An increase was also observed for deaths caused by hypertensive disease (1.17, 95% confidence interval: 1.09 to 1.26), but not for heart failure, cerebrovascular disease, or other diseases of the circulatory system. CONCLUSIONS: There was an increase in deaths caused by ischemic heart disease and hypertensive diseases in some regions of the United States during the initial phase of the COVID-19 pandemic. 33462863: Hypertension is a multifaceted condition influenced by genetic and environmental factors and estimated to cause 9.4 million deaths globally every year. 33567538: The establishment of an effective salt reduction strategy with lifestyle education is needed to reduce hypertension, which is the primary cause of death in Tunisia. 33692847: Discontinuation or death caused by hypertension was rare, although previous studies have reported that hypertension was a risk factor for acute and chronic cardiovascular diseases and ischemic stroke. 33714244: INTRODUCTION: Hypertension is considered to be the most common pathology of the circulatory system and the most common cause of death or cardiovascular diseases' development. 33747565: Backgrounds: High blood pressure is one of the most important causes of death around the world. 33809913: In SARS-CoV-2-infected patients, obesity, hypertension, and diabetes are dangerous factors that may result in death. 33836976: Hypertension is the main cause of death worldwide and the approach that the Family Physician makes of hypertensive patients, given his or her key role as a gateway to the health system, is a crucial determinant in their evolution. 33872425: The overall prevalence of hypertension is 45.4% in the United States with nearly 80,000 deaths due to hypertension in 2015. 33920763: Hypertension causes many deaths worldwide and has shown an increasing trend as a severe non-communicable disease. 33954415: METHODS: We extracted data on the number of deaths due to hypertension among adults aged 45 or older annually from 2000 to 2018 from Mississippi Vital Statistics. BACKGROUND: In Mississippi, hypertension as a leading cause of death moved from 15th in 2000 to 11th in 2018, but research on temporal trends is limited. 33964896: The number of deaths due to hypertensive disorders of pregnancy was approximately 27.83 thousand in 2019, representing a 30.05 % decrease from 1990. 33964914: Particularly, comparing with the expected mortality in the absence of COVID-19 outbreak, the observed deaths from pneumonia and influenza substantially decreased by 49.2%, while deaths due to hypertension and myocardial infarction increased by 14.5 and 8.6%, respectively. 34054370: Despite hypertension remaining the leading cause of death worldwide, awareness of hypertension and its control rate is still suboptimal in Malaysia. 34111216: In Brazil, the prevalence of SAH is 23.7%, which caused 203,000 deaths and 3.9 million DALYs in 2015. Stroke accounted for the highest cost attributable to SAH and the third highest PAR, representing 47% of the total cost of circulatory diseases attributable to SAH. 34201492: Moreover, high blood pressure (BP) remains a leading cause of death globally. 34220374: Hypertension is a major preventable cause of death worldwide. 34327016: Hypertension is the second leading cause of death in Ghana, partly accounting for two-thirds of all medical admissions and more than 50% of deaths. 34337061: Hypertension and the Risk of All-Cause and Cause-Specific Mortality: An Outcome-Wide Association Study of 67 Causes of Death in the National Health Interview Survey. Background: Few studies have assessed the association between hypertension and risk of detailed causes of death. 34343391: Hypertension is the most common cause of death and disability worldwide with its prevalence rising in low to middle income countries. 34346156: Cardiovascular disease (CVD), such as hypertension and atherosclerosis, are the leading cause of global death. 34370651: School pass-out group had significant knowledge about dangerous natural course of hypertension (p = 0.00069), hypertension can lead to death if untreated (p = 0.015), benefits of cessation of smoking (p = 0.03), advantage of limiting alcohol (p = 0.019) and performing regular exercise (p = 0.013) reduces blood pressure. 34400442: OBJECTIVE: Hypertension has become the leading cause of death worldwide. 34458742: High blood pressure and consequential cardiovascular diseases are among the top causes of death worldwide. 34475436: Using death certificates and national population public data sets, a total of 335,863 deaths due to hypertension were found in Mexico, disaggregated by sex and age, during the time period covered in this study. 34496000: Among the NCDs, hypertension was the leading cause of death with 2,243 and 2,472 cases in 2017 and 2018. 34751917: Hypertension remains the leading cause of global mortality, with elevated systolic blood pressure (BP) leading to 10.8 million deaths each year. 34825625: Hypertension has been a significant cause of death due to elevated blood pressure worldwide. 34852885: Despite a 17% overall reduction in maternal deaths in South Africa between 2011 and 2016, there was a 14% increase in deaths due to hypertension. 3502585: These results suggest that hypertension is a common cause of death among urban blacks in South Africa but that it is not commonly associated with ischemic heart disease. 35057722: The study results together with results of international studies showed that differences in standardized mortality ratios for death from AH are largely due to different approaches to determining the primary cause of death. 35154522: Introduction: Hypertension is the leading direct cause of death in the world and one of the most important risk factors for cardiovascular disease (CVD). 3530550: Death may be caused by severe uncontrollable hypertension or by concomitant problems. 35435219: The proportion of deaths due to hypertensive diseases showed the greatest percentage increase, with largest change in breast cancer patients (+191.1%). 35557081: Preeclampsia (PE), new onset hypertension during pregnancy, is the leading cause of death and morbidity for the mother and low birth weight in offspring. 35557241: Hypertension remains the leading cause of death globally, accounting for 10.4 million deaths per year. 35606307: Hypertension (HYP) is the first cause of death and disability worldwide. Despite improvement in HYP management over time, only half of treated hypertensive patients are adequately controlled, which translates in 30,000 annual cardiovascular deaths attributable to HYP. 35651628: Hypertension is a main cause of death in the United States with more than 103 million adults affected. 35685669: At least 45% of deaths due to heart disease and 51% of deaths due to stroke are the result of hypertension. 35742125: Hypertension and cancer are two of the leading global causes of death. 35818993: Hypertension (high blood pressure) is a major risk factor for cardiovascular disease, which is the leading cause of death worldwide. 35872101: BACKGROUND AND AIMS: Cardiovascular disease (CVD) and hypertension are the main causes of global death. 35899158: SDG-targeted NCDs were considered the underlying causes of death, and hypertension was considered a multiple cause of death. 35916004: Most deaths due to postpartum eclampsia and hypertensive disorders occurred within the first week (44.3% on day 1 and 37.1% on days 2-7). 35932508: Hypertension is the main cause of human death and the Renin- Angiotensin- Aldosterone System (RAAS) has a key role in the control of human blood pressure. 35944931: BACKGROUND: Elevated blood pressure, or hypertension, is the leading cause of preventable deaths globally. 36026761: OBJECTIVE: Hypertension is a leading cause of death worldwide. 36055373: BACKGROUND: Hypertension is the leading cause of death throughout the world. 36082119: Hypertension is the most prevalent cardiovascular disorder and the leading cause of death worldwide in both sexes. 36124099: Covid-19 infection is more likely to affect the elderly than younger people, and pre-existing medical conditions, such as cardiovascular disease, diabetes, high blood pressure, and respiratory diseases, might lead to death due to COVID-19 infection. 36148456: Background: Hypertension is a major cause of death and disability worldwide. 36229530: Hypertension has remained the number one cause of cardiovascular death in the Philippines for over three (3) decades. 36277949: In Africa, hypertension is a leading cause of death from a non-communicable disease. 36329155: Hypertension, characterised by a constant high blood pressure, is the primary risk factor for multiple cardiovascular events and a major cause of death in adults. 36342266: Arterial hypertension is a leading cause of death globally. 36438268: Lastly, 2,499 deaths were attributable to hypertension ( p < 0.001). 36443558: Obesity is defined as having an excess of adipose tissue and is associated with the development of diabetes, hypertension, and atherosclerosis, which are the main causes of death worldwide. 36472973: The study showed that while improving test accuracy avoids 0.6% of HTN-induced deaths over 10 years (13,856,507 [9,382,742; 17,395,833]), almost 40 million (39,650,363 [31,34,233, 49,298,921], i.e., 12.7% [9.9, 15.8]) of the HTN-induced deaths could be prevented by increasing coverage and completion of a screening event in the same time frame. 36483311: Method: In this cross-sectional study, we extracted all death reports due to hypertension based on age, gender, and the year of death based on ICD-10 from the EDRS system (Electronic Death Registration System). 36615030: BACKGROUND: Arterial hypertension (AHT) is the leading preventable cause of death worldwide. 36639981: Findings will be used to inform future public health policies to support implementation of scalable community-based interventions to reduce salt intake and control hypertension, the leading-cause of death in India. 36647044: Subsequently, we obtained the cause-specific mortality in the same year from the Tianjin All Cause of Death Registration System (CDRS), and the population attributable fraction was used to estimate the annual cardiovascular disease (CVD) deaths caused by hypertension. 36774606: A 33-year-old woman with a history of high blood pressure since she was 8 years old, hypothyroidism, polycystic ovary syndrome, metabolic syndrome, multiple nevi, and a maternal family history of death at age 50 due to malignant high blood pressure and heart failure. 36788612: Hypertension is the leading cause of death in human being, which shows high prevalence and associated complications that increase the mortality and morbidity. 36811857: Conclusions and Relevance: In this cross-sectional study of maternal mortality in Hong Kong, suicide and hypertensive disorder were the dominant causes of death. 36839189: Reducing population-level sodium intake can reduce hypertension, an important preventative strategy to lower the risk of cardiovascular diseases, the leading cause of death in the United States. 36863553: Hypertension is a modifiable cardiovascular risk factor and cause of death worldwide. 36905441: Hypertension (HT) continues to be a leading cause of cardiovascular death and an enormous burden on the healthcare system. 36934596: Cardiovascular diseases, in particular hypertension and hypercholesterolemia, are two of the main causes of death worldwide. 36962115: Smoking and hypertension are two major risk factors for cardiovascular disease, the leading cause of death in Nepal. 37008311: Few data were analyzed on deaths and disability-adjusted life years (DALYs) caused by hypertension in East Asia. Conclusions: The deaths and DALYs due to hypertension declined in China, Japan, and South Korea in the past 29 years, with China having the greatest burden. 37128890: ABSTRACT: Hypertension and its complications are a leading cause of death in the human population. 37206362: Background: Hypertension is one of the main causes of cardiovascular death. 37244992: BACKGROUND: Hypertension is a major public health problem, resulting in 10 million deaths annually. 37266632: Hypertension is a leading cause of death worldwide. 37318780: Hypertension is the leading risk factor for cardiovascular disease yet also one of the most readily preventable causes of death. 37361179: Ozone-associated risks in total deaths caused by hypertensive diseases reduced in warm season, while risks in IHD in males increased at high temperature. 37428721: Hypertension is a major risk factor for cardiovascular disease, which is a common cause of death in Zambia. 37442759: ABSTRACT: Cardiovascular diseases, including heart failure, coronary artery disease, atherosclerosis, aneurysm, thrombosis, and hypertension, are a great economic burden and threat to human health and are the major cause of death worldwide. 37445491: Cardiovascular disease (CVD), including hypertension, is a leading cause of death worldwide and imposes an enormous burden on our societies [...]. 37454754: As the most common cause of LVH, hypertension accounts for more cardiovascular deaths than any other modifiable risk factor. 37456481: The research focused on individuals aged 25 years or older with a mention of hypertension and cardiovascular disease as the underlying cause of death between 1999 and 2019. 37551050: Hypertension is the leading cause of death worldwide, affecting 1.4 billion people. 37568172: BACKGROUND: Hypertension is the leading cause of death and disability. 37594686: High blood pressure is the leading cause of death and disability globally and an important treatable risk factor for cardiovascular, cerebrovascular and chronic kidney diseases. 37599662: Background and Aims: Hypertension is the third leading cause of death in the world and is estimated to be increased by about 60% by 2025. 37627036: INTRODUCTION: Hypertension, a leading cause of death, was investigated in this study to understand the role of specific brain regions in regulating blood pressure. 37636820: Background: Hypertension is a global leading cause of death which disproportionately affects refugees. 37754800: Hypertension remains the leading cause of death worldwide. 37795487: Introduction: Hypertension (HT) remains the leading cause of death worldwide. 37882129: Hypertension was the main direct cause of death (36.5%; n=27/74), followed by pregnancy related sepsis (27.4%; n=21/74) and obstetric haemorrhage (20.6%; n=15/74). 37935316: These risk factors, including obesity, dyslipidemia, hypertension, and insulin resistance (IR), are significant contributors to premature cardiovascular disease and represent a leading cause of non-relapse deaths in childhood cancer and HCT survivors. 38088763: OBJECTIVES: Hypertension is a leading cause of death and disease burden followed by dyslipidemia. 38094854: Background: Hypertension is the leading cause of death from cardiovascular disease. 3810363: Hypertensive disorders of pregnancy were the most frequent cause of death (30%). 38140354: There is a close link between cardiovascular diseases and hypertension and dyslipidaemia, and cardiovascular events are the leading cause of death among subjects with type 2 diabetes (T2D). 38152897: High blood pressure causes over 10 million preventable deaths annually globally. 38186879: Hypertension is a major risk factor for cardiovascular disease, the leading cause of death worldwide, and its prevalence is rapidly increasing following the pandemic rise in obesity. 38189116: Preeclampsia is a hypertensive disorder of pregnancy that affects approximately 2-5% of all pregnancies, contributes to 4 of the top 10 causes of pregnancy-related deaths, and remains a long-term risk factor for cardiometabolic diseases. 38352851: Introduction: Hypertension is the leading cause of death in the cardiovascular system. 38390740: BACKGROUND: Death certificate data indicate that hypertension may have increased as a contributing cause of death among US adults. 38408686: Analysis of the specific risk factors associated with aneurysm death revealed that the percentage of deaths attributable to smoking decreased from 45.6% in 1990 to 34.6% in 2019, and deaths attributable to hypertension decreased from 38.7% to 34.7%. 38489104: Hypertension is a major risk factor for cardiovascular disease and the leading cause of death in Colombia. 38504228: The most frequent cause of death in women were DM as the UC and associated cause of death, AH as the UC, and CIHD and Alzheimer's disease as associated causes of death, while the most frequent causes of death in men were substance dependence as the UC and associated cause of death, and cancer as an associated cause of death. 38573329: BACKGROUND: Hypertension is a major cause of death worldwide. 3934702: The goals of NHBPEP and the 1990 prevention objectives for the nation center around the same basic theme: high blood pressure is a serious condition leading to major diseases and premature death. There is good evidence of progress in preventing disease and premature death from hypertension, in bringing hypertension under long term control, and in giving Americans a better understanding of the consequences of uncontrolled high blood pressure. 402043: Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care. 432566: In spite of treatment of hypertension (greater than 165/110 mmHg) there was an association between high blood pressure and premature death, particularly when cause of death was cardiovascular disease. 444914: Reports suggest that hypertension and death due to hypertensive disease are commoner among black than among white people. 6412360: The present social and economic burden resulting for the individual and the public from neglected therapeutic opportunities, from excess morbidity and early death due to inadequately treated hypertension, can and must be reduced in the interests of the community at large. 7158104: The postmortem diagnosis of hypertension is of importance both for the determination of basic disease or terminal cause of death and for statistical investigations based on autopsy material or for comparisons between clinical and epidemiological data as well. 7233893: (2) Severe hypertension and advanced age are the two most important predisposing factors leading to intracerebral hemorrhage; the deceased patient had neither. The plaintiff alleged that failure of the attending physician to manage her husband's hypertension properly resulted in his death from intracerebral hemorrhage. 7294103: During the next few years her neurologic and visual condition progressively worsened and she developed hypertension, seizures, ataxia, and lactic acidemia, leading to death at the age of 16 years. 7298128: On the other hand, sinoaortic denervation following lateral NTS lesions produced the first demonstration of fulminant hypertension in the dog, which led to death within hours. 7672896: For hypertensive disease, diabetes and asthma, when using multiple causes of death some further areas were found to have high SMR and the level of significance was higher. 7759336: The study was terminated after the initial 3 horses developed severe tachycardia and hypertension, which resulted in the death of 1 horse from pulmonary edema. 8016506: Cardiovascular complications, related to the increased incidence of hypertension and hyperlipidemia, remains the main cause of death in kidney transplant patients. 8193527: Cardiovascular diseases are the leading causes of death in the United States, with hypertension being amongst the most prevalent of the cardiovascular risk factors. 8205466: Cardiovascular disease remains the major cause of death in elderly people, with hypertension the main treatable risk factor. 8268868: Morbidity and mortality data place hypertension as the leading cause of death and disability in virtually all countries in Latin America. 8288134: Hepatocellular hemorrhagic necrosis was found in 11 cases, that correspond to 55% of 20 cases of death due to hypertensive disease of third trimester of pregnancy: eclampsia, in 81.8% was diffuse; in 18.1% it was focal: it was present at 18 years to 38 years of age; at 25.5 years of age, average; 36.3% were primipara, 36.3% multiparae. 8513316: Hypertension is the leading cause of death in the elderly in Western countries. 8553142: Haemorrhage (25%), infection (24%) and hypertensive disease (18%) were the most important causes of death. 8574532: Severe hypertension followed aortic closure and extra-anatomic bypass and resulted in the eventual death of the patient 16 months later from dissection of the ascending aorta with pericardial tamponade. 8736451: Hypertension is a significant cause of death particularly in elderly urban Sierra Leoneans in Freetown and deaths from hypertension may be increasing. 8900086: The differences among the groups in the rates of death from coronary heart disease were greater than those for death due to stroke or hypertension. 8974756: Arterial Hypertension remains a serious public health problem in Spain, given its high degree of prevalence (20% to 30% of individuals suffer from hypertension, the figure increasing with age) and contributes to the main cause of death in the country, that being cardiovascular disease. 9214569: Cardiovascular disease (CVD), including coronary heart disease, stroke, and hypertensive disease, is the leading cause of death in Louisiana and in the United States and, in 1994, accounted for 43.7% and 45.2% of all deaths among persons aged > or = 45 years in Louisiana and in the United States, respectively. 9576116: Hypertensive vascular disease was the autopsy cause of death in 42% of blacks compared with 23% of whites (P<.001). Hypertensive vascular disease as a cause of death in blacks versus whites: autopsy findings in 587 adults. 9673823: Nicotine is involved in many cardio-respiratory diseases, including hypertension and sudden infant death syndrome (SIDS), which is the most common cause of death in infants between 1 month and 1 year of age. 9926911: Although mortality from hypertension as the main cause of death accounts for 1% to 4% of all deaths, mortality from stroke, mainly caused by hypertension, accounts for 10% of all deaths, indicating a failure in the treatment of hypertension. 32059997: Thus, salt-sensitive hypertension is induced in CKD via activation of the renal WNK1- SPAK-NCC phosphorylation cascade by TNF-alpha, reflecting a link with the immune system. Although chronic kidney disease (CKD) is a common cause of salt-sensitive hypertension, the involvement of the WNK phosphorylation cascade is unknown. Moreover, a high-salt diet did not adequately suppress activation of the WNK1-SPAK-NCC phosphorylation cascade in this model, leading to salt-sensitive hypertension. 32127862: The other factors that work in concert with hypertension to cause CKD are yet to be clearly elucidated. Introduction: Hypertension is a cause and consequence of chronic kidney disease globally. 32167996: Blood pressure targets in chronic kidney disease: an update on the evidence.PURPOSE OF REVIEW: Hypertension is the leading modifiable cause of cardiovascular events and of mortality and is generally considered as a direct cause of chronic kidney disease. 32765290: CKD causes hypertension and cardiovascular disease; and hypertension causes CKD. 33121630: Chronic kidney disease is encountered by the primary care physician, in no small part owing to the high rates of hypertension and diabetes, the 2 most common etiologies of chronic kidney disease in the United States. 33273787: Diabetes and hypertension are the two most common causes of CKD. 33308177: Additionally, appropriate dietary patterns should also be advised to avoid the development of non-communicable diseases such as hypertension and obesity that are known principal causes of Chronic Kidney Disease (CKD). 33570513: The two most frequent aetiologies of CKD, DM and hypertension, and many other predisposing factors, are more frequent in the Eastern region, resulting in more prevalent CKD Stages 3-5. 33712668: Cox analysis showed that the renal risk of LNSBP for CKD outcomes remained significant even after adjusting for background factors, including age, sex, medical history of hypertension and diabetes, smoking status, eGFR, 24-h proteinuria, and etiology of CKD (HR 1.18; 95% CI 1.06-1.32; P = 0.002; per 10 mmHg). 33981475: Diabetes and hypertension are the major causes of CKD throughout the region with a higher prevalence of infectious causes in Afghanistan and a high burden of CKD of an unknown cause in Sri Lanka and parts of India. 34094519: The second peak is between 50 and 70 years of age, and CKD is usually the result of diabetes mellitus and systemic arterial hypertension (59.6%). 34181718: BACKGROUND: Hypertension is a leading cause of chronic kidney disease worldwide. 34235163: Background: Although it is widely known that hypertension is an important cause of chronic kidney disease (CKD), little detailed quantitative research exists on the burden of CKD due to hypertension. The distribution disparity in the burden of CKD due to hypertension varies greatly among countries. Methods: We extracted the disability-adjusted life-year (DALY) numbers, rates, and age-standardized rates of CKD due to hypertension from the Global Burden of Disease Study 2019 database to investigate the time trends of the burden of CKD due to hypertension from 1990 to 2019. Conclusion: Improving the average achievements and equality of distribution in health, education, and income, as well as increasing the number of physicians per 10,000 people could help to reduce the burden of CKD due to hypertension. These findings may provide relevant information toward efforts to optimize health policies aimed at reducing the burden of CKD due to hypertension. Disease Burden of Chronic Kidney Disease Due to Hypertension From 1990 to 2019: A Global Analysis. Results: Globally, from 1990 to 2019, DALY numbers caused by CKD due to hypertension increased by 125.2% [95% confidential interval (CI), 124.6 to 125.7%]. Objective: The objective of the study is to estimate the global disease burden of CKD due to hypertension and to evaluate the association between the socioeconomic factors and country-level disease burden of CKD due to hypertension. 34515350: In the present study, we examined the role of phosphatase and tensin homolog (PTEN), a major regulator of PI3K signaling, in the pathogenesis of renal inflammation and fibrosis in an experimental model of hypertension induced by AngII. Hypertension is a major cause of chronic kidney disease. 34950960: SIRT6 prevents and delays progressive CKD induced by hyperglycemia, kidney senescence, hypertension, and lipid accumulation by regulating mitochondrial biogenesis, and has antioxidant, anti-inflammatory, and antifibrosis effects. 35118089: Kinin B1 receptor (B1R) activation has been shown to have a role in the development of hypertension, one of the major etiologies for chronic kidney disease. 35200681: Hypertensive nephropathy is a chronic kidney disease caused by hypertension. 35244176: Our results show the benefit of EV enrichment for miRNA detection and the potential of total urine and urinary EV-associated miRNAs as biomarkers of altered kidney physiology, renal fibrosis and glomerular injury, and disease progression in hypertension and obesity induced CKD. 35317361: Background: Chronic kidney disease (CKD) is a progressive loss of renal function, mainly due to hypertension, diabetes, and primary kidney disease. 35443397: Hypertension (60%) was leading cause of CKD. 35546745: INTRODUCTION: Hypertension is a leading cause of cardiovascular disease and chronic kidney disease resulting in premature death and disability. 36402925: Association between microscopic hematuria and albuminuria in patients with chronic kidney disease caused by diabetes and hypertension: the Fukuoka Kidney disease Registry Study. CONCLUSIONS: MH with erythrocytes >= 10/HPF was significantly associated with increased prevalence of macroalbuminuria in patients with non-dialysis-dependent CKD caused by diabetes and hypertension. BACKGROUND: The association between microscopic hematuria (MH) and albuminuria in patients with chronic kidney disease (CKD) caused by diabetes and hypertension remains unclear. 36515817: Inflammation, oxidative stress, and hypertension trigger the development of chronic kidney disease (CKD). 36626329: Logistic regression showed that gestational hypertension was independently associated with CKD due to hypertension (aOR 2.76, CI 1.45 - 5.24). 36800948: CKD due to hypertension accounted for 18.7% of CKD DALYs and CKD due to diabetes (types 1 and 2) accounted for 22.7%, while CKD from glomerulonephritis accounted for the most DALYs at 33%. 36875008: Background: Diabetes mellitus and hypertension are the most prominent conditions causing chronic kidney disease and eventually end-stage renal disease. 37146904: After adjustment, stage 5 CKD due to hypertension (aOR: 7.33; 95% CI: 4.86-10.69; p<.001; power=1) displayed higher odds of infection than any other comorbidity. 37572115: Chronic kidney disease (CKD) is one of the main causes of mortality worldwide; its etiology is multifactorial, but diabetes, obesity, and hypertension are the main causes of CKD in adults, although there are other risk factors that are mainly associated with an individual's lifestyle. 37717572: Females had a higher ASIR, while males had a higher age-standardized DALY rate, the gap of which was most distinctive in CKD due to hypertension. 37868481: CKD that requires dialysis was caused mainly by hypertension (78, 35%), diabetes mellitus type 2 (52, 24%), bilateral small kidney disease (40, 18%), and others (34, 16%). 37947985: Bariatric surgery can reverse diabetes mellitus and improve hypertension, which are the main causes of CKD. 38031057: Global incidence and death estimates of chronic kidney disease due to hypertension from 1990 to 2019, an ecological analysis of the global burden of diseases 2019 study. The association between SDI and burden of CKD due to hypertension was estimated using a Pearson correlation analysis. 38178018: Correction: Global incidence and death estimates of chronic kidney disease due to hypertension from 1990 to 2019, an ecological analysis of the global burden of diseases 2019 study. 38238661: Given the growing prevalence of CKD in Mexico and Latin America caused by SAH, there is a need for context-specific approaches to address the effects of SAH, given the diverse population and unique challenges faced by the region. 38330931: Hypertension was the most common etiology of CKD and 34% of patients had previous cardiovascular disease. 38576797: Comorbidities like diabetes mellitus and hypertension are the usual triggers of CKD. 11229626: After baseline measurements of HR, serum creatinine and electrolytes (potassium and sodium), patients received valsartan 80 mg/day plus spironolactone 100 mg/day for concomitant chronic heart failure due to hypertension. 18030872: [Effect of elevated bilirubin levels on the long-term outcome in patients with chronic heart failure due to hypertension]. 19048834: Arterial hypertension (AH) was the cause of CHF in 44 (13%) patients, coronary heart disease in 112 (33%) patients, and combination of the two disorders in 184 (54%) patients. 20491332: They were divided into two subgroups: 21 patients with the etiology of CHF caused by hypertension and 26 patients with the etiology of CHF caused by ischemic heart disease. 20541587: These results indicated that sympathetic variability may be significantly different between salt-sensitive hypertension-induced CHF and healthy individuals, which suggests that sympathetic variability may be used to predict abnormality of the sympathetic regulatory system. To assess sympathetic variability in chronic heart failure (CHF), we evaluated a distribution of inter-spike intervals (ISIs) in renal sympathetic nerve activity (RSNA) in salt-sensitive hypertension-induced CHF (DSSH-CHF) rats. A power-law distribution of inter-spike intervals in renal sympathetic nerve activity in salt-sensitive hypertension-induced chronic heart failure. 20729727: Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. 21283019: CONCLUSION: Ageing male SHRs in contrast to the female SHRs, better mimic the chronic heart failure in humans produced by chronic hypertension. 28290905: MATERIAL AND METHODS: Patients (n=100) with class III-IV CHF and left ventricular ejection fraction (LV EF) <40% due to ischemic heart disease (IHD), dilated cardiomyopathy (DCMP), or arterial hypertension (AH) after compensation of HF before discharge were distributed into groups of low (NT-proBNP <1400 picog/ml, n=30) or high (NT-proBNP more or equal 1400 picog/ml, n=70) risk. 30659413: Hypertension and valvular heart disease were the most common causes for CHF. 36729410: Oxidative stress is one of the most important pathological processes in chronic heart failure caused by hypertension. 38597756: In the majority of patients, ischemic heart disease (98.1 and 91.1% in 2002 and 2021, respectively, p<0.001) and hypertension (80.5 and 98.2%, respectively, p<0.001) were diagnosed as the cause for CHF. 10431527: CONCLUSIONS: Hypertension is still a frequent disorder in pregnancy which may lead to serious complications. 10723231: It may be difficult to differentiate between the primary central nervous system involvement and complications secondary to concomitant arterial hypertension, renal insufficiency and iatrogenic effects of immunosuppressive therapy. 11063175: Coarctation of the aorta is the most common cardiovascular cause of hypertension, and its importance lies in the fact that it is correctable, and that its persistence often leads to dangerous complications and early death. 11255610: CONCLUSION: Since the prevalence of obesity is high in Saudis and since obesity and hypertension occur together and cause serious complications, it is strongly suggested that measures are adopted to decrease prevalence of obesity and its underlying complications. 11416592: Up to 75% of diabetes related cardiovascular complications may be attributable to hypertension. 11465240: Hypertension is a complex pathophysiological state that leads to serious complications, including heart failure, coronary artery disease, and abnormal renal function. 11775408: These three pathologies imply a risk for cardiovascular complications much higher than that due to an isolated arterial hypertension. 12022207: Hypertension is a major public health problem both in the developing and developed countries of the world and if untreated, can lead to various fatal complications like cerebral stroke, encephalopathy, ischaemic heart disease (IHD), renal failure and sudden cardiac death, etc. 12109779: The development of hypertension is accompanied by changes in the rheological properties of blood, particularly by increased red blood cell (RBC) aggregation leading to further pathological complications. 12313673: Hypertensive disease in pregnancy was found to be the leading cause of complications, existing in 10.4% of the pregnancies. 12750170: Severe elevation of red blood cell number is often associated with hypertension and thromboembolism resulting in severe cardiovascular complications. 1291659: AIM: To examine new concepts concerning structural changes in cerebral blood vessels during chronic hypertension, and to examine mechanisms that lead to cerebral vascular complications, in light of the hypothesis that hypertensive vascular hypertrophy may be harmful. 12948429: Hypertension is present in 60% to 70% of the population over 60 years of age and may result in cardiovascular complications such as stroke, coronary heart disease, and heart failure. 136891: This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. 14584294: Both mother and foetus are exposed to lethal from complications frequently caused by hypertension and anaemia. 14626575: Arterial hypertension is one of the most important factors leading to chronic graft nephropathy and causing cardiovascular complications following renal transplantation. 15545151: Both patients were characterized by severe hypertension; therefore, in both cases, degree of hypertension is likely to be causative for this vascular complication. 15815755: Beside lipid disorders and cigarette smoking, hypertension represents the most important risk factor leading to cardiovascular complications. 15854165: The incidence of hypertension is 25-30% in the adult Caucasian population and complications due to hypertension are even greater in African Americans. 15992627: They also have aortic complications such as aneurysm and dissection, which result from a diffuse arteriopathy and continued hypertension that may be caused by underlying endothelial dysfunction. 16238681: CONCLUSION: In this large study of European type 1 diabetic subjects, increased concentrations of tHcy were independently related to macroalbuminuria, renal function and hypertension, which suggests that tHcy might play an important role in the pathogenesis of vascular complications in type 1 diabetes. 16352114: Obesity and hypertension both lead to cardiovascular complications. Endothelial, vascular and renal dysfunctions, all consequences of high blood pressure, further worsen hypertension. Multiple mechanisms involved in obesity-induced hypertension. 16636541: Left ventricular (LV) diastolic dysfunction (LVD) is a common complication secondary to hypertension. 17203817: This increase is associated with increased number of patients with 'diseases of modern civilization', such as diabetes and hypertension, which lead to kidney complications (e.g. diabetic and hypertensive nephropathy). 17371336: BACKGROUND: Hypertension is one of the main causes of cardiovascular complications leading to death and allograft dysfunction. 17643514: CONTEXT: Uncontrolled hypertension attributable to low medication adherence may cause such serious complications as cardiovascular disease and stroke. 1811303: Hypertensive disease can lead to various complications ranging from a headache to myocardial infarct or hemiplegia. 18151410: Cerebral complications resulting from hypertension caused by vasopressor drugs in obstetrics. 18309090: Therefore, hypertension is associated with a decrease in the number of circulating progenitor cells and in the BM-MNC proangiogenic potential, probably leading to vascular complications in this setting. 18691776: Participants with controlled BP were more knowledgeable about threshold, risk factors, and complications as a result of hypertension, had increased awareness, and took medications and BP measurements on regular basis with more inclination to follow or initiate treatment. 18708940: Most patients obtained complete or partial remission after therapy including one accompanied with EBV infection; 5 patients died: 3 of disease progression, 1 of severe infection, and 1 of complications caused by diabetes and hypertension. 1916312: The occurrence of hypertension, leading to various life-threatening complications in the elderly is a widely recognized problem. 19195642: The patient has been managed by conventional steroid suppressive therapy and antihypertensive drugs with limited success; hypertension remained uncontrolled and led to severe complications. 19287815: The research focused mainly on epidemiology, determinants of the aetiology of hypertension, clinical features, varying responses to hypotensive agents among the racial groups, complications that result from hypertension and the control of hypertension. 19596343: Finally, recent Canadian data showing a reduction of the cardiovascular complications attributable to hypertension suggest a possible link of causality with the implementation of the CHEP. 20036896: Cold temperatures make hypertension worse and trigger cardiovascular complications (stroke, myocardial infarction, heart failure, etc.). 20070154: Left ventricular hypertrophy (LVH) is a complication that may result from chronic hypertension. 21079637: Hypertension and diabetes mellitus frequently occur together, leading to increased complications and mortality in patients with both these conditions. 21146149: In a rat model of TBI, we have established that radiation nephropathy is a significant lethal complication, which is caused by hypertension and uremia. 21273751: Sustained severe hypertension and depletion of blood volume resulting from excess catecholamine release from the pheochromocytoma may have caused the complications. 21332058: As a result of high blood pressure it can lead to severe complications, including aortic dissection. 21592975: The high sympathetic activity engenders three intermediate mechanisms, chronic hypertension, left ventricular hypertrophy and arrhythmias, particularly atrial fibrillation, which eventually leads to CV complications and death. 21613355: CONTEXT: The co-occurrence of insulin resistance (IR) and hypertension is a heritable condition leading to cardiovascular complications. 21719861: INTRODUCTION: In the facelift patient, uncontrolled perioperative hypertension is a difficult, acute condition that can lead to significant complications. 21879671: Extreme obesity is a frequent comorbidity, while hypertension is associated with the highest risks since it may lead to a life-threatening complication--eclampsia. 22193449: Hypertension is a common cardiovascular disease and can induce many complications, such as stroke and coronary heart disease. 22231770: A diagnosis of congenital adrenal hyperplasia (11beta-hydroxylase deficiency) was made due to hypertension with virilized genitalia. This case is presented for its rarity where hypertension can cause complication of cardiac failure, if diagnosis is delayed despite early features of pseudoprecocious puberty. 2285101: Most common complications are due, either to induced arterial hypertension or to arterial catheterism (vasospasm or embolism). 23053479: Chronic delivery of angiotensin II (Ang II, 400 ng/kg/min) or N(omega)-nitro-L-arginine-methyl-ester (L-NAME, 0.1 g/L) was used for a 2-week period to induce hypertension. Arterial hypertension is a major risk factor that can lead to complication of peripheral vascular disease due, in part, to endothelial dysfunction. 23082005: Both animal and human studies have indicated that PA is associated with a variety of cardiovascular and renal complications that reflect the capability of elevated aldosterone to induce tissue damage exceeding that induced by hypertension itself. 23105866: Hypertension causes complications such as coronary atherosclerosis and thrombosis wherein inflammatory factors play significant role. 23109761: If left untreated, it can result in life-threatening complications secondary to severe hypertension.We report the case of a 3-year-old girl with congenital mid-aortic syndrome, who was diagnosed by chance in the course of a viral illness, and whose high blood pressure values were first dismissed as inaccurate. 23415058: They included 34 complications due to arterial hypertension (35%), among them 10 cases of pre-eclampsia, eight of eclampsia, seven of Hemolysis-Liver Enzymes-Low Platelet (HELLP) syndrome and two of retroplacental hematoma ; 26 postpartum haemorrhages (27%); and 36 miscellaneous diagnosis including two sepsis, four acute pulmonary oedema, four cardiomyopathy, three pulmonary embolism, and three acute liver steatosis. 23700822: UNLABELLED: The hypertension is a civilization disease, slowly destroying the cardio-vascular system and leading to serious complications, which may result in patient death. 23700849: Psoriasis may cause recurrent miscarriages, chronic hypertension, diabetes or obesity leading to perinatal complications and premature birth. 238547: Complications attributable to hypertension were confined to this latter group. 24388946: Because neurogenic OH is often accompanied by supine hypertension, the treatment program should aim toward minimizing OH and the potential fall injuries related to cerebral hypoperfusion without exacerbating nocturnal hypertension that may lead to excessive cardiovascular complications. 24697027: It is important to control BP in this group of children because early diagnose helps to decrease the risk of multiple organ complications caused by HT. 24827813: However, a longer period of administration or earlier onset of treatment might be needed to delay the development of complications due to hypertension. 25028642: Sodium and fluid retention in dialysis patients is associated with hypertension and vascular changes that may ultimately lead to serious cardiovascular complications. 25637333: Hypertension is the most common condition that leads to multiple organ complications, disability, and premature death. 26074961: These complications reflect the ability of inappropriate elevation of plasma aldosterone to cause tissue damage beyond that induced by high blood pressure itself, thereby setting the stage for major cardiovascular and renal disease. 26315109: Disease activity increases the risk of obstetric and maternal complications, mainly due to arterial hypertension. 2638500: The knowledge about hypertension most related was causes of disease and its complications. 26427798: Higher prevalence of poor blood pressure control and an increasing number of reported cases of complications due to hypertension have also been observed. 26454916: Uncontrolled hypertension in turn can lead to kidney failure and other complications. 26515144: Hypertension frequently results in severe complications in cardiovascular system and histopathological changes in the heart. 26618349: Ang II stimulation of the sympathetic system leads to renal and cardiovascular complications that are secondary to uncontrolled hypertension. 26622407: Diabetes and hypertension are complex and serious diseases that may ultimately lead to renal complications. 26995439: Hyperactive sympathetic nervous system aggravates hypertension and it can cause complications like left ventricular hypertrophy, heart failure, arrhythmias and atherogenesis. 27153123: Despite major scientific advances in its prevention, treatment and care, hypertension remains a serious condition that might lead to long-term complications such as heart disease and stroke. 27476173: ADPKD shows significant progression with age when complications due to hypertension are most significant. 27722964: Hypertension is a common but complex human disease, which can lead to a heart attack, stroke, kidney disease or other complications. 28600736: Hypertension is a leading cause of cardiovascular complications in children on dialysis. 28656594: Metabolic syndrome is coexistence of abdominal obesity, hyperglycemia, hyperlipidemia and hypertension that causes cardiovascular diseases, diabetes and their complications, low quality and short lifespan. 28837424: OBJECTIVE: Preeclampsia is a severe hypertensive disorder of pregnancy which may lead to brain complications such as eclampsia. 29049041: There is emerging evidence to suggest that the successful management of several cardiovascular risk factors [obesity, hypertension (HTN), diabetes mellitus, and obstructive sleep apnea (OSA)] can lead to fewer complications and atrial fibrillation prevention. 29702856: OBJECTIVE: Uncontrolled hypertension (HTN) results in strokes, myocardial infarction (MI), and other complications, which are the leading cause of disability, death, and severe economic consequence. 29709920: Hypertension is one of the most prevalent diseases worldwide and can cause harmful complications within the vascular system. 29886833: Uncontrolled hypertension is frequently the cause of cardiovascular complications. 30273141: Hypertension can lead to severe complications, such as stroke and heart failure. 30281670: Hypertension causes vascular complications, such as stroke, cardiovascular disease, and chronic kidney disease (CKD). 30658606: Hypertensive disorders of pregnancy can lead to fatal complications for both the mother and fetus. 30767907: Hypertension is one of the most important chronic diseases requiring management via the nationwide health maintenance program, and health care providers should inform patients about their risks of a complication caused by hypertension. 30770942: Arterial hypertension represents one of the most frequent chronic diseases that can lead to complications, such as stroke, dementia, heart attack, heart failure and renal failure. 30934719: Hypertension is one of the most common cardiovascular diseases, which will cause severe complications if not treated in a timely way. 30980603: Beside the well-known complications of poorly controlled, long-standing hypertension, milder abnormalities induced by early-stage hypertension have also been described. 31187045: Metabolic syndrome (MS) is a collection of cardiovascular risk factors comprising insulin resistance, dyslipidemia, obesity, and hypertension, which may cause further complications in diabetes. 31198451: Hypertension can cause various complications; one of them is cognitive function impairment. 31398197: BACKGROUND: Uncontrolled high blood pressure (UBP) can lead to various cardiovascular complications causing an estimated nine million deaths per year worldwide. 31431679: Hypertension is the single biggest cause of various cardiovascular complications and at the same time one of the most preventable phenomena. 31467877: Hypertension, the main cause of maternal complications, affected mostly nonwhite women. 31572179: Hypertension is one of the most common cardiovascular diseases, resulting in serious complications such as cardiovascular damage and chronic kidney disease. 3164019: Cardiovascular complications caused by hypertension need to be anticipated during routine dental therapy. 31729722: INTRODUCTION: Hypertension is a major public health concern leading to multiple acute complications. 31926088: Background Hypertension is one of the major health problems of the world and one of the most important causes of death in Indonesia. Complication due to hypertension leads to myocardial infarction, stroke, and renal failure. 32205566: Vascular remodeling is one of the most critical complications caused by hypertension. 32323658: Uncontrolled or poorly managed hypertension leads to several complications such as coronary heart disease, peripheral vascular disease and kidney disease. 32331360: Therefore, noninvasive and continuous BP measurement methods are needed to ensure appropriate diagnosis and early management before hypertension leads to irreversible complications. Elevated blood pressure (BP) is a major cause of death, yet hypertension commonly goes undetected. 32354545: After the Fontan, systemic venous hypertension induces pathophysiologic changes in the lymphatic system that can result in complications of pleural effusion, ascites, plastic bronchitis, and protein losing enteropathy. 32405229: Withdrawing or switching RAAS inhibitors would have uncertain benefits, but it would definitely have many disadvantages such as uncontrolled hypertension, cardiac function deterioration and renal function impairment, which could potentially induce more complications in patients with COVID-19 than the infection of coronavirus itself. 32461198: Withdrawing or switching RAAS inhibitors would have uncertain benefits, but it would definitely have many disadvantages such as uncontrolled hypertension, cardiac function deterioration and renal function impairment, which could potentially induce more complications in patients with COVID-19 than the infection of coronavirus itself. 32492902: Hypertension always leads to other health complications. 32566645: Background: In sub-Saharan Africa, the prevalence of hypertension has assumed epidemic levels and currently accounts for numerous complications such as stroke, heart failure, and kidney damage. 32660065: SARS-CoV-2 induced endothelial cell injury could exacerbate endothelial dysfunction, which is a hallmark of aging, hypertension, and obesity, leading to further complications. 32740890: Notably, if patients present with pre-existing specific comorbidities like diabetes or high blood pressure, rates of COVID-19 induced complications and deaths are escalated. 32741300: Maternal complications (32%) were mainly due to hypertensive disorders of pregnancy (HDP; 19/121; 15.7%). 32766319: Improving hypertension surveillance from a data management prospective: Data requirements for implementation of population-based registry.BACKGROUND: Hypertension (HTN) has become a major public health problem which can cause serious complications when it is not well-controlled. 32863338: Not all the patients showed target organ complications caused by hypertension. 336168: The presence of renal impairment or hypertension, or both, usually leads to complications, especially in the mother. 33813841: Preeclampsia is a heterogeneous disease characterized by new onset of hypertension along with signs of organ damage, affects 2% to 8% of pregnancies, and can result in serious complications to the mother and her child. 33907133: INTRODUCTION: Hypertension can lead to different degrees complications of cardiovascular and cerebrovascular, and increase the risk of sudden death. 33912502: Objective: Uncontrolled chronic diseases such as hypertension and diabetes mellitus can lead to severe complications. 34395624: However, in some patients with a history of heart disease, systemic hypertension, or cerebrovascular disease, these may lead to dangerous complications. 34833952: Moreover, cardiac fibrosis is closely related to hypertension, myocardial infarction, viral myocarditis, atherosclerosis, and diabetes, which can lead to serious complications such as heart failure, arrhythmia, and sudden cardiac death, thus seriously threatening human life and health. 35035931: Hypertension either as a cause of kidney disease or as a complication of chronic kidney disease is the most frequently encountered comorbidity of KT patients. 35046380: Hypertension can cause organ complications, called hypertension-mediated organ damage (HMOD). 35124478: According to clinical experience, long-term hypertension will cause cardiac hypertrophy and other complications, and heart structure remodeling will significantly change the energy characteristics of the heart chambers, and impair heart function. 35132316: Because of this erroneous cognition, many young patients fail to pay attention to their own hypertension, fail to take correct and standardized treatment, and suffer from a series of complications caused by hypertension. 35409698: Most importantly, uncontrolled HPT can lead to severe complications (stroke, heart attack, kidney disease, and heart failure), mainly ignoring the signs in nascent stages. 35556453: CONCLUSION: The study determines that platelet aggregation is one of the physiological events that occurs in hypertension and may be one of the causative factors of complications like cerebrovascular accidents, ischemic heart diseases etc. 35742943: Both hypertension and type 2 diabetes, if treated inappropriately, lead to serious complications, increasing the mortality of patients and generating much higher costs of health systems. 35866827: Preeclampsia is a hypertensive disorder of pregnancy that can lead to multiorgan complications in the mother and fetus. 36335800: OBJECTIVES: Preeclampsia (PE) is a hypertensive disorder of pregnancy that can cause severe complications and adverse fetal/maternal outcomes. 36484353: Preeclampsia, characterized by high blood pressure and proteinuria during pregnancy, causes serious complications in both the mother and the fetus. 36594299: This study was done to evaluate the effects of hypertension and to find out the major complications occurring due to hypertension. 36811694: Acknowledgment of pediatric hypertension early is critical, as it can result in serious complications long-term if left undiagnosed. 36890456: BACKGROUND: Arterialsclerosis caused by hypertension can lead to many complications, such as heart attack, stroke and so on. 37022208: Ongoing evaluation and nursing care are key in the prevention of complications resulting from hypertensive disorders in pregnancy. 37235676: Elevated blood pressure can lead to many complications and is the main risk factor for stroke, heart failure and nephropathy. 37255909: Pheochromocytoma (PCC) is a neuroendocrine tumor that may present with headaches, palpitations, and hypertension, and if left unresected, it can lead to serious complications and fatal cardiac mortality. 37425261: Introduction: Adolescent high blood pressure (HBP) can lead to several end-organ complications if it continues into adulthood. 37453193: The complications caused by hypertension are important risk factors for cardiovascular disease accidents. 37932696: BACKGROUND: Patients with bilateral primary aldosteronism (PA) generally are treated with antihypertensive drugs, but optimal treatment for patients with complications due to refractory hypertension has not been established. 38094531: Dry weight (DW), one of the dialysis parameters, should be optimized to reduce the complications caused by high blood pressure. 38232920: Pulmonary hypertension, a condition marked by high blood pressure in the lungs, can lead to heart failure and other complications. 38303535: Elevated blood pressure often leads to lethal complications (heart failure, stroke, renal disorders, etc.) if left untreated. 38460862: Hypertension, a prevalent cardiovascular ailment globally, can precipitate numerous complications, notably hypertensive cardiomyopathy. 38464676: Purpose: Hypertension (HT) can cause renal complications or deterioration of kidney function. 38496804: Background: HT is a systemic disease that presents with persistent high blood pressure, which has become an important health problem due to its cause of serious complications and high prevalence in the community. 38547158: PURPOSE OF REVIEW: Hypertension remains one of the most common clinical problems leading to significant posttransplant complications. 3881092: The authors suggest that the abnormalities in basement membrane form and function caused by hyperglycemia form the necessary background upon which other factors, such as hypertension and hyperlipidemia, then act to cause irreversible complications. 576851: The HDFP is continuing its efforts to find to what extent sustained treatment of those with elevated blood pressure can reduce mortality or complications due to hypertension. 6214041: These findings indicate that inhibition of blood coagulation effectively protects rats with experimentally decreased renal mass from the development of progressive renal failure and hypertension and support the concept that the glomerular thrombosis plays an important role in the pathogenesis of these complications. 6519756: By lowering blood pressure, a number of hypertensive complications can be prevented, including congestive heart failure and such consequences of hypertensive arteriolar disease as nephropathy, intracerebral hemorrhage, and lacunar stroke. 6750812: The need to prevent complications resulting from hypertension is stressed. 694688: More effective screening and therapeutic programmes should be initiated in the Indian population because of the high prevalence of hypertension which may lead to complications if untreated, and because 58% of the hypertensive subjects were untreated or had discontinued therapy. 7314924: The high prevalence of hypertension in the elderly population as well as the grave consequences complications caused by hypertension should call our attention to the recording and treatment of arterial hypertension in the elderly. 7404085: The high prevalence of diastolic blood pressures of 105 mmHg or more, together with the high prevalence of hypertension in White male subjects aged under 40 years, could be an important factor in the aetiology of ischaemic heart disease in White males in the 25-34-year age greup. More effective screening and therapeutic programmes should therefore be initiated in the White population because of the high prevalence of hypertension which may lead to complications. 7970077: There are three clinical stages of SOH: slight, moderate and severe, caused by a pathogenetic mechanism which is thought to involve the action of prostaglandins and the renin-angiotensin system leading to an alteration in capillary permeability with increased ovarian diameter. The use of gonadotropins in therapy has led to the appearance of a complication due to hyperstimulation, referred to as \syndrome due to ovarian hypertension\ (SOH). 8749228: Nifedipine may be an important adjunct to the conservative management of the complications caused by chronic venous insufficiency and hypertension. 9225654: Prophylactic treatment with medication causing least harm to the mother and fetus to prevent serious complication due to hypertension in pregnancy when increased risk is identified would be of value and further improve maternal and fetal outcome. 9284413: Hypertensive disease causes vascular complications, which are clinically important. 9404410: UNLABELLED: Severe hypertension may lead to macroangiopathy complications especially when a major vascular risk factor as diabetes exists. 9495622: As a consequence, these vessels may play a role in myocardial, cerebral and renal complications of hypertension. 10503066: The prevalence of a normal LVEF associated with CHF as a result of prior myocardial infarction or hypertension was 22% in men aged 60 to 69 years, 33% in men aged 70 to 79 years, 41% in men aged 80 to 89 years, and 47% in men aged 90 years or older. 11817974: Diabetes with and without hypertension is an important cause of LV dysfunction and CHF. 12473553: For CHF occurring in the absence of myocardial infarction, the lifetime risk is 1 in 9 for men and 1 in 6 for women, which highlights the risk of CHF that is largely attributable to hypertension. 1349931: A 75-year-old woman with longstanding hypertension, resulting in congestive heart failure and renal failure. 1360979: The most common chief complaints on admission were dyspnea, headache, palpitation, and edema which were due to hypertension and congestive heart failure. The majority of the patients required immediate medical treatment to control congestive heart failure due to hypertension at initial presentation. 1381791: Angiotensin-converting enzyme inhibitors have been shown to be effective therapy for hypertension, and also for severe congestive heart failure, whether due to hypertension or to other causes. 14621191: Three patients who suffered from congestive heart failure caused by severe hypertension were treated with a combination therapy consisting of angiotensin converting enzyme inhibitor (ACEI) and angiotensin II receptor blocker (ARB). 1535655: BACKGROUND: The long-term effects of hypertension on the heart culminate in congestive heart failure. 15913489: Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. 16106138: Coronary artery disease has supplanted hypertension as the leading cause of congestive heart failure in the United States. 16285604: Similarly, 5-year and 10-year survival rates of patients with CHF caused by valvular heart disease, hypertension, and dilated cardiomyopathy were 62% and 44%, 58% and 53%, and 70% and 65%, respectively. 16379701: Hypertension was the most common cause of congestive heart failure. 1715483: Arterial hypertension is the most common cause of congestive heart failure and an important risk factor in coronary artery disease (CAD). 1832580: OBJECTIVE: It is now believed that diabetes sensitizes the myocardium so that superimposed hypertension with its attendant vascular changes results in progressive myocyte damage leading ultimately to congestive heart failure. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 21331710: As a consequence of the sustained high BP, there is an increased risk of mortality and morbidity that is characterized by myocardial infarction, congestive heart failure, stroke, end-stage renal failure, and peripheral vascular disease (1-3). 22977362: Hypertension is the major cause of congestive cardiac failure all over the world. 23102190: CHF is often caused by hypertension, diabetes, or coronary heart disease. 25280267: Oliguria secondary to captopril and rapid-onset congestive heart failure due to persistent hypertension led to the introduction of intravenous agents labetalol and nitroprusside. 2576672: Left ventricular hypertrophy may be a serious consequence of chronic untreated hypertension since it may accentuate the risk of congestive heart failure, arrhythmias, coronary ischaemias and sudden death. 27614538: Patients were selected if they had a history of CHF or suspected abnormal diastolic function due to chronic hypertension. 27841876: In Dahl salt-sensitive rats that were fed a high-salt diet, a model for hypertension-induced congestive heart failure, spermidine feeding reduced systemic blood pressure, increased titin phosphorylation and prevented cardiac hypertrophy and a decline in diastolic function, thus delaying the progression to heart failure. 28414679: CASE: A 40 year old woman with a history of HIV, congestive heart failure secondary to an unknown congenital heart defect, and hypertension presented to our emergency department with worsening edema. 29624034: The?most common complication in adulthood is cardiac decompensation, which can be explained as a consequence of longstanding?hypertension and changes in coronary blood vessels. 31451679: It is well established that chronic hypertension can lead to congestive heart failure (CHF). 33250480: Nephrectomy can be an effective treatment for a WT patient with hypertension causing hypertensive cardiomyopathy, and then cardiac function will be improved within several weeks. In this report, a pediatric case of WT with hypertension causing hypertensive cardiomyopathy and congestive heart failure is presented. The patient was diagnosed with cardiomyopathy caused by hypertension. 3718040: Four babies had extensive aortic thrombosis and hypertension producing congestive aortic thrombosis and hypertension producing congestive heart failure. 4028530: Cardial decompensation caused by hypertension and polyglobulia associated with multiple renal oncocytomas. 4036842: Systemic hypertension is a common cause of congestive heart failure. 6990626: Classical writings suggest that the Roman emperor Hadrian died from congestive heart failure resulting from hypertension and coronary atherosclerosis. 7554808: Coronary artery disease, hypertension, valvular heart disease, and cardiomyopathies are the commonest causes of CHF in elderly patients. 8311732: The patients were divided in two groups according with the presence of AH as cause of CHF: group A, 18 patients with CHF due to AH and group B, 12 patients with CHF due to idiopathic dilated or chagasic cardiomyopathy without previous AH. In patients with CHF due to AH, proteinuria was more frequent, more severe and did not improve after the treatment, suggesting renal lesion. 8678395: The pathogenetic sequelae of diabetes and hypertension are devastating to the heart and often lead to premature congestive heart failure, sudden cardiac death, and acute myocardial infarction. 8754362: Congestive heart failure (CHF) continues to be a lethal end stage of cardiovascular diseases caused by hypertension, coronary heart disease, valve deformity, diabetes and cardiomyopathy. 8763514: Valve disease, coronary artery disease and hypertension are the most frequent causes of congestive heart failure. 8837575: Levels of IL-2 and IL-2-sR are not elevated when congestive heart failure is due to coronary artery disease or hypertension. 8970426: In this study of 301 black patients with congestive heart failure (CHF), systemic hypertension is the most common cause of CHF and is the primary etiology of CHF in 61%. 9233121: The consequences of untreated hypertension include myocardial infarction, stroke, congestive heart failure, peripheral vascular disease and renal disease. 9256850: Coronary heart disease and hypertension are the most common etiologies of CHF in older adults, and they often coexist. 9336607: Primary care physicians who see elderly patients are likely to see cases of congestive heart failure, since this condition is typically the result of long-standing hypertension or coronary artery disease. 9431757: RESULTS: The top 10 diseases encountered in 12,280 patients were: pneumonia, HIV/AIDS, pulmonary tuberculosis, hypertension, Diabetes mellitus, malaria, gastro-enteritis, congestive cardiac failure secondary to cardiomyopathy, congestive cardiac failure secondary to hypertension, and asthma. 9529748: Cardiovascular diseases in our medical in-patients at Kenyatta National Hospital are common and especially so with hypertension which plays an important role in the aetiology of congestive heart failure and cerebravascular accidents. 9540127: Hypertension-induced congestive heart failure. 1654935: Data suggest that there are enhanced L-type calcium currents in SHR compared to WKY controls even in the prehypertensive state and that, in this form of gentic hypertension, there are fundamental changes in the membrane signal that triggers contraction. 25427636: However, hypertension may also result in left ventricular dyssynchrony (LVD) which is characterized by delayed activation of certain ventricular segments leading to uncoordinated contraction. 31542964: Increased Vascular Contractility in Hypertension Results From Impaired Endothelial Calcium Signaling. 31555955: BACKGROUND: Hypertension as a known risk factor for cardiovascular diseases can result in left ventricular dyssynchrony (LVD) leading to uncoordinated contraction. 3157632: The left ventricular ejection dynamics, the extent and pattern of left ventricular contraction were compared with eight patients with secondary myocardial hypertrophy due to arterial hypertension (group II) and eight normal subjects (group III). 4090589: Occasionally, peculiar cytoplasma deformations could be found surrounded by circumscribed, consecutive endothelial gaps, allowing speculation of increased contraction-like states of intraendothelial filament tension due to hypertension. 4281576: [Mitochondrial function and contractility in the hypertrophic myocardium due to hypertension]. 7762002: Animal studies have demonstrated that low-level lead exposure produces hypertension and that lead can cause contraction of vascular smooth muscle directly. 7843009: To get clinical evidences of the hypothesis, the reversal or contraction of glaucomatous optic cup after reduction of intraocular pressure (IOP) was examined (The change is primarily caused by intraocular hypertension--induced distortion and posterior ectasia of the lamina cribrosa which moves forward reversely, leading to dilated optic cup contraction.). 8831104: Effects of hypertension on hypercholesterolemia-induced changes in contraction of rabbit aorta and carotid artery. 8986928: Finally, in isolated aortae, chronic combined drug treatment was associated with an increased basal release of nitric oxide and a decrease in the hypertension-induced endothelium-dependent contractions in response to acetylcholine. 9366285: In an attempt to compensate for the increased peripheral resistance frequently noted in hypertension, the heart may hypertrophy, with the left ventricular enlargement accompanied by fibrosis and resulting in reduced contractility. 1359140: Hypertension is a known risk factor in the genesis of coronary artery disease. 15039815: Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. 16392277: In obese patients with type 2 DM (T2DM) there can be associated complications of hyperinsulinaemia, dyslipidaemia, and hypertension, which can lead to coronary artery disease and stroke. 17713747: Arterial hypertension is the leading cause of coronary artery disease and cardiac failure, and coronary artery disease is the cause of heart failure in 50% of cases. 18369738: OBJECTIVE: Hypertension induces coronary artery disease (CAD) and progression of arterial wall calcification. 25621195: BACKGROUND: Endothelial dysfunction is associated with vascular risk factors such as dyslipidemia, hypertension, and diabetes, leading to coronary atherosclerosis. 26587454: However, the risks for cerebrovascular disease and coronary artery disease which are attributable to hypertension were the highest in Korea. 26619661: Abstract Hypertension is the major cause of cardiovascular disease. Persistent hypertension leads to cardiovascular remodeling and resulted in heart diseases such as coronary artery disease, heart failure, and arrhythmia. 2662954: In absolute terms, coronary artery disease is the most important consequence of hypertension. 29087287: Conclusion: Turkish Cypriot patients with coronary artery disease may be more affected by secondary factors, such as diabetes, hypertension, obesity, and sedentary life style when compared with genetic factors, which may be responsible for coronary artery disease. 31322087: Clinical manifestation of atherosclerotic heart disease mainly due to stage III hypertension, history of myocardial infarction were combined with pneumonia, chronic obstructive pulmonary disease with the outcome in pneumosclerosis and emphysema, as well as the presence of cholecysto-cardial syndrome, chronic gastritis, chronic cholecysto-pancreatitis, abdominal ischemic syndrome, rheumatoid arthritis, diabetes mellitus, and chronic pyelonephritis. 31929865: Background: Hyperlipidemia and hypertension are the most important causes of ischemic heart disease. 31969096: Systematic Understanding of the Mechanisms of Flos Chrysanthemi Indici-mediated Eeffects on Hypertension via Computational Target Fishing.AIM AND OBJECTIVE: Hypertension-induced stroke and coronary artery disease are significant causes of global morbidity and mortality. 32131408: Metabolic Fingerprint of Turner Syndrome.Girls with Turner syndrome (TS) are at increased risk of developing insulin resistance and coronary artery disease as a result of hypertension and obesity frequently seen in these patients. 33273852: Background: Globally, sixty-two percent of cerebrovascular disease and forty-nine percent of ischemic heart disease are attributable to increased blood pressure. 33907634: These genetic polymorphisms have a direct association with CAD development or indirect association through causing atherosclerosis and hypertension which, in turn, are complicated by CAD later on. 3402354: To determine the importance of systemic arterial hypertension (SAH) in the pathogenesis of coronary atherosclerosis (CA), the coronary stenosis (CSI), coronary diffuse atheromatous (CDAI) and coronary tortuosity (CTI) indices were assessed by selective coronary angiography (SCA) in 132 survivors of a definite first myocardial infarction (MI). 34091009: The present study aims to understand the underlying vasoprotective effects of nutritional NO 2 - and NO 3 - co-therapy in mice with angiotensin-II (AT-II)-induced arterial hypertension. High-dose AT-II (1 mg/kg/d, 1w, s. c.) was used to induce arterial hypertension in male C57BL/6 mice. Arterial hypertension is one of the major health risk factors leading to coronary artery disease, stroke or peripheral artery disease. 35135760: Another high-quality publication found an association between occupational sitting and ischaemic heart disease in a subgroup already at risk due to hypertension. 35356999: Persistent arterial hypertension leads to structural and functional remodeling of the heart resulting in myocardial ischemia, fibrosis, hypertrophy, and eventually heart failure. 35677685: In contrast to historical teaching, recent studies have shown that excess aldosterone production is associated with increased burden of ischemic heart disease disproportionate to the effects caused by hypertension alone. 37344814: BACKGROUND: Cardiovascular diseases, such as stroke and ischemic heart disease attributable to hypertension, are major causes of premature death in Japan and worldwide. 7064799: The role of hypertension and downward changes of blood pressure in the genesis of coronary atherosclerosis and acute myocardial ischemic attacks. 7585300: Eventually the combination of dyslipidemia ('high triglyceride-low high density lipoprotein' in Asia Pacific rim), plus smoking plus hypertension (part salt related) may trigger a CAD epidemic. 8576788: This does not mean that hypertension is the cause of coronary artery disease. 10760631: Hypertension and coronary disease remain the leading causes of the disease, and heart failure due to myocardial infarction has increased in prevalence. 10955415: To assess the risk of myocardial infarction in users of post-menopausal hormone replacement therapy who are at high risk of coronary disease because of hypertension, diabetes mellitus, or smoking, we used data from a previously published case-control study of women 45-74 years. 12480731: The consequences of hypertension include cerebrovascular disease, coronary heart disease, and general atherosclerosis. Hypertension and related factors in the etiology of Alzheimer's disease. 12806484: Independent associations with treatment of hypertension were found for, in decreasing order of magnitude: less time elapsed since the last blood pressure measurement, greater number of physician visits in the past 12 months, higher body mass index, female gender, history of coronary disease, changes in diet due to arterial hypertension, and higher family income. 15931015: Hypertension was least recognized: only 5% of the 180 women who had hypertension acknowledged it as a cause of their CHD. 16679101: The metabolic syndrome represents a constellation of risk factors caused by insulin resistance, dyslipidemia, hypertension, and obesity, resulting in elevated coronary disease risk. 17299955: [Economic burden of coronary heart disease and stroke attributable to hypertension in China]. 19766467: It has been demonstrated that hypertension can lead to coronary heart disease, heart failure, stroke, and memory loss. 22157565: Around 54% of stroke and 47% of coronary heart disease are attributable to high BP. 23641033: RISK FACTORS: Self assigned ethnicity, age, sex, smoking status, systolic blood pressure, ratio of total serum cholesterol to high density lipoprotein cholesterol concentrations, body mass index, family history of coronary heart disease in first degree relative under 60 years, Townsend deprivation score, treated hypertension, type 1 diabetes, type 2 diabetes, renal disease, rheumatoid arthritis, coronary heart disease, congestive cardiac failure, valvular heart disease, and atrial fibrillation RESULTS: The QStroke algorithm explained 57% of the variation in women and 55% in men without a prior stroke. 25063306: ETHNOPHARMACOLOGICAL RELEVANCE: Xin-Ji-Er-Kang (XJEK), a Chinese herbal formula, is effective against hypertension induced coronary heart disease, viral myocarditis and toxic myocarditis. 26259287: Obesity is associated with numerous comorbidities, including hypertension, lipid disorders and type II diabetes, and is also a major cause of cardiovascular disease, coronary disease, heart failure, atrial fibrillation, and sudden death. 2676261: Attention is drawn to implications of recent guidelines for cholesterol-lowering for the design of trials of lipid-lowering in hypertensive patients, and to some recent evidence for genetic linkage between hypertension and hyperlipidemia in the pathogenesis of coronary heart disease. 26876916: In recent years, about 7.3 million people died due to coronary heart disease, 9.4 million deaths due to high blood pressure and 6.2 million due to stroke, where obesity and atherosclerotic progression remain the chief pathological factors. 27627083: The mechanisms causing this complication are complex and include coronary heart disease, myocardial changes induced by hypertension, increased aortic stiffness, arrhythmias, renal failure and last but not least by direct metabolic alterations causing diabetic cardiomyopathy. 29973522: Hypertension can cause coronary heart disease. 3599374: Therefore, it appears that the incidence of CHD caused by hypertension and by hypercholesterolemia are mixed in Japan. 737618: The increased frequency of coronary heart disease in the obese is largely attributable to the commonly associated hypertension, diabetes mellitus and lipoprotein abnormalities, rather than the adiposity. 7468582: Some of the excess risk of coronary heart disease in diabetes is probably due to hypertension. 805354: This is of great importance in view of the significance of high serum lipid levels and hypertension as risk factors in the etiology of coronary heart disorders. 19927134: Although hypertension is well known as a cause of vascular dementia (VaD), recent findings highlight the role of hypertension in the pathogenesis of Alzheimer's disease (AD) as well as mild cognitive impairment (MCI). 22507914: In the present research work, for the first time we are reporting the genesis of VaD by deoxycorticosterone acetate (DOCA)-salt induced experimental hypertension. Experimental hypertension induced vascular dementia: pharmacological, biochemical and behavioral recuperation by angiotensin receptor blocker and acetylcholinesterase inhibitor. It may be concluded that DOCA-salt hypertension induces VaD in rats. Furthermore, we have also investigated the beneficial effect of telmisartan, an angiotensin II type 1 receptor blocker (ARB) and donepezil, an acetylcholinesterase inhibitor (AChEI), on DOCA-salt hypertension induced VaD in rats. ARBs and AChEIs may be considered as potential pharmacological agents for the management of hypertension induced VaD. 22526544: CONCLUSIONS: DOCA-salt hypertension induces vascular dementia in rats. METHODS: DOCA was used to induce hypertension and associated vascular dementia. Defensive effect of natrium diethyldithiocarbamate trihydrate (NDDCT) and lisinopril in DOCA-salt hypertension-induced vascular dementia in rats. OBJECTIVES: This study investigates the effect of natrium diethyldithiocarbamate trihydrate (NDDCT), a nuclear factor kappa-B (NF-kappaB) inhibitor, as well as lisinopril, an angiotensin converting enzyme (ACE) inhibitor, on deoxycorticosterone acetate (DOCA) hypertension-induced vascular dementia in rats. 23201648: This research work investigates the salutiferous effect of aminoguanidine (AG), an iNOS inhibitor and 4'-hydroxy-3'-methoxyacetophenone (HMAP), a NADPH oxidase inhibitor in Hypt induced VaD in rats. Role of iNOS and NADPH-oxidase has been reported in various pathological conditions but there role in hypertension (Hypt) induced VaD is still unclear. Pharmacological inhibition of inducible nitric oxide synthase (iNOS) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, convalesce behavior and biochemistry of hypertension induced vascular dementia in rats. It may be concluded that AG, an iNOS inhibitor and HMAP, a NADPH-oxidase inhibitor may be considered as potential agents for the management of Hypt induced VaD. 24614908: Hypertension has been traditionally associated with the etiology of vascular dementia, however, vascular risk factors including hypertension are increasingly being implicated in AD. 25446433: Hypertension (HT) is a prevailing risk factor for cognitive impairment, the most common cause of vascular dementia; yet, no possible mechanism underlying the cognitive impairment induced by hypertension has been identified so far. 25659733: This study has been structured to investigate the role of agomelatine, a melatonergic MT1/MT2 agonist and nicorandil, a selective ATP sensitive potassium (KATP) channel opener in renal artery ligation (two-kidney-one-clip: 2K1C) hypertension induced endothelial dysfunction, brain damage and VaD. 27144579: In addition, oral administration of TWK10-fermented soymilk extract in DOCA-salt hypertension-induced VaD rats resulted in a significant decrease in blood pressure (p < 0.05), which was regulated by inhibiting ACE activity and promoting NO production, in addition to decreased escape latency and increased target crossing (p < 0.05). In conclusion, these results demonstrated that TWK10-fermented soymilk extract could improve learning and memory in DOCA-salt hypertension-induced VaD rats by acting as a blood pressure-lowering and neuroprotective agent. 27189349: OBJECTIVE: The present study has been structured to explore the effects of bosentan, an ET-1 antagonist on two-kidneyone- clip: 2K1C method induced hypertension provoked vascular dementia (VaD). 27874975: Structural and functional brain alterations in a murine model of Angiotensin II-induced hypertension. Hypertension is a main risk factor for the development of cerebral small vessel disease (cSVD) - a major contributor to stroke and the most common cause of vascular dementia. Our data strongly support the suitability of this particular mouse model of AngII-induced hypertension as an appropriate animal model for early-onset cSVD and hence, vascular cognitive impairment, pathologies commonly preceding vascular dementia. 27937042: Prevention of hypertension-induced vascular dementia by Lactobacillus paracasei subsp. paracasei NTU 101-fermented products. OBJECTIVE: This study investigated the effect of ethanol extract of Lactobacillus paracasei subsp. paracasei NTU 101-fermented products (NTU101F) in hypertension-induced VaD in rats. RESULTS: Oral administration of NTU101F in DOCA-salt hypertension-induced VaD rats resulted in a significant decrease in blood pressure by 18.3-23.2% (p < 0.001), which was regulated by increasing eNOS density (about 3-fold) in the aorta, promoting NO production, and decreasing of matrix metallopeptidase 9 activity (about 2-fold) in the hippocampus, in addition to improve the kidney function and structure, decrease escape latency and increase the times spent in the target quadrant by 23.5-27.8% (p < 0.05). CONCLUSION: Overall, our findings suggest that NTU101F could exert neuroprotection in the brain and attenuate hypertension-induced VaD. 34118020: Hypertension (HT) is one of the main causes of vascular dementia, lead to cognitive decline. 34897090: Hypertension is a major risk factor for the pathogenesis of vascular dementia and Alzheimer's disease. 35396697: This study investigates the role of ulinastatin (UTI) and quercetin alone as well as in combination in hypertension-induced endothelial dysfunction and vascular dementia (VaD). Therefore, the utility of these agents might be studied further to understand their full potential in hypertension-induced VaD. METHOD: Two-kidney one-clip (2K1C) renovascular model was set up to induce hypertension in the Albino Wistar rats (males). 35556073: INTRODUCTION AND OBJECTIVE: Cardiovascular diseases and hypertension are the major contributors to the pathogenesis of vascular dementia. 35557207: INTRODUCTION: A reduction in blood flow to the brain in hypertension leads to vascular dementia, but what drives this is unknown. Opportunities to restore the spark-to-BK coupling could be a novel approach to prevent vascular dementia caused by hypertension. 37549299: Uncoupling of Ca 2+ sparks from BK channels in cerebral arteries underlies hypoperfusion in hypertension-induced vascular dementia. The deficit in cerebral blood flow (CBF) seen in patients with hypertension-induced vascular dementia is increasingly viewed as a therapeutic target for disease-modifying therapy. 38192137: Montelukast Ameliorates 2K1C-Hypertension Induced Endothelial Dysfunction and Associated Vascular Dementia. 9324122: Hypertension accelerates the development of diabetic retinopathy; hypertensive/diabetic cerebral disease leads to vascular dementia, transient ischemic attacks, and strokes. 11432121: Hypertension and diabetes are the leading causes of small-artery disease, subcortical brain ischemia, and stepwise or slowing progressive decline in cognitive function. 11786083: BACKGROUND: Mechanical stretch, a consequence of capillary glomerular hypertension, is thought to be the common final pathway for glomerulosclerosis in systemic hypertension, diabetes, reduced nephron number and focal segmental glomerulosclerosis. 15276118: Our study demonstrated the early appearance of both left ventricular systolic and diastolic dysfunction in diabetic patients at rest and the contributory effects of diabetes to myocardial impairment produced by hypertension, as well as the high usefulness of tissue Doppler imaging in detection and quantitation of myocardial dysfunction in diabetics. 15487691: In the early years of the 20th century, the debate continued whether macular changes were directly related to diabetes or whether they were due to hypertension and arteriosclerosis. 15855808: The magnitude of GLUT1 overexpression caused by hypertension is higher than that induced by diabetes alone. BACKGROUND/AIM: Diabetes and mesangial stretch caused by hypertension increase mesangial matrix deposition which is induced by local production of transforming growth factor beta 1 (TGF-beta1). 15890893: BACKGROUND: We hypothesized that serum gamma-glutamyltransferase (GGT) would positively predict the risk of microalbuminuria, a frequent consequence of both diabetes and hypertension, because serum GGT predicted diabetes and hypertension in dose-response relationships. 16937598: Approximately 47 million Americans have metabolic syndrome, a constellation of obesity, hypertension, dyslipidemia, and insulin resistance leading to diabetes. 18154717: Various diseases such as arterial hypertension, diabetes and obesity result in renal diseases which are often irreversible and resistant to currently available therapies. 19721377: Patients with lifestyle-related diseases such as hypertension, diabetes, and hyperlipidemia are at high risk for the pathogenesis of a life-threatening atherosclerotic disease. 20445714: BACKGROUND: Obesity and arterial hypertension are a serious risk factor for insulin resistance patients leading to diabetes and other disorders. 21435165: Critical ischemic disease is often caused by arteriosclerosis due to hypertension or diabetes. 22991477: OBJECTIVE: To determine the frequency of incorrect reporting of hypertension as cause of diabetes on death certificates in the USA. RESULTS: The percentage of cases in which both hypertension and diabetes were included in part I of the death certificate, in which hypertension was reported on the line below diabetes on the death certificate-that is, suggesting that hypertension was a cause of diabetes-increased from 15.5% in 1985 to 36.1% in 2000 and 38.2% in 2005. 27960152: BACKGROUND/AIMS: Hypertension is a major cause of stroke, and diabetes can increase incidence of this disease. 28656594: Metabolic syndrome is coexistence of abdominal obesity, hyperglycemia, hyperlipidemia and hypertension that causes cardiovascular diseases, diabetes and their complications, low quality and short lifespan. 29149254: 2017;186(10):1115-1124) clearly documented that both gestational diabetes and hypertension lead to diabetes and hypertension and that the combination of both during pregnancy leads to very high rates of subsequent diabetes and hypertension. 30078514: Globally and in most Global Burden of Disease study regions, age-standardized DALY rates decreased, except in High-income North America, Central Latin America, Oceania, Southern Sub-Saharan Africa, and Central Asia, where the increased burden of CKD due to diabetes and to a lesser extent CKD due to hypertension and other causes outpaced burden expected by demographic expansion. 31380241: Relationship Between Portal HTN and Cirrhosis as a Cause for Diabetes. 33158933: This is similar to the consequences of hypertension, diabetes, obesity and ageing that are the common precursors to HFpEF. 36102254: Metabolic syndrome (MetS) is a common feature in obesity, comprising a cluster of abnormalities including abdominal fat accumulation, hyperglycemia, hyperinsulinemia, dyslipidemia, and hypertension, leading to diabetes and cardiovascular diseases (CVD). 36706989: BACKGROUND: Poor wound healing is a significant complication of diabetes, which is commonly caused by neuropathy, trauma, deformities, plantar hypertension and peripheral arterial disease. 38015048: The metabolic syndrome (MetS) refers to the co-occurrence of risk factors, including hyperglycaemia, increased body weight, hypertension and dyslipidemia, which eventually lead to diabetes and cardiovascular disease, a common health problem worldwide. 10624386: The prevalent causes of end-stage renal disease (ESRD) in the elderly are diabetes mellitus and nephrosclerosis due to long-term arterial hypertension. 1328365: Exclusion criteria were diabetes mellitus, organ damage secondary to hypertension and diseases that may have interfered with compliance and the interpretation of results. 1328366: Exclusion criteria were diabetes mellitus, organ damage secondary to hypertension, and diseases that might have interfered with compliance and the interpretation of results. 14737848: Diabetes mellitus doubles the risk of cardiovascular diseases, even in hypertensive patients who are already at high risk because of their high blood pressure. 17187749: About 5.9% of the women were at a high-risk because of polluted housing condition, 1.9% because of heart diseases Class capital I, Ukrainian or II, 5.2% because of diabetes mellitus, 4.2% because of hypertension and 14.9% because of previous cesarean section. 27195949: Diabetes mellitus increases the mortality secondary to heart failure independent of hypertension and coronary artery disease. 29721501: Result: Mice in the DM group exhibited increased blood glucose levels, cardiac dysfunction, and high blood pressure at 1, 3, and 6 months after DM induction. 35193593: A total of 1,659,045 deaths due to CKD were recorded between 1980 and 2014 (477,332 due to diabetes mellitus, 1,056,150 due to hypertension, 122,795 due to glomerulonephritis, and 2,768 due to other causes). 35371924: Hypertension often leads to diabetes mellitus that strongly puts the patients at an increased risk of cardiovascular, kidney, and/or atherosclerotic diseases. 38560076: The previously postulated hypotheses of triple vessel disease (TVD), diabetes mellitus (DM), and concentric left ventricular hypertrophy (LVH) due to Hypertension (HTN) being protective against VSR were explored. 5714359: [Significance of hypertension in the pathogenesis of diabetes mellitus]. 15589689: All together, the present results showed that hypertension associated to type 1 or type 2 diabetes exacerbated the damage caused by diabetes or hypertension alone on liver lipid metabolism. 16137672: In this study we examined diabetes- and hypertension-induced changes in cardiac structure and function in an animal model of type 2 diabetes, the Goto-Kakizaki (GK) rat. 18160587: Obesity is a complex, multifactorial chronic disease frequently associated with cardiovascular risks, hypertriglyceridemia, low high-density lipoprotein-cholesterol, high blood pressure, and the insulin resistance that appears to be central to the pathogenesis of Type II diabetes. 19095606: RESULTS: In type 2 diabetes, the prevalence of hypertension due to both hyperglycemia and insulin resistance is increased. 23897568: BACKGROUND: The obesity and hypertension have become the causes for the development type 2 diabetes. 24057947: Type 2 diabetes is associated with a high prevalence of comorbidities resulting from hypertension, dyslipidemia, and hyperglycemia. 31119677: The metabolic and physiologic responses to healthy dietary habits and physical exercise have become an increasingly interesting research area, since equilibrated diet and regular physical activity are commonly recommended for their antioxidant capacity and for the prevention and treatment of several disorders as insulin resistance, dyslipidemia, obesity, and hypertension that may result in cardiovascular disease and type II diabetes. 31671730: Not only that organizations, such as the world health organization (WHO) have identified high blood pressure as one of the main risk factors of the cardiometabolic syndrome, but there is also a link between the occurrence of insulin resistance/impaired glucose tolerance and hypertension that would consequently lead to type-2 diabetes (T2D). 32740722: Role of FTO and MC4R Polymorphisms in Escalating Obesity and Their Indirect Association With Risk of T2D in Indian Population.INTRODUCTION: Obesity plays a pivotal role in the development of metabolic syndrome-excessive body fat, spikes in blood glucose levels and hypertension-and ultimately leads to cardiovascular diseases and type 2 diabetes (T2D), if left unattended. 37730735: Metabolic syndrome represents a cluster of conditions such as obesity, hyperglycaemia, dyslipidaemia, and hypertension that can lead to type 2 diabetes mellitus and/or cardiovascular disease. 12707391: By contrast, the inhibition of renal pentosidine formation assessed both by immunohistochemistry and HPLC suggests a critical role of advanced glycation end product (AGE) formation together with hypertension in the genesis of diabetic nephropathy. 1794213: A role for hypertension in the progression of established renal damage in IDDM is now accepted; however the role of hypertension in the genesis of diabetic nephropathy is not yet clear. 18922888: Both hyperglycemia and glomerular hypertension are crucial determinants in the pathogenesis of diabetic nephropathy and impose cellular stresses on renal target cells. 19906946: Both systemic and glomerular hypertension are believed to be important in the pathogenesis of DN. 21228783: Diabetes and hypertension frequently coexist and constitute the most notorious combination for the pathogenesis of diabetic nephropathy and retinopathy. 21659766: Hyperglycemia and mechanical stress deriving from glomerular hypertension are the key factors underlying pathogenesis of DN. 2401396: This supports our hypothesis that hypertension is very unlikely to be the cause of diabetic nephropathy. 27520943: DN caused by hypertension and unmitigated inflammation in diabetics, renders the kidneys unable to perform normally, and leads to renal fibrosis and organ failure. 3117203: Arterial pressure is raised early in the subset of insulin dependent diabetics at risk of later development of progressive renal failure, suggesting that liability to arterial hypertension may play a part in the aetiology of diabetic kidney disease. 36181985: A total of 208 plants used for kidney-related problems by 10 Mayan groups were found, representing 143 native species, where only 42 have reported pharmacological activity against kidney damage, mainly approached by in vitro and in vivo models of chemical- or drug-induced nephrotoxicity, diabetes nephropathy, and renal injury produced by hypertension. 7626982: ERF/NO is likely to promote the dilation of glomerular arterioles, which results in the development of hyperfiltration and intraglomerular hypertension, causing diabetic nephropathy progression. 10578411: The patient's history of diabetes mellitus, hypertension and hypercholesterolaemia, and the finding of murmurs over peripheral arteries at physical examination led to a presumptive diagnosis of cerebellar ischaemia in the context of generalized atherosclerosis. 10681640: A clinical syndrome combining hypertension and hypokalemic alkalosis led to the diagnosis of primary hyperaldosteronism, caused by a right-sided, 2 cm large, apparently benign aldosterone-producing adenoma. 10735332: In view of the coexisting diagnoses of critical aortic stenosis, labile hypertension, and renal failure, ECT represented a substantially increased risk in this patient because of severe arterial hypertension and tachycardia. 1124783: A case report of a 51-year-old male hospitalized with hypertension and hypokalemia is presented with reports of laboratory findings which lead to the diagnosis of pseudoaldosteronism. 1192621: On the other hand, the investigation of a case of hypertension whose genesis was previously unclear can lead to the diagnosis of a hitherto unrecognized renal disease. 12088941: The initial hypertension in the supine position followed by severe hypotension after hydralazine administration, ultimately responsive to vasopressin, led to a diagnosis of Shy-Drager syndrome. 14978420: Persistence of low potassium levels and hypertension led to the diagnosis of primary hyperaldosteronism related to an adrenal cortical tumor. 15458452: Patients' symptoms, a family history of PKD, and discovery of PKD during evaluation for hypertension or hematuria were the most frequent factors that led to the diagnosis. 15735772: Arterial hypertension was the principal manifestation who lead to the diagnosis, which was confirmed through the conventional angiography. 17609400: Three of the five patients had a stroke before the diagnosis of TSH-oma, probably due to hypertension, or smoking and contraceptive treatment. 185706: In fact, it is above all the hypertension which should lead to diagnosis. 19078445: Additional clinical features, including skin pigmentation, mild hypertension, and hyponatremia, as well as further laboratory testing led to a diagnosis of autoimmune Addison's disease. 20093878: Continued episodes of dizziness and later-appearing bouts of severe headache, palpitations, diaphoresis, severe hypertension, and marked tachycardia led to diagnosis and management of MEN type 2a complicating pregnancy. 2063853: We conclude that there has not been a decrease in the incidence of hypertension as a causative diagnosis for patients entering ESRD programs and that this may be a reflection that treatment of hypertension does not prevent the development of ESRD in some patients. Hypertension as a causative diagnosis was a constant proportion of the increase. Hypertension as a causative diagnosis of patients entering end-stage renal disease programs in the United States from 1980 to 1986. To determine whether the incidence of hypertension as a causative diagnosis of end-stage renal disease (ESRD) is also decreasing, we examined the records of the Health Care Financing Administration (HCFA) from 1980 to 1986 regarding the causative diagnoses of patients entering ESRD programs. 21315290: Clinical case presentation of a 47-year-old woman referred to the cardiology unit with the diagnosis of aortic aneurysm with regurgitation secondary to hypertension was found to have MFS. 2148673: Severe systemic hypertension was the main symptom leading to a diagnosis of TRAS. 21962616: Hypokalemic hypertension is a common condition leading to the diagnosis of secondary hypertension. 22231770: A diagnosis of congenital adrenal hyperplasia (11beta-hydroxylase deficiency) was made due to hypertension with virilized genitalia. This case is presented for its rarity where hypertension can cause complication of cardiac failure, if diagnosis is delayed despite early features of pseudoprecocious puberty. 22923005: The presence of a heart murmur and hypertension had led to diagnosis and surgical repair of an atrial septal defect at age 5 and of aortic coarctation at age 12. 2295097: The presenting features of convulsions, confusion, agitation with hypertension and proteinuria led to a diagnosis of eclampsia for which a caesarean section was performed. 23263535: BACKGROUND: Clinic-based blood pressure (CBP) has been the default approach for the diagnosis of hypertension, but patients may be misclassified because of masked hypertension (false negative) or 'white coat' hypertension (false positive). 26303089: The diagnosis is confirmed by genetic testing, which allows in many cases targeted treatment to prevent severe cardiovascular consequences of high blood pressure or aldosterone excess. 26975032: OBJECTIVES: To examine the prevalence, diagnosis, treatment, and control of hypertension and to assess the CVD mortality attributable to hypertension in China. Uncontrolled hypertension was associated with relative risks for CVD mortality of 4.1 (95% CI, 3.7-4.6), 2.6 (95% CI, 2.4-2.9) and 1.9 (95% CI, 1.8-2.0) at ages 35 to 59, 60 to 69, and 70 to 79 years, respectively, and accounted for about one-third of deaths due to CVD (approximately 750 000) at 35 to 79 years of age in 2010. IMPORTANCE: Hypertension is a leading cause of premature death in China, but limited evidence is available on the prevalence and management of hypertension and its effect on mortality from cardiovascular disease (CVD). 27381309: Massive hypertension, orthopnea, edema and blurred vision finally led to the diagnosis of an end stage renal disease. 27453714: Hypokalemic Hypertension Leading to a Diagnosis of Autosomal Dominant Polycystic Kidney Disease. 27549377: RESULTS: This narrative review focused its attention on the diagnosis, the pathophysiology, the clinical consequences of arterial hypertension, and on the factors that must be considered for a better blood pressure control. 29157938: With the diagnosis of adrenal cyst causing uncontrolled high blood pressure, a right laparoscopic adrenalectomy was performed. 29709926: Although the plasma aldosterone concentration and plasma renin activity were within the normal ranges, percutaneous balloon dilatation of the stenotic lesion resolved his hypertension, leading to a diagnosis of renovascular hypertension caused by segmental renal ischemia due to extra-renal artery stenosis. 30147302: Purpose: Hypertension is an increasing threat to global public health, a leading cause of premature death, and an important modifiable risk factor for cardiovascular and cerebrovascular disease. Results: Overall, most patients reported hypertension awareness prior to diagnosis and were conscious about consequences of hypertension. 3058194: Diagnosis was reached by angiography performed because of hypertension, with or without impaired renal function. 30673043: Diagnosis and management of systemic hypertension due to renovascular and aortic stenosis in patients with Williams-Beuren syndrome. 30723799: Conclusion: The integrated hypertension care intervention at private clinics is feasible, and leads to improved diagnosis and treatment in low-income country urban setting. 30793467: The VAMPIRE(r) algorithm proved useful for an objective diagnosis of retinal vasculature changes secondary to systemic hypertension in cats, and could be an additional diagnostic test for feline systemic hypertension. 31560040: These findings, in addition to hypertension, resulted in a diagnosis of metabolic syndrome. 31564065: This review will summarize current data on the diagnosis, epidemiology, pathophysiology, and clinical consequences of hypertension and volume overload in HD patients. 3816893: Preoperatively most patients complained of urinary tract infection with or without fever, but sometimes investigation for hypertension or urolithiasis also led to the diagnosis. 3977497: A seven-year history of intermittent severe headaches, diaphoresis, and anxiety together with persistent severe hypertension led to the diagnosis of pheochromocytoma. 4053131: Our results support an aggressive approach to the diagnosis and surgical treatment of renal artery fibromuscular dysplasia causing hypertension. 8893935: Phaeochromocytoma as a catecholamine-secreting tumour causing severe hypertension is exceedingly rare in children. We highlight the problems encountered in making the diagnosis in an 11-year-old Chinese girl who presented with sustained hypertension, heart failure and transient renal impairment with two normal 24-hour urinary vanillyl mandelic acid (VMA) results before a third produced the diagnosis. 9020017: RESULTS/CONCLUSIONS: The arterial hypertension that had led to the diagnosis of this neoplasm remitted after surgery and can be considered to be a paraneoplastic manifestation. 10993857: BACKGROUND: In arterial hypertension, left ventricular hypertrophy (LVH) includes myocyte hypertrophy and fibrosis, which leads to LV diastolic dysfunction and, finally, heart failure. 11447089: CONCLUSIONS: Systemic HTN induces LV hypertrophy, myocardial fibrosis, and isolated diastolic dysfunction in the absence of local or systemic activation of Ang II or ET. 15854105: PURPOSE: To provide advanced practice nurses with a greater understanding of the pathophysiology, diagnostics, and management of diastolic dysfunction resulting from hypertension. 15956824: PURPOSE OF REVIEW: Hypertension leads to left ventricular hypertrophy, diastolic dysfunction, and eventually clinical heart failure (hypertensive heart disease). 16053992: BACKGROUND: Left ventricular (LV) hypertrophy and diastolic dysfunction, which are common cardiac consequences of hypertension, are modified by insulin resistance. 16910416: It is now clear that hypertension, coronary artery disease and other diseases and conditions commonly produce diastolic dysfunction in the absence of significant systolic dysfunction. 17659790: In conclusion, this study provides a new insight into the left ventricular proteome profile associated with systemic hypertension induced diastolic dysfunction in a renovascular hypertension rat model. 17919764: Although patients with type 2 diabetes demonstrate cardiac diastolic dysfunction, it is well known that cardiac diastolic dysfunction is produced by hypertension and aging. 18948553: Chronic intake of a phytochemical-enriched diet reduces cardiac fibrosis and diastolic dysfunction caused by prolonged salt-sensitive hypertension. 20118106: Hypertension, diabetes and obesity cause cardiac diastolic dysfunction (DD) which could reduce exercise capacity. 21893687: The present study also demonstrates that levosimendan, alone or in combination with valsartan, can correct diastolic dysfunction induced by salt-dependent hypertension. 23213108: METHODS AND RESULTS: LV tissue samples were procured from normal dogs (CTRL) and old dogs with hypertension-induced LV hypertrophy and diastolic dysfunction (OHT/HFpEF). 23436107: Hypertension is identified as the main precursor of left ventricular hypertrophy and therefore can lead to diastolic dysfunction and heart failure. 23747907: Similar to clinical echocardiographic observations, hypertension in rats results in left ventricular hypertrophy (LVH) and diastolic dysfunction and aldosterone receptor blockade reduces LVH in SHR. 25593786: However, earlier stages of disease may be causally related or contribute to peripheral or cerebral embolism, pre-hypertension and hypertension, and increased left ventricular afterload resulting in left ventricular hypertrophy and diastolic dysfunction. 26093301: Hypertension induced hypertrophy and diastolic dysfunction and is associated with cardiac oxidation and reduced NO production. 2879938: Diastolic dysfunction of the left ventricle is characterized by a marked decrease in ventricular compliance, often a result of hypertension and left ventricular hypertrophy; the end result is an increase in left ventricular filling pressure and pulmonary venous pressure. 30710427: Most importantly, we identify the efficacies of ATp300 inhibitors C646 and L002 in reversing hypertension-induced cardiac hypertrophy and fibrosis, and discover new anti-hypertrophic and anti-fibrotic candidates. Previously, we reported that acetyltransferase p300 (ATp300) inhibitor L002 prevents hypertension-induced cardiac hypertrophy and fibrosis in a murine model. Acetyltransferase p300 inhibitor reverses hypertension-induced cardiac fibrosis. In this short communication, we show that treatment of hypertensive mice with ATp300-specific small molecule inhibitor L002 or C646 reverses hypertension-induced left ventricular hypertrophy, cardiac fibrosis and diastolic dysfunction, without reducing elevated blood pressures. 33218338: BACKGROUND: Diastolic dysfunction can be caused by hypertension or diabetes mellitus, and it is also often found with increasing age. 35370704: Dahl salt-sensitive (DSS) rats fed with a diet containing 8% NaCl AIN-76A developed left ventricular remodeling and diastolic dysfunction caused by hypertension. Conclusion: CANA can improve myocardial hypertrophy, fibrosis, and left ventricular diastolic dysfunction induced by hypertension in DSS rats, possibly through the activation of the AMPK/SIRT1/PGC-1a pathway to regulate energy metabolism and oxidative stress. 35554763: In fact, obesity and hypertension promote remodeling and cardiac stiffening due to excess collagen deposition, fibrosis, and microvascular dysfunction, that ultimately lead to diastolic dysfunction. 36290749: A Polyphenol-Rich Extract from Muscadine Grapes Prevents Hypertension-Induced Diastolic Dysfunction and Oxidative Stress. Thus, MGES may serve as a medical food to protect the heart from hypertension-induced diastolic dysfunction caused in part by excessive reactive oxygen species production. Male Sprague Dawley rats were treated for four weeks with drinking water, angiotensin II (Ang II) to induce hypertension, MGES, or both Ang II and MGES. 37485733: The impaired relaxation indicates that, in this cohort, the long-term changes in haemodynamic load of co-existing T2D and hypertension cause diastolic dysfunction demonstrable at rest, whereas either disease on its own does not. 11821367: BACKGROUND: In Mexico, hypertension is a major cause of disability and death in the elderly, but the most effective way to promote behaviour change in old people is unknown. 12486305: Pharmacological targeting of the natruiretic peptide system is now leading to novel advances in the treatment of hypertension and of heart failure - two of the most common causes of human disability and death. 1794700: The specific differences between the 3 groups of female weavers in morbidity with temporary disability caused by hypertension can be explained by the complex action heating microclimate and extensive noise. 18787731: Obesity is associated with a wide variety of comorbidities such as type 2 diabetes, systemic hypertension, cardiovascular disease, certain cancers and sleep apnea, most of which may lead to disability or death. 19129998: Hypertension remains the leading cause of mortality and the third largest cause of disability in both developed and developing countries. 20257751: Sustained hypertension; predisposing factors and causes of disability and death. 20505676: Hypertension and smoking are major causes of disability and death, especially in the Asia-Pacific region, where there is a high prevalence of a combination of these two risk factors. 20626345: Hypertension, the leading cause of mortality and the third largest cause of disability, is poorly controlled worldwide. 21857120: Hypertension is one of the leading causes of disability or death due to stroke, heart attack and kidney failure. 22406133: Cardiovascular disease and hypertension are among the leading conditions causing disabilities in older subjects. 22558581: BACKGROUND: Increase in the prevalence of hypertension, obesity and obesity related diseases has become significant cause of disability and premature death in both developing and newly developed countries, with over bearing demand on national health budgets. 23944045: Hypertension is a common and frequently-occurring disease, as well as one of main causes for disability and death. 25174471: RESULTS: Among all the deaths due to cardiovascular diseases and DALYs, 64.0% of them were caused by high blood pressure. 25420484: Hypertension is now the foremost cause of disability and is responsible for the highest percentage of attributable death among risk factors. 27495110: Hypertension usually coexists with other chronic conditions and can cause disability in relation to activities of daily living. 28102522: The increasing prevalence of hypertension, a significant cause of disability and premature death throughout the world, is a major public health concern. 29214054: Background: Hypertension is one of the leading causes of disability and death in both developed and developing countries that need urgent strategies to implement interventions that control it. 29860726: In the contingent of people with disabilities due to hypertension, the proportion of elderly disabled is 43,4%, while the proportion of disabled people of middle and young age is less - 29,1 and 27,4%, respectively. [Disability of elderly people due to hypertensive disease in the Russian Federation.] 30629703: BACKGROUND: Hypertension is a major cause of preventable disability and death globally and affects more than one in four adults in England. 30729041: Background: Hypertension (HTN) has been identified as the leading risk factor for mortality and the third cause of disability worldwide. 30732939: Hypertension is one of the most common chronic diseases in adults and a leading cause of disability and mortality worldwide. 30785635: BACKGROUND: Hypertension, or high blood pressure, is a major cause of disability and the leading risk factor for death around the world. 3206817: [A 4-year study of work disability due to hypertension in the Northern Bohemia brown coal basin]. 3560632: Five-year follow-up of an organized population of males between 35 and 54 years of age and medication of patients with arterial hypertension (AH) demonstrated possibilities of considerably reducing the incidence of cerebral insult (by 42.9%) and myocardial infarction (by 15.5%) and the respective mortality rates (by 56.1% and 23.8%), invalidism associated with cardiovascular diseases (by 36%), temporary disability because of AH (by 38.2%). 10472616: The analysis of sick absenteeism in the branches selected in view of hazardous working conditions shows that: (1) in many branches chemical hazards in the work environment are responsible for an increased sick absenteeism due to diseases of the circulatory system, particularly among men, mental disorders and neoplasms, both among men and women, and complications of pregnancy among women; (2) physical work overload increases sick absenteeism mainly due to diseases of the musculoskeletal and peripheral nervous systems, as well as due to cardiac disease and arterial hypertension; and (3) hot microclimate contributes to sick absenteeism because of diseases of the circulatory system, including cardiac disease and arterial hypertension, particularly among men, as well as acute and chronic respiratory diseases. 10526697: In addition, we have learned much from epidemiologic studies that have helped identify risk factors for hypertension and have thus provided insight into mechanisms that are involved in the pathogenesis of this disease. 10592842: The protective effect of the extract of Uncariae ramulus et Uncus (URE) against endothelium disorder due to hypertension was investigated. 10662254: These studies suggest that several of the ocular or optic nerve head ischemic or ocular vascular disorders previously thought to be manifestations of arterial hypertension may, in fact, be due to a combination of systemic arterial hypertension and hypotension, with arterial hypertension acting as a predisposing factor and arterial hypotension actually producing the disorders. 10760631: Hypertension and coronary disease remain the leading causes of the disease, and heart failure due to myocardial infarction has increased in prevalence. 10872167: However, a wide differential diagnosis exists for the MRI appearances of CADASIL, including multiple sclerosis and small-vessel disease secondary to hypertension. 11432121: Hypertension and diabetes are the leading causes of small-artery disease, subcortical brain ischemia, and stepwise or slowing progressive decline in cognitive function. 11770402: Conjunctivitis of various causes was the main disease to use glucocorticoid, all 215 eyes had the defect of visual field caused by hypertension, damage of optic disc and retinal nerve fiber layers, just like primary open-angle glaucoma. 12405428: Despite the important role of hypertension as a cause of disease, its pathogenesis remains largely unknown. The application of genetic approaches to rare monogenic (Mendelian) forms of hypertension and hypotension has begun to delineate molecular pathways underlying human blood pressure variation, defining disease pathogenesis and identifying targets for therapeutic intervention. 12592180: CONCLUSION: In developing countries, hypertension in pregnant women is a severe condition responsible for disease and handicaps which could be avoidable at little cost through a better policy of detection and good quality multidisciplinary management. 13236368: [Present problems in treatment of hypertension and diseases secondary to hypertension]. 14650599: There was a high possibility that his accompanying disease, an alteration in hemostasis due to alcoholic liver cirrhosis and hypertension, would induce thymic cyst hemorrhage. 14978906: The etiology of the LV-RA communication was congenital and valvular diseases were acquired changes caused by sclerosis due to infected endocarditis or hypertension. 15242243: Apart from age, many modifiable factors, such as hypertension, smoking, diabetes, dyslipidemia, obesity, physical inactivity, alcohol abuse and hyperhomocysteinemia, have been recognised as playing a role in the pathogenesis of this disease. 15478018: Pharmacological studies of cardiovascular disorders, including hypertension, cardiac failure, ischemia, myocardial infarction and left ventricular hypertrophy, indicate that reduced activity of the local kallikrein-kinin system (KKS) may be instrumental in the induction of these disorders. 15673046: UNLABELLED: Hypertension is the most important cause of disease in the expectant mother and the fetus, and it unfavorably affects the perinatal morbidity and mortality. 15963942: Inhibition of the mammalian soluble epoxide hydrolase (sEH) is a promising new therapy in the treatment of disorders resulting from hypertension and vascular inflammation. 16197546: Evaluation of a strict protocol approach in managing women with severe disease due to hypertension in pregnancy: a before and after study. 16467500: An understanding of the molecular mechanisms underlying hypertension and related organ complications is a key aspect for developing new, effective, and safe antihypertensive agents able to cure the cause of the disease. 16690767: Experimental models of hypertension, such as spontaneously hypertensive rats (SHR), show alterations in cellular sodium transport that affects Na(+)-coupled cotransport processes and has been involved in the pathogenesis of this disease. 17034366: The consideration that hypertension and/or other cardiovascular diseases are late consequences of abnormal ontogeny of the cardiovascular system could explain why so many complex interactions among genes and environmental factors play such a significant role in the pathogenesis of these diseases. 17066054: Genetic testing, which is increasingly available, can facilitate timely diagnosis and treatment of these relatively uncommon disorders, such that the underlying defect can be corrected or ameliorated and the long-term consequences of poorly controlled hypertension prevented. 1715487: The purpose of this article is to review the evidence that the resistance vasculature is altered in hypertension, the role that it may play in the pathogenesis of the disease, and the effect of antihypertensive treatment on the abnormalities. 17196688: CONCLUSION: Stress perfusion CMR allows non-invasive differentiation between patients with significant CA stenosis and patients with SVD caused by hypertension and/or diabetes based on the temporal and spatial extent of perfusion deficits. 17378993: Compared with coronary disease in whites, HF in African Americans is marked by increased prevalence, earlier onset, increased risk for hospitalization and mortality, and increased prevalence of hypertension as the underlying cause of disease. 17728801: Hypertension is a disorder controlled by multiple genes and inflammation and vascular remodelling of arteries have been implicated in pathogenesis of this disease. 17851966: Hypertension and diabetes mellitus could contribute to the etiology of this disorder. 1792767: Results indicate that the functional state of the liver in vasorenal hypertension is disturbed as a result of the main renal disease and also under the effect of arterial hypertension as a destabilizing factor leading to disorders of the hemodynamics and furthering potentiation of lipid peroxidation processes in the body. 17952226: OBJECTIVES: To estimate the burden of disease attributable to high blood pressure (BP) in adults aged 30 years and older in South Africa in 2000. Estimating the burden of disease attributable to high blood pressure in South Africa in 2000. Overall, 50% of stroke, 42% of IHD, 72% of hypertensive disease and 22% of other CVD burden in adult males and females (30+ years) were attributable to high BP (systolic BP >or= 115 mmHg). 18154717: Various diseases such as arterial hypertension, diabetes and obesity result in renal diseases which are often irreversible and resistant to currently available therapies. 18342073: Doppler ultrasonography and angiography show arteriovenous fistulas that classically develop at shunts, explaining the role of traumatism and high vascular pressure in the genesis of this disease. 18387084: Although increasing evidence suggests that salt-sensitive hypertension is a disorder of the central nervous system (CNS), little is known about the critical proteins (e.g. ion channels or exchangers) that play a role in the pathogenesis of the disease. 18456100: METHODS: Worldwide burden of disease attributable to high blood pressure (> or =115 mm Hg systolic) was estimated for groups according to age (> or =30 years), sex, and World Bank region in the year 2001. About 54% of stroke and 47% of ischaemic heart disease worldwide were attributable to high blood pressure. 18502988: Vascular risk factors such as hypertension, diabetes, and smoking may be associated with the pathogenesis of the disease. 1867228: Importantly, the incidence of coronary disease has been reduced to only a small extent, suggesting that factors beyond high blood pressure are important in the genesis of atherosclerotic disease in hypertensive patients. 1889858: This paper reviews the evidence that the resistance vasculature is altered in hypertension and the role that the vasculature may play in the pathogenesis of the disease. 18922528: Aortic stiffening is the most important determinant of elevated systolic blood pressure which in turn is the main contributor to the burden of disease attributable to hypertension. 19165175: It is thought that hypertension and volume overload are major causes of this disease, but here we sought to identify additional mechanisms using a mouse model of chronic renal insufficiency. 19290795: Hypertension is the first single modifiable cause of disease burden worldwide. 19431240: In case of cardioembolic pathogenesis, it was characterized by the markedly less severe signs of the disease and in case of the disease due to isolated arterial hypertension--by the lower rate of vascular white matter abnormalities on neuroimaging. 19665687: SAHS patients experience increases in hypertension, obesity, and dyslipidemia, and the oxidative state has been related to the genesis of these disorders. 1971810: By analyzing the characteristics of pressure natriuresis in hypertensive patients and by comparing these curves to those observed in various forms of experimental hypertension of known origin, it is possible to gain insight into the etiology of this disease. 19721377: Patients with lifestyle-related diseases such as hypertension, diabetes, and hyperlipidemia are at high risk for the pathogenesis of a life-threatening atherosclerotic disease. 2009242: Unlike various other risk factors for vascular disease, hypertension retains its predictive power as age increases, but since the baseline risk is higher, the number of cases of disease attributable to hypertension is much higher in the elderly than in the young. 20445714: BACKGROUND: Obesity and arterial hypertension are a serious risk factor for insulin resistance patients leading to diabetes and other disorders. 20563545: Substantial consequences of hypertension are microangiopathy, interstitial fibrosis and left ventricular hypertrophy. Arterial hypertension often leads to diseases of kidneys, vessels and brain. 20924360: Mitral stenosis was reported as the most frequent cause of PH several decades ago, but PH with left-sided heart disease is now usually caused by systemic hypertension and ischemic heart disease. 21137169: [Serum lipoprotein profile in newly recognized arterial hypertension. The role of atherogenic lipoproteins in the pathogenesis of disease]. 21180035: Hypertension is a major public health problem and leading cause for diseases involving cardiovascular & renal system. 21435165: Critical ischemic disease is often caused by arteriosclerosis due to hypertension or diabetes. 2190362: The multifocality of the hematomas and lack of underlying disease suggest that the hemorrhages resulted from cocaine-induced acute hypertension or arterial spasm, possibly potentiated by heavy ethanol consumption. 2245518: The availability of genetically homologous animal models for hypertension has greatly promoted studies on the etiology and pathogenesis of high blood pressure disease. 2265421: Evidence has been provided that adequate physical activity prevents diseases caused by hypokinesia (hyperlipoproteinaemia, ischaemic heart disease, myocardial infarction, obesity and to a certain extent also hypertension) and that it retards the ageing process, in particular osteoporosis. 23173587: Several systems are amplified by the concomitant obesity and hypertension, thus generating a perpetual vicious circle which further contribute to the pathogenesis/progression of microvascular disease. 24465859: Improved detection is needed to reduce the burden of disease attributable to hypertension. 24522941: Renovascular disease is a cause of hypertension in 10 % to 15 % of prepubertal children. Interventions to address hypertension and causes of renovascular disease continue to advance. 24835972: Hyperuricemia is a biochemical hallmark of gout, renal urate lithiasis, and inherited purine disorders, and may be a result of enormous ATP breakdown or purine release as a result of cardiovascular disease, hypertension, kidney disease, eclampsia, obesity, metabolic syndrome, psoriasis, tumor lysis syndrome, or intense physical training. 25064267: Collectively, these results indicate that Rio Mamore virus strain HTN-007 in adult Syrian golden hamsters can cause a nonlethal disease that is pathologically similar to hantavirus pulmonary syndrome. 25160207: An accurate measurement of the blood pressure, in fact, is a prerequisite for appropriate management of hypertension, a condition causing many serious diseases. 25466736: DISEASES CAUSED by hypertension may cost the NHS more than L2 billion a year, according to figures from Public Health England (PHE). 25621148: Preexisting hepatosplenic disease due to Schistosoma infection is likely important because of portopulmonary hypertension and/or because it allows egg embolization to the lung by portocaval shunts. 25880433: BACKGROUND: The people of low and middle income countries bear about 80% of the global burden of diseases that are attributable to high blood pressure. 25932893: Hypertension is a chronic condition that can lead to heart disease, stroke, and other diseases that can result in premature death. 26031157: Allforms of arterial hypertension develop by common algorithm independently from causes of disorders of blood flow, microcirculation in distal section of arteries. 26088410: Furthermore, developing evidence-based guidelines is not enough to affect positively the burden of disease caused by hypertension. 26185735: KKidney disease could result from hypertension and ischemia/hypoxia. 26304517: The appropriate initial treatment of a middle-aged individual with symptomatic paroxysms of atrial fibrillation, diabetes, and hypertension should focus on eliminating the underlying causes of disease to safely reduce morbidity and prolong life. 2638500: The knowledge about hypertension most related was causes of disease and its complications. 26893930: The 'hypertensive emergencies' have been grouped together in three subsets: (1) diseases that result from acute hypertension that is caused by faulty regulation of the peripheral circulation (acute primary hypertension), (2) diseases that produce hypertension (acute secondary hypertension) and 3) diseases that have hypertension as an effect of the acute stress caused by the principle disease (acute associated hypertension). 27075454: The underlying cerebral structural change associated with cognitive decline may be a consequence of the cerebral small-vessel disease induced by high blood pressure and may be detected on magnetic resonance imaging as white matter hyperintensities, cerebral microbleeds, lacunar infarcts or enlarged perivascular spaces. 27085816: RESULTS: The risks factors for CMBs are complicated, including those that cause large-vessel disease, such as hypertension and old age, and those that cause small-vessel disease, such as amyloid deposits, endothelial lesions, and atrial fibrillation. 27492552: The objective was to estimate the disease burden attributable to hypertensive disorders of pregnancy in two referral hospitals in Uganda. 27498679: Hypertension leads to small vessel disease resulting in progressive damage to the white matter, cortex, and hippocampus. A few studies have been done with the two-clip, two-vessel occlusion renal model for induction of hypertension. 27895434: Hypertension, an emerging problem of recent era, and many pathophysiological factors are participating to produce the disease. 28214547: Overall, our study suggests that uncontrolled hypertension leading to CSVD might represent a risk factor for TLE. 28265034: The main vascular risk factor for SVD is brain hypoperfusion from cerebral blood vessel narrowing due to chronic hypertension. 28273684: Therefore, study of the early stages of development of hypertension is of particular interest, because it helps in understanding the aetiology of the disease. 28498854: Hypertension is a leading cause of global disease, mortality, and disability. Experiments driven by these findings and using angiotensin-II induced hypertension in mice showed altered kidney mRNA expression of six genes, suggesting their potential role in hypertension. 28584618: BACKGROUND: Hypertension (HTN) is a major cause of noncommunicable diseases. 28993004: Yet, despite the increase in literature on CAA-related cognitive and psychiatric symptoms, the specific characteristics of symptoms in CAA are difficult to assess because of the substantial prevalence of comorbidities such as small vessel disease due to high blood pressure, Lewy body disease and, of course, AD, all of which act as important confounding factors. 29035901: The American College of Obstetricians and Gynecologists Task Force on Hypertension in Pregnancy has refined preeclampsia diagnostic criteria accordingly, and as the disorder's pathogenesis has been more clearly defined, new targets for screening, diagnosis, prevention, and treatment have emerged. 29388934: The most frequent variant of neurogenic dysfunction of the bladder in the children is the hyper-reflexive one; it is this variant in which the most pronounced disorders of urodynamics due to intravesical hypertension and detrusor hypoxia are observed. 29483399: In this review, we identify the pathophysiological changes in CSVD that are caused by hypertension and further explore the relationship between CSVD and cognitive impairment. Hypertension-Induced Cerebral Small Vessel Disease Leading to Cognitive Impairment. 29760448: In this Review, we discuss the complex interplay between the brain, the gut, the microbiota and the kidney in CKD and hypertension and explain our brain-gut-kidney axis hypothesis for the pathogenesis of these diseases. 2977586: Capillary hypertension is suggested to be the underlying cause of microvascular disease affecting the kidney, the retina, and other organs and tissues in diabetic patients and animals. 29906243: Measures of the adipokine chemerin are elevated in multiple cardiovascular diseases, including hypertension, but little mechanistic work has been done to implicate chemerin as being causative in such diseases. 29973407: Hypertension is suggested as the cause of sporadic SVD, but a recent alternative hypothesis invokes dysfunction of the blood-brain barrier as the primary cause. 30188091: Elaboration of new methods of correction of microcirculatory disorder in the brain caused by persistent high blood pressure is a topical task both for medicine and for biology. 30414594: Since taking antihypertensive medication (AHM) could prevent aging-related diseases caused by hypertension, we hypothesized that using AHM could also reduce the AA. 30763152: Disease in the eye resulting from hypertension is the most easily identifiable form of TOD and can often be the reason the cat is presented to the veterinarian. 30842611: Hypertension requires strict treatment because it causes diseases that can lead to death. 30987567: In addition, HTN can induce disorders of brain microcirculation resulting in cognitive dysfunction. 31043901: These results suggest that a large BP screening campaign based on convenience sampling could be a useful and reasonably inexpensive tool to help raise awareness in the general population and thereby help address the burden of disease caused by hypertension. 31066871: Observation: The major risk factors for the disease are increased hemodynamic forces, typically owing to poorly controlled hypertension, and heritable genetic variants. 31571663: When compared to the BPN/3J strain, the hypertensive BPH/2J mice showed a complete loss of outer layers of the neural retina at 21 weeks of age, which was indicative of a severe vision-threatening disease potentially caused by hypertension. 31655775: However, the mechanisms underlying the physiopathology of hypertensive occlusive vascular renal disease are complex and distinction between the different causes of RVD should be made. 32016791: RECENT FINDINGS: HHD is a condition that arises as a result of elevated blood pressure and constitutes a key underlying mechanism for cardiovascular morbidity and mortality. 32054378: Here we discuss new reports pointing to participation of Sigma1 receptor in muscle specific processes like contraction, EC-coupling, calcium currents and in diseases like left ventricular hypertrophy, transverse aortic stenosis and hypertension-induced heart dysfunction. 32346448: The aim of the present study was to compare the effect of hesperidin (HES) and crocin (CRO) alone and in combination, on blood pressure in a rat model of high-fat diet (HFD)-induced hypertension, using invasive carotid artery measurements. Hypertension is the most important cause of such conditions. 32431784: Also, this study shows that diabetes and hypertension have a certain role in the pathogenesis of multivessel diseases, therefore, preventive measures for diabetes and hypertension can be effective strategies in reducing the burden of premature STEMI. 33116810: Background: Hypertension is one of the leading causes of disease in the world. 33595132: This disorder can be caused by high blood pressure, heart disease, vascular problems, psychological and hormonal factors such as problems with testosterone and prolactin levels. 34070965: Chronic kidney disease (CKD), a damaged condition of the kidneys, is a global public health problem that can be caused by diabetes, hypertension, and other disorders. 34881086: Therefore, it is necessary to search for new antihypertensive means to reduce the burden of disease caused by hypertension. 35242281: As the too early exposure of premature infants to high arterial oxygen pressure leads to characteristic diseases, we studied the adaptation of the oxygen sensing system and its targets, the hypoxia-inducible factor- (HIF-) regulated genes (HRGs) in the developing lung. 35256446: INTRODUCTION: Obstructive sleep apnoea (OSA) is a highly prevalent disease that causing systemic hypertension. 35285667: Hypertensive disorders of pregnancy are among the most serious conditions that pregnancy care providers face; however, little attention has been paid to the concept of tailoring clinical care to reduce associated adverse maternal and perinatal outcomes based on the underlying disease pathogenesis. 35326161: Hypertension remains the leading cause of disease burden worldwide. Oxidative Stress-Induced Hypertension of Developmental Origins: Preventive Aspects of Antioxidant Therapy. 35406662: High blood pressure is one of the major public health problems that causes severe disorders in several tissues including the human kidney. 35474167: Some diseases are caused by high blood pressure, including impairment of heart and kidney function, cerebral hemorrhage and myocardial infarction. 35844869: Identified gaps, perceived barriers, and facilitators provide a useful starting point for strengthening efforts to address the significant burden of disease attributable to diabetes and hypertension. 3593034: This diagnosis should be considered much more frequently because it is possible to prevent the encephalopathy avoiding systemic hypertension that is probably intimately linked with the genesis of the disease. 35936394: As a reliable indicator of human physiological health, blood pressure (BP) has been utilized in more and more cases to predict and diagnose potential diseases and the dysfunction caused by hypertension. 36026628: OBJECTIVE: The burden of disease attributable to hypertension in the Philippines has continuously increased over the last three (3) decades. 367013: In 50 patients with transient disorders of cerebral circulation due to hypertensive disease (27 cases), and combinations of hypertensive disease with atherosclerosis (23 cases) the authors by means of diluting Ewans blue stain (T-1824) studied the indices of general hemodynamics compared to that of REG data . 36754555: INTRODUCTION: Hypertension (HTN) is the leading cause of disease and death on a global scale. 36819391: Congestive heart failure (CHF) is a complex, heterogeneous medically ill condition that can occur due to diverse primary (cardiomyopathies, coronary artery diseases, and hypertension) and secondary causes (high salt intake and noncompliance toward treatment) and leads to significant morbidity and mortality. 37514810: High blood pressure is a critical health threat that can lead to diseases including heart attacks, strokes, kidney disease, and vision loss. 3794335: We conclude that there is a significant difference in the ANG II binding capacity during the development of hypertension in the SHR as compared with the WKY rat and therefore it may play a role in the pathogenesis of this disorder. 3866842: Disease of arterioles and small arteries affects predominantly the kidney and brain, and is due directly to the hypertension itself. 3934702: The goals of NHBPEP and the 1990 prevention objectives for the nation center around the same basic theme: high blood pressure is a serious condition leading to major diseases and premature death. There is good evidence of progress in preventing disease and premature death from hypertension, in bringing hypertension under long term control, and in giving Americans a better understanding of the consequences of uncontrolled high blood pressure. 3946211: Although the physiologic mechanism for the observed predictive influence of postural BP on the development of hypertension are unknown, these findings may have important influences on identifying subjects at risk and also providing insight into disease pathogenesis. 4617851: [Role of hypertension in the genesis of bone pain in osteomyelitis and other diseases]. 599801: Comparatively new hemodynamic aspects of hypertensive disease connected with the contribution of the heart itself to the pathogenesis of the disease are discussed. 6096059: It is suggested that small deep infarcts visible on CT may be caused by cardiac emboli and artery-to-artery emboli from carotid lesions, besides small vessel disease due to hypertension. 6715764: Systemic hypertension, which may induce various diseases in the elderly, had a striking effect on atrophic changes of brain matter in elderly subjects. 6945938: Establishment of various models for hypertensive diseases such as spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) clarified the importance of genetic factors in the pathogenesis of these diseases and further accelerated studies on their genetic mechanisms. 7257862: Screening of relatives belonging to families with a high frequency of hypertension seems to have a potential practical value and may furthermore provide information about the etiology of the disease. 7392386: The level of catecholamines and serotonin in the blood is considerably increased in the initial stages of hypertensive disease, which points to their participation in the pathogenesis of this disease. 7432667: These support the view that changes in these parameters is not dependent on the concomitance of other diseases, but due to hypertension itself. 7468768: This study provides evidence that the combination of diabetes mellitus and hypertension produces significantly greater myocardial lesions than either disease alone. 8488853: Importantly, the incidence of coronary artery disease has been reduced to only a small extent, suggesting that factors beyond high blood pressure are important in the genesis of atherosclerotic disease in hypertensive patients. 8744539: The application of genetic strategies to studies of the pathogenesis of hypertension has proceeded on multiple fronts in the past year and has provided new insight into disease pathogenesis. 8817009: On the basis of increased plasma levels in hypertension and heart failure, adrenomedullin is suspected to contribute to the pathogenesis of these diseases. 8896708: Finally, the characteristics of small arteries in hypertension are reviewed, with special attention to the structural abnormalities and their possible participation in the pathogenesis of the disease. 8905981: Severe small artery diseases, which cannot be attributable only to hypertension, were present. 9045385: The predominance of nephrotic syndrome and frequent recurrences or hypertension, long-term course in different causes of the disease suggests several pathogenetic variants of nephrotic syndrome. 9404973: Patients with cirrhotic disorders caused by portalvenous hypertension show extensive collaterals and increased intravascular blood volume. 9928756: We discuss the possible pathophysiological causes of a rise in PRA in this clinical setting and suggest that underlying arteriolar disease due to prolonged hypertension may be the cause of increased and non-suppressible PRA in primary aldosteronism. 10805898: It was considered that the media became friable in this patient because of the presence of Takayasu's arteritis and that hypertension that persisted for a long time caused the independent development of aortic dissections in the ascending and abdominal aortae. 12384138: Among these abnormalities, the conjunction of dilatation of the aorta with hypertension may lead to aortic dissection. 16053789: Hypertension was the most important cause of AD. 18706125: Rapid rise in blood pressure and history of hypertension are the most common causes of aortic dissection in athletes. 1899675: Hypertension appears to be a prerequisite in the pathogenesis of aortic dissection, and control of ventricular contraction velocity may be prophylactic. 20082464: Superimposed risk factors, such as hypertension, may weaken the aortic wall and eventually lead to aortic dissection. 23998655: Pre-eclampsia superimposed on chronic hypertension was solely possible cause of ruptured AAD in this case. 25785767: OBJECTIVES: Physical exercise accompanied by arterial hypertension is known to trigger acute aortic dissections. 26097568: Acute aortic dissection is a life-threatening condition mainly caused by hypertension, atherosclerotic disease and other degenerative diseases of the connective tissue of the aortic wall. 30558735: Type A aortic dissection caused by uncontrolled hypertension secondary to pheochromocytoma is a rare entity. 35800890: Single Cell RNA Sequencing Reveals the Pathogenesis of Aortic Dissection Caused by Hypertension and Marfan Syndrome. Aortic dissection (AD) is mainly caused by hypertension and Marfan syndrome. 36343070: Hypertension is one of the high-risk factors causing AD. 37829691: Aortic dissection due to unstable hypertension secondary to pheochromocytoma is rare and complicates the procedure. 8650586: Inadequate treatment of giant-cell arteritis and underlying hypertension (treated or untreated) are potential factors leading to aortic dissection in these patients. 11920902: Myocardial infarction and hydrops are considered to be consequences of hypertension in the recipient. 12151377: We speculate that the ventricular separation has evolved in response to the need of maintaining high oxygen delivery while protecting the pulmonary circulation from oedema as result of high vascular pressures. 12344838: Hypertension in its most severe form produces convulsions, proteinuria, and edema and may lead to fetal and maternal death. 12784673: Reversible posterior leukoencepalopaty syndrome is caused by vasogenic edema of the subcortical association fibers and by cytotoxic edema of the cortical gray matter, due to hypertension, renal dysfunction, drugs and so on. 12987351: [Cerebromeningeal edema caused by arterial hypertension]. 1360979: The most common chief complaints on admission were dyspnea, headache, palpitation, and edema which were due to hypertension and congestive heart failure. The majority of the patients required immediate medical treatment to control congestive heart failure due to hypertension at initial presentation. 16341373: SRL does not cause glucose intolerance, hypertension or renal failure, but it may cause dyslipidemia, hepatic artery thrombosis, thrombocytopenia, anemia, leukopenia, oral mucosa ulcers, edema, arthralgias and wound complications. 16485542: The findings of normal DWI and high ADC values were compatible with vasogenic edema due to hypertension. 16768758: Microscopy showed white matter pallor with parenchymal cysts, enlarged perivascular spaces and focal acute hemorrhages consistent with edema secondary to acute hypertension. 18676082: The normal DWI findings and high ADC values were consistent with vasogenic edema due to severe hypertension. 19462818: Since these alterations suggested the presence of vasogenic edema induced by hypertension, we diagnosed him as having reversible posterior leukoencephalopathy syndrome (RPLS) induced by hypertension. Therefore, we considered that hypertension was induced by oral CBZ therapy. 21577345: Normal diffusion-weighted imaging findings and high apparent diffusion coefficient values suggested that the main pathomechanism was vasogenic edema owing to severe hypertension. 22234407: CONCLUSION: It is imperative to recognize such cases where hypertension causes edema within the posterior fossa resulting in secondary hydrocephalus. 22824983: Lastly, acute hypertension during pregnancy caused greater edema formation in both brain cortices that was not attributed to changes in sympathetic innervation. In the present study, we examined the effect of pregnancy on the effectiveness of cerebral blood flow autoregulation using laser Doppler flowmetry and edema formation by wet:dry weight in acute hypertension induced by phenylephrine infusion in the anterior and posterior cerebrum from nonpregnant (n=8) and late-pregnant (n=6) Sprague-Dawley rats. 2386223: Superoxide dismutase reduces permeability and edema induced by hypertension in rats. Treatment 30 min after hypertension with SOD or polyethylene glycol-conjugated SOD reduced edema caused by hypertension. 23960851: High arterial blood pressure and hypoxic vasodilatation increase the hydrostatic pressure in the microcirculation, which increases water flux from vessel to tissue and induce edema. 26617168: Posterior reversible encephalopathy syndrome (PRES) is a complex clinical condition with vasogenic subcortical oedema caused by hypertension. 27552021: These images are interpreted as vasogenic edema, which is caused by arterial hypertension or eclampsia, neurotoxicity related to immunosuppressive agents or chemotherapy, among other causes. 28044115: Repeat kidney biopsy showed diffuse endocapillary and extracapillary proliferative and membranous lupus nephritis (ISN-RPS class IV-G+V) and endothelial swelling secondary to severe hypertension but no evidence of TMA. 29531864: The pathophysiology involves subcortical vasogenic edema secondary to hypertension and endothelial damage. 3416726: This protective action on the vascular wall is of importance, since one of the direct vascular consequences of arterial hypertension is a fragilisation of vessel walls, tissue oedema and even vascular rupture. 34445693: This is important when the endothelium experiences changes in external stresses caused by high blood pressure, leading to edema, or by immune or cancer cells in inflammation or metastasis. 38061857: This seemed to confirm the diagnosis of the disc oedema being caused by hypertension and a highly asymmetrical presentation of hypertensive retinopathy. 7417061: In hypertension, transmural pressure increases in the capillaries, leading to edema and, in premature infants, eventual rupture of vessels and IVH. 7660303: The presence of the cotton wool spots in the arcades is highly suggestive of hypertension as the etiology of the disk edema. 8443976: All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth. 852471: the fact, that ICP does not play any role in acute hypertension, indicates that an abrupt elevation of filtration pressure within the capillaries must be the decisive factor leading to edema. 8887253: Hypertension also contributes to an increase in endothelial cell permeability leading to intimal edema. 12022207: Hypertension is a major public health problem both in the developing and developed countries of the world and if untreated, can lead to various fatal complications like cerebral stroke, encephalopathy, ischaemic heart disease (IHD), renal failure and sudden cardiac death, etc. 12816279: Hypertension-induced encephalopathy is a recognized pathological process commonly focused in the parietal and occipital lobes of the cerebral hemispheres. In the appropriate clinical setting, hypertension as the inciting cause of cerebellar encephalopathy should be considered. 13290696: [A case of pseudotumorous encephalopathy caused by arterial hypertension]. 13546061: [Unusual aspects of encephalopathy caused by arterial hypertension]. 16376285: Hypertension-induced cerebellar encephalopathy and hydrocephalus in a male. 16876020: Hypertension-induced cerebellar encephalopathy. 18097471: Together, these results suggest that deltaPKC plays a role in the development of hypertension-induced encephalopathy and may be a therapeutic target for the prevention of BBB disruption. 18097480: In this issue of the JCI, Mochly-Rosen and colleagues demonstrate a novel molecular strategy for preserving the BBB in a model of hypertension-induced encephalopathy (see the related article beginning on page 173). 21119009: We found that activation of protein kinase Cdelta (PKCdelta) induced aberrant mitochondrial fragmentation and impaired mitochondrial function in cultured SH-SY5Y neuronal cells and in this rat model of hypertension-induced encephalopathy. 23453196: Arterial hypertension and preeclampsia are the main causes of posterior reversible encephalopathy. 31360275: Severe hypertension is a major cause, among a long list of recognized causative factors of posterior reversible encephalopathy (PRES). 33622758: Posterior reversible encephalopathy is suspected to occur due to elevated blood pressure and overproduction of inflammatory markers, both of which have been reported in the setting of COVID-19 infection. 35166476: The paper describes a case of dyscirculatory encephalopathy with multiple small focal cerebral ischemic changes caused by both hypertension and athero-stenosis of several arteries in both the brain carotid systems and the vertebrobasilar system, namely tandem stenoses. 36949864: Posterior reversible encephalopathy syndrome or reversible cerebral vasoconstriction syndrome is a rare encephalopathy, possibly caused by excessive hypertension, usually encountered in the obstetric or cerebrovascular department. 6506976: Clinical and polygraphical (EEG, EOG, EMG, ECG, REG) studies of nocturnal sleep and of the hemodynamics were carried out in 60 patients with dyscirculatory encephalopathy induced by hypertension and atherosclerosis. 7640750: [Encephalopathy induced by arterial hypertension: clinical, radiological and therapeutical aspects]. 8691497: Lacunar strokes occur more in blacks reflecting increased incidence of hypertension and are leading causes of multi-infarct encephalopathy and dementia. 10070914: Interdialytic weight gain and hypertension as a cause of ESRD were independent predictors of predialysis systolic blood pressure. 10095172: METHODS: We investigated 256 chronic hemodialysis patients, including 123 patients with a history of hypertension as a cause of ESRD. 10207266: Data from the First Report on Dialysis and Transplant in Sicily showed that hypertension is the cause of end-stage renal disease in 8% of dialysis patients and that the incidence of hypertension, as a cause of end-stage renal disease, increased with age. 10547649: During the last few years there has been a renewal of interest in blood-pressure-induced kidney damage due to a progressive increase in the incidence and prevalence of hypertension and vascular diseases as a cause of end-stage renal disease (ESRD). 10578218: Hypertension is an important cause of end-stage renal disease (ESRD) in the USA and in Sub-Saharan Africa. Both in the USA and South Africa hypertension was found to be the most common cause of ESRD, but it is not clear whether this is related to the higher incidence and severity of hypertension in black people. 10619598: Diabetes and hypertension are the leading causes of end-stage renal disease in the Western world. 10620213: In multivariate analysis, the following factors were independently and significantly predictive of DWGF: white recipient, age at transplantation, ESRD caused by hypertension or diabetes mellitus, length of pretransplant dialysis, delayed graft function, acute rejection, panel reactive antibody> 30%, African American donor race, age> 45 years, and donor death caused by cerebrovascular disease. 10720601: The incidence of end-stage renal disease attributable to hypertension is 5-fold greater in African Americans than in whites. 11071968: BACKGROUND: Multiple studies suggest that hypertension-induced end-stage renal disease (ESRD) is heritable. 11168948: BACKGROUND: Renal damage from hypertension is the second most common cause of end-stage renal failure in the United States. 11206613: Bilateral simultaneous nephrectomy is a rare procedure usually performed for end-stage renal disease, most often because of persistent hypertension after renal transplantation. 11370956: Diabetes and hypertension are the most common causes of end-stage renal disease in the United States. 11386927: CONTEXT: Incidence of end-stage renal disease due to hypertension has increased in recent decades, but the optimal strategy for treatment of hypertension to prevent renal failure is unknown, especially among African Americans. 11773939: Approximately 40% of stroke cases, 39% of myocardial infarction cases and 28% of end stage renal diseases are attributable to hypertension. 11799511: CASE REPORT: A 43-year-old man with end-stage renal disease secondary to hypertension was scheduled for primary placement of a left upper extremity arteriovenous fistula. 11816509: The most common diseases responsible for End Stage Renal Disease were: hypertension (22%), chronic glomerulonephritis (19%) and diabetic nephropathy (15%). 12152908: Diabetes mellitus and hypertension, the main causes of end-stage renal disease in the United States, are more prevalent in African Americans. 12152917: Although African Americans make up 12.6% of the US population, the incidence of diabetes-related ESRD is four times higher than for whites, and the prevalence of ESRD due to hypertension is twice that of white patients. 12164884: BACKGROUND: Arterial hypertension is an important cause of end-stage renal failure. 12435255: CONTEXT: Hypertension is a leading cause of end-stage renal disease (ESRD) in the United States, with no known treatment to prevent progressive declines leading to ESRD. 12496670: RECENT FINDINGS: The most recent United States Renal Data Systems data show hypertension as the primary cause of end-stage renal disease in African-Americans until 1997, diabetes now being the most prevalent etiology. 12501871: BACKGROUND: Diabetes mellitus and hypertension are leading causes of end stage renal disease in the United States. 12506150: Similar 12-mo mortality risks were noted in the groups with diabetes mellitus or hypertension as the causes of ESRD and among patients > or = 65 yr. 12577136: Diabetes and hypertension lead to increased end-stage renal disease, requiring more vascular access procedures. 12819306: The increase in ESRD incidence in the United States is primarily attributable to diabetes and to hypertension. Information on the association of hypertension with renal dysfunction and ESRD in the United States may be useful in predicting future trends in the incidence of ESRD due to hypertension in Singapore. 12864889: Chronic glomerulonephritis and hypertension are principal causes of CRF in tropical Africa and East Africa, together with diabetes mellitus and obstructive uropathy. In a six-year study of 3632 patients with ESRD, based on SADTR statistics, hypertension was reported to be the cause of ESRD in 4.3% of whites, 34.6% of blacks, 20.9% mixed race group and 13.8% of Indians. 12965065: Diabetes mellitus and hypertension were the most common causes of end-stage renal failure. 14516404: A 68-year-old male had end-stage renal disease secondary to hypertension. 14586719: BACKGROUND: Insufficiency of renal function and high blood pressure influence each other and eventually result in life-threatening endstage renal disease. 15115580: ESRD in the geriatric population most commonly results from diabetes, hypertension, glomerular and tubulointerstitial nephritis. 15363056: There was no significant change in incidence of treated ESRD in Indigenous or non-indigenous persons aged less than 25 years, in non-indigenous persons aged 25-64 years for ESRD caused by hereditary polycystic disease or hypertension, or in type 1 diabetics aged over 55 years. 15485598: In contrast to the striking decline in mortality rates from both stroke and coronary heart disease, the prevalence of hypertension as a cause of end-stage renal disease (ESRD) has increased such that it is now the second most common cause of ESRD in the United States. Over the past several decades, it has become clear that hypertension is both a cause and a consequence of kidney disease. 15719254: Bone marrow transplant nephropathy (BMTN) classically presents more than 100 days after transplantation as an acute nephritis with hypertension, azotaemia and anemia that usually results in end stage renal failure (ESRF). 15719329: Hypertension is considered as a cause of end-stage renal disease (ESRD) in 34.6% of Blacks, 4.3% Whites, 20.9% of mixed race people, and 13.9% of Indians. 15752232: The causes of chronic kidney diseases reflect this change and diabetes, together with hypertension, is now the major cause of end-stage renal failure worldwide, not only within the developed world, but also increasingly within the emerging world. 15752243: Glomerulonephritis is still the most common cause of ESRD in China; however, epidemiologic studies have revealed that the prevalence of diabetes and hypertension, which both are major causes of ESRD in many developed countries, are increasing dramatically. 15956825: PURPOSE OF REVIEW: Hypertension is vastly prevalent worldwide and constitutes the second leading cause of end-stage renal disease. 16014104: Both hypertension and diabetes are leading causes of end-stage renal disease worldwide, and their incidences are increasing, especially in underdeveloped communities. 16222601: Diabetes mellitus and arterial hypertension are the leading causes of end-stage renal disease in industrialized countries. 16452996: Underlying this trend are increasing rates of hypertension and diabetes mellitus, the two most common causes of ESRD. 16640171: Hypertension and diabetes are the two most important causes of ESRD, and antihypertensive treatment plays a crucial role in preventing Chronic Renal Failure (CRF) and ESRD. 16958293: BACKGROUND: In Mexico, diabetes mellitus type 2 and hypertension are leading causes of end-stage renal disease. 16965728: Hypertension is the second leading attributable cause of end-stage renal disease in the United States today. 16983949: Diabetes mellitus and hypertension were the underlying cause of end-stage renal disease in 55% of the patients. 17117899: The prevalence of HT in this sample was 67.4%, varying according to the etiology of End-Stage Renal Disease: diabetic 81%, vascular 81%, glomerulonephritis 61%, PKD 52%, unknown and others 64%. 17219852: The study revealed that hypertension, followed by obstructive uropathy, are the leading causes of ESRD. 17242449: Given that diabetes and hypertension are the 2 most common causes of end-stage renal disease, it is not surprising that obesity is also highly prevalent in the US hemodialysis population. 17266625: Hypertension plays major causative roles in development of cardiac failure and end-stage renal disease (ESRD). 17295666: Almost 70% of new cases of treated end-stage kidney disease are due to diabetes, hypertension or glomerulonephritis. 17452891: Multivariate analysis showed that increased recipient age, higher body mass index, African-American race, hepatitis C infection, hypertension as cause of end-stage renal disease, cold ischemia >or=30 hours, and use of tacrolimus each increased risk of complications. 17452897: Elderly patients with diabetes and those with hypertension as a cause of end-stage renal disease also experienced a large benefit. 17524851: During the study decades we noted an increase in the number of kidney transplantations (from 22 to 3690), age of recipients (from 30 to 40), male-to-female ratio of recipients (from 0.58 to 0.67), male-to-female ratio of donors (from 0.48 to 0.52), diabetes mellitus (from 0% to 27%), and hypertension (from 4% to 15%), as causes of ESRD, as well as the use of cadaveric kidneys (0% to 11%). 17524868: Furthermore, the peak in the relative frequency of diabetes mellitus and hypertension as the etiology of end-stage renal disease among those having undergone transplantation between 1999 and 2000 may have been responsible for the peak in rehospitalization costs and length of hospital stay. 17524900: This study was designed to investigate the correlation between ESRD secondary to HTN and sleep quality among kidney transplant recipients. BACKGROUND: That hypertension (HTN) as a leading cause of end-stage renal disease (ESRD) is linked to sleep disorders in the general population can be the basis of a hypothesis that HTN may be a contributing factor to the poor quality of sleep in some kidney transplant recipients. 17656472: Although diabetes and hypertension remain the most commonly reported cause of ESRD, rates of end-stage atherosclerotic renovascular disease seem to be on the rise in older patients. 17657116: Peak incidence of ESRD due to hypertension has shifted to a higher age-group. 18165208: Arterial hypertension is a significant cause of end-stage renal failure; effective treatment of hypertensive patients reduces the rate of progression of this disorder. ss-Blockers, particularly nonselective agents, are associated with deterioration of renal function in patients with chronic renal failure. 18198742: CONCLUSION: Hypertension, diabetes mellitus and chronic glomerulonephritis were the commonest causes of ESRD across most of the English-speaking Caribbean countries. 18212446: Hypertension is the fourth common cause of end-stage renal disease. Hypertension was responsible for 935 hospital admissions in 1997. 18271837: End-stage renal disease secondary to hypertension had been diagnosed at the age of 64 for which the patient was initiated on maintenance hemodialysis. 18334239: Using data from the US Renal Data System, we examined trends in ESRD incidence, including ESRD caused by diabetes or hypertension. 18648345: Proteinuria is a major long-term clinical consequence of diabetes and hypertension, conditions that lead to progressive loss of functional renal tissue and, ultimately, end-stage renal disease. 18679391: Although the ESRD epidemic is attributed in greater part to the increasing rate of diabetes, hypertension remains the second most common reported cause of ESRD and is present in approximately 90% of cases of diabetes-related ESRD. Although the role of hypertension as a primary cause of CKD is debated, hypertension is commonly recognized as the most important CKD progression factor. 1882825: Changing patterns of end-stage renal disease due to hypertension. We analyzed the records of all residents of Jefferson County, Alabama, accepted for renal replacement therapy between 1982 and 1987 and compared them with those accepted between 1974 and 1978 to determine any changes in the distribution and frequency of end-stage renal disease (ESRD) due to hypertension (H-ESRD). 1928071: It has been proposed that once functioning renal mass has been reduced below a critical level, either as the result of disease, congenital absence of a kidney, or surgical ablation, that hyperfiltration and glomerular hypertension lead to progressive glomerular sclerosis and end-stage renal failure. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 19368146: There was a statistically significant association between the HPA-1b allele and hypertension as the primary cause of ESRD (65% of patients with hypertension vs 23% of all other patients carried the HPA-1b allele, p=0.02, Fisher's exact test). 19422271: BACKGROUND: Diabetes and hypertension are the 2 major causes of endstage renal disease. 19745105: BACKGROUND: End-stage renal disease (ESRD) due to hypertension is common and displays familial aggregation in African Americans, suggesting genetic risk factors, including adrenergic activity alterations which are noted in both hypertension and ESRD. 20065899: Seventy percent of cases of end-stage renal disease are due to diabetes and hypertension, conditions which are usually managed by primary care providers. 2017628: A 61-year-old man who had end-stage renal disease secondary to diabetes mellitus and hypertension developed peritonitis due to infection with Rhizopus as a complication of receiving continuous ambulatory peritoneal dialysis (CAPD). 20219618: With increasing cyst size, further activation of the RAAS occurs, blood pressure increases, and a vicious cycle ensues with enhanced cyst growth and hypertension ultimately leading to ESRD. 20339374: In fact, hypertension and diabetes mellitus are the main causes of ESRD in western societies and together account for approximately more than 50% of ESRD incidence in the United States and Japan. 20433426: Incidence and prevalence on RRT are continuously increasing, and hypertension and diabetes are becoming the leading cause of ESRD. Hypertension and diabetes are increasing and have become the leading cause of renal failure in incident patients at day 91, unadjusted, in 2007 (26.8 and 21.4% respectively). 20517291: BACKGROUND: A 62-year-old man with a history of end-stage renal disease secondary to hypertension who was on continuous ambulatory peritoneal dialysis (CAPD), presented to a peritoneal dialysis clinic with subacute onset of abdominal pain, mainly in the epigastric region. 2063853: We conclude that there has not been a decrease in the incidence of hypertension as a causative diagnosis for patients entering ESRD programs and that this may be a reflection that treatment of hypertension does not prevent the development of ESRD in some patients. Hypertension as a causative diagnosis was a constant proportion of the increase. Hypertension as a causative diagnosis of patients entering end-stage renal disease programs in the United States from 1980 to 1986. To determine whether the incidence of hypertension as a causative diagnosis of end-stage renal disease (ESRD) is also decreasing, we examined the records of the Health Care Financing Administration (HCFA) from 1980 to 1986 regarding the causative diagnoses of patients entering ESRD programs. 20714753: He progressed to end-stage renal failure despite plasmatherapy and underwent bilateral nephrectomy because of uncontrolled hypertension. 21079654: Identifying the precise prevalence of CKD attributable to hypertension is difficult owing to the absence of uniform criteria to establish a diagnosis of hypertensive nephropathy. The prevalence of hypertension, chronic kidney disease (CKD) and end-stage renal disease (ESRD) attributable to hypertension continues to rise worldwide. 21251296: Diabetes and hypertension are among the leading causes of end stage renal disease, although autoimmunity, renal atherosclerosis, certain infections, drugs and toxins, obstruction of the urinary tract, genetic alterations, and other insults may initiate the disease by damaging the glomerular, tubular, vascular or interstitial compartments of the kidneys. 21331710: As a consequence of the sustained high BP, there is an increased risk of mortality and morbidity that is characterized by myocardial infarction, congestive heart failure, stroke, end-stage renal failure, and peripheral vascular disease (1-3). 21335249: Percentages of diabetes mellitus and hypertension as causes of ESRD increased, whereas those of chronic glomerulonephritis and urologic disease decreased. 21499197: RESULTS: Recipient end-stage renal disease from hypertension, as compared with other recipient end-stage renal disease causes, was associated with modest, significant increases in the age- and gender-adjusted relative risks of hypertension diagnosis (aHR, 1.37%; 95% confidence interval [CI], 1.08-1.74) after donor nephrectomy among related donors. 21531530: METHODS: Patients undergoing one- and two-stage BBAVF at two institutions were compared retrospectively with respect to age, sex, body mass index, use of preoperative venous duplex ultrasound, diabetes, hypertension, and cause of end-stage renal disease. 21599823: We also know that Diabetes Mellitus (DM) followed by Hypertension (HTN) are the two most frequent causes of end-stage renal disease (ESRD). 21677297: BACKGROUND: Diabetes Meillitus (DM) and hypertension (HT) are important causes of end-stage renal disease (ESRD) and renal replacement therapy (RRT) is the standard active treatment. 22066080: We describe a 62-year-old female with end-stage renal disease due to hypertension. 22186319: Diabetes clustered with hypertension and nephropathy has become the leading cause of end-stage renal disease globally. 2258879: Hypertension is the commonest cause of end-stage renal failure in black South Africans and the most common preventable cause of end-stage kidney disease in the country. Hypertension as a cause of end-stage renal failure in South Africa. The survival at 36 and 72 months was the same whether hypertension was the cause of end-stage renal failure or not, and whether the hypertension was malignant or benign. 2261145: Hypertension causes approximately 25% of end-stage renal disease (ESRD) and develops in virtually every patient with advanced renal insufficiency from any cause. 22790459: He developed endstage renal disease due to hypertension and was treated with hemodialysis for 3 y. 23082445: Hypertension has been identified as one of the causes for end stage renal failure (ESRF) and is likely to worsen kidney function. 23146984: Diabetes mellitus (32.9%) and hypertension (24.1%) were the most common known causes of ESRD in our patients. 23299034: Diabetes and hypertension, the 2 leading causes of ESRD, contribute to the pathogenesis of ischemic heart disease (IHD) in these patients, as do other traditional risk factors (eg, dyslipidemias, smoking, and sedentary lifestyle). 23360312: Diabetes and hypertension are the main causes of chronic end-stage kidney disease in humans. 23425705: OBJECTIVE: Hypertension is an important cause of end-stage renal disease. 23816745: Increased efforts and awareness should be focused on the prevention and treatment of diabetes mellitus and hypertension as they are the main causes of ESRD. 23934421: RESULTS: Hypertension and diabetes were the leading causes of end-stage renal disease. 23984264: A 34-year-old man with end-stage renal disease as a result of the focal segmental glomerulosclerosis and uncontrolled hypertension that precluded the transplantation surgery and the patient's post-transplant blood pressure and the renal function remained within normal limits following the transplant for 6 months of follow-up. 24809889: A 56-year-old woman with hypertension-induced end stage renal disease presented with skin thickening and mottled discoloration. 24821181: The exact reasons of the rising prevalence of ESRD patients are unknown, but it can be attributed to an increase in the prevalence of diabetes mellitus and hypertension as the most common causes of ESRD. 24864612: Diabetes mellitus and Hypertension was the cause of ESRD in 29 (72.5%). 25001132: Role of renin-angiotensin-aldosterone system gene polymorphisms and hypertension-induced end-stage renal disease in autosomal dominant polycystic kidney disease. A number of genetic variations involved in renin-angiotensin-aldosterone system (RAAS) pathway genes have clinical or physiological impacts on pathogenesis of hypertension-induced ESRD in ADPKD. The present review deals with RAAS gene polymorphisms focused on hypertension-induced ESRD in ADPKD in different populations. 25065406: CASE PRESENTATION: 66-year-old African-American female with a history of ESRD secondary to hypertension developed a blood infiltration on the arterial side of her arteriovenous fistula followed by sudden onset of diffuse abdominal pain with nausea and vomiting during her regular HD treatment. 25185727: Age >49 years, female gender, hypertension as the cause of ESRD, and initiation on hemodialysis was associated with a greater risk of GIB. 25327089: Hypertension (37.1%) was leading cause of ESRD. 25380885: Zonulin was not affected by sex, type of immunosuppressive therapy, presence of diabetes, coronary artery disease, heart failure, hypertension, or cause of end-stage renal disease. 26024705: On the other hand, hypertension is one of the main causes of ESRD. 26361686: We report a case in which a man had undergone allogenic stem cell transplantation from his brother 16 years ago due to chronic myeloid leukemia, and who then developed ESRD due to arterial hypertension and underwent renal transplantation (Rtx) from the same brother. 26419536: The study showed that hypertension is a leading cause of ESRF in Sudan followed by chronic glomerulonephritis. Hypertension and diabetes mellitus are the leading causes of ESRF among patients over 40 years old. 2664194: Hypertension is the most common cause of end-stage renal disease (ESRD) at this center (57%). 26674015: Hypertension is one of the leading causes of end stage renal disease. 26787576: Hypertension and diabetes were the main causes of ESRD. 26941817: Nowadays, diabetes mellitus (DM) and hypertension are considered as the most common causes of end-stage renal disease (ESRD). 27275220: For females, the predictor variables selected are hypertension & (Diabetic*Hypertension), which means that hypertension and hypertensive diabetic are significant causes of ESRD. 27287605: Patterns of End-Stage Renal Disease Caused by Diabetes, Hypertension, and Glomerulonephritis in Live Kidney Donors. 27355680: It is not only associated with the future burden of end-stage renal disease but also affects mortality and cardiovascular outcomes caused by hypertension. 27932159: CASE REPORT: A 50-year-old man with end-stage renal disease secondary to hypertension and focal segmental glomerulosclerosis underwent living-related KT. 28060446: Recipient 2 was a 62-year-old woman with a history of end-stage renal disease caused by hypertension and insulin-dependent diabetes. 28169886: OBJECTIVE: Persistent hypertension in adulthood is a leading cause of end-stage renal disease (ESRD). 28245797: BACKGROUND: Hypertension is one of the most important causes of end-stage renal disease, but it is unclear whether elevated blood pressure (BP) also accelerates the gradual decline in the glomerular filtration rate (GFR) seen in the general population with increasing age. 28256256: We designed a histological & immunohistochemical study to evaluate effectiveness of MSCs therapy in withhold of end-stage renal disease (ESRD) secondary to hypertension which has become a growing & striking public health problem. 28338771: BACKGROUND: Hypertension is a major cause of end-stage renal disease, and blood pressure (BP) control is crucial in patients with chronic kidney disease (CKD). 28408734: CASE REPORT A 50-year-old Hispanic male with a history of end-stage renal disease secondary to hypertension underwent deceased donor kidney transplantation. 28937072: Diabetic nephropathy (57%) and hypertension (12.4%) are emerging as the most common causes of end-stage renal disease (ESRD) in our data, followed by undetermined causes in those who presented as ESRD (10.9%), and then by rejected transplant in 4.6%. 29095051: Background Obesity increases risk of hypertension and diabetes, the leading causes of end-stage renal disease. 29265049: Hypertension was the main cause of end-stage renal disease (ESRD) constituting 36.4%, followed by diabetes (27.3 %), and toxic nephropathy (4.5%). 29903699: RPS causes high blood pressure that may lead to severe chronic kidney disease and end-stage renal disease (ESRD). 29942501: It is well known that one of the main determinants of mortality and morbidity in chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients is fluid overload acting on the cardiovascular system causing hypertension, increased arterial stiffness, left ventricular hypertrophy and eventually heart failure. 29989454: This study intends to assess the impact of environmental factors on the onset of hypertension-induced end-stage renal disease (ESRD) and to compare the level of oxidative stress with nonhypertensive diabetic ESRD. Environmental impact on the onset of hypertension-induced end-stage renal disease. 30152431: Chronic glomerulonephritis and hypertension accounted for about 77.5% of etiology of ESRD in these patients. 30152440: A 59-year-old female with end-stage kidney disease secondary to hypertension was started on PD in 2003. 30870849: Severe hypertension can lead to irreversible kidney failure and end-stage renal disease (ESRD) and vice versa. 31031388: A 67-year-old male patient with endstage renal disease that was caused by hypertension was on maintenance hemodialysis (HD) for 22 months. 31335778: This was consistent among subgroups of recipients at higher risk for adverse outcomes due to hyperfiltration: African American recipients (aHR 1.10, 95% CI 0.70-1.73, p=0.68) and those with ESRD caused by hypertension (aHR 1.10, 95% CI 0.65-1.85, p=0.73) or diabetes (aHR 0.80, 95% CI 0.56-1.13, p=0.20). 31599090: These studies help define an age-related nephropathy that overlaps with hypertension as a potential cause of end-stage renal disease when glomerulosclerosis is advanced. 3265607: Uncontrolled hypertension was an important cause for rapid deterioration to end stage renal failure within 3 years, compared to 8 years when hypertension was controlled. 34553555: Most cases of ESKD are due to diabetes and hypertension that occur more than 10 years after donation. 7792029: The predominant symptoms of the index patient were hypertension and mild renal insufficiency at age 48, resulting in end-stage renal failure at age 63 due to giant bilateral angiomyolipoma of the kidneys. 7939913: In the Southeast, hypertension is the most common cause of ESRD, followed closely by diabetes mellitus occurring most frequently in older minority patients, particularly blacks. 7987102: These findings have important implications for the provision of renal services in districts with a high proportion of ethnic minorities and for the management of diabetes mellitus and hypertension, two important causes of end stage renal failure in these populations. 8017304: Investigators have reported that patients with end-stage renal disease and left ventricular hypertrophy due to hypertension have diminished lateral/septal count ratios on stress and delayed imaging mimicking lateral myocardial infarction in approximately 35% of patients. In conclusion, myocardial thallium-201 distribution is normal in patients with left ventricular hypertrophy due to hypertension. The purpose of this study was to compare myocardial SPECT thallium-201 distribution in a broader group of patients with left ventricular hypertrophy resulting from hypertension with normal file subjects in order to determine the prevalence of abnormal studies and to compare the lateral/septal count ratio. 8095060: Overall, 6.5% of patients with end-stage renal disease due to hypertension were seropositive for a hantavirus. 8172207: Clinical documentation of end-stage renal disease due to hypertension. 8327642: Although hypertension accounts for approximately 15-20% of end-stage renal disease and renal impairment occurs in 15% of patients with essential hypertension, there are few data available on the clinical features of patients with benign hypertensive nephrosclerosis, the histological consequence of hypertension on the kidney. 8398008: Progressive renal failure is a significant complication of hypertension, a major cause of end-stage renal disease. 8465818: First-, second-, or third-degree relatives with ESRD were more prevalent among cases with ESRD due to hypertension and type II diabetes mellitus compared with CGN (P < or = 0.05). 8719761: African Americans and Native Americans have shown the most dramatic increase; diabetes being the major reason for both races, but for African Americans, hypertension is the leading cause of ESRD. 9039100: In contrast, endstage renal disease resulting from hypertension continues to increase. 9165646: Hypertension and glomerulonephritis are the next most commonly attributed causes of ESRD, but these diagnoses are not necessarily based on consistent or uniform criteria. 9181281: A 63-year-old black male with end-stage renal disease secondary to hypertension was placed on chronic dialytic therapy and tolerated rHuEPO treatment well for two years. 9211180: PARTICIPANTS: Patients with ESRD due to hypertension (n = 214), diabetes (n = 239), other specified causes (n = 181), unknown causes (n = 82) and control subjects drawn from the general population (n = 361). This result supports the hypothesis that nonmalignant hypertension of long duration may cause renal insufficiency. 9314428: African Americans (blacks) have a disproportionately high incidence of end-stage renal disease due to hypertension. 9394313: BACKGROUND: Hypertension is a significant cause of end-stage renal failure and effective treatment of hypertensive will reduce the progression rate of chronic renal failure in various kidney disorders. 9395579: Hypertension is an important cause of end-stage renal disease in the black population whilst analgesic nephropathy is important in the white population. 9412644: CONCLUSIONS: T2 high intensities on MR images of ESRD may reflect subcortical small-vessel alterations induced by hypertension. 9623542: CONCLUSION: The results demonstrate high incidence and prevalence rates of ESRD mainly as a result of NIDDM and systemic arterial hypertension. BACKGROUND: End-stage renal disease (ESRD) on long-term dialysis is a substantial problem in Reunion because of the high incidence and prevalence of this disease due to non-insulin-dependent diabetes mellitus (NIDDM) and systemic arterial hypertension. 9681290: However, hypertension is the most frequently reported cause of ESRD in African Americans. 9828579: Hypertension remains a major cause of ESRD among African Americans, and progression to ESRD may be rapid in patients with marked proteinuria. 9839285: Long-lasting hypertension may induce ESRD in some patients through hypertensive nephrosclerosis. 9839286: This lower survival of patients with renal vascular disease seems to be related to higher cardiac mortality, which is in alignment with the diagnosis of hypertension as cause of renal failure. The incidence of hypertension as cause of ESRD has doubled in the ERA-EDTA Registry in the past two decades, going from 7 to 13%. It is very possible that this is not a real increase in the incidence of hypertension as cause of ESRD, but rather a consequence of greater acceptance of older patients, a phenomenon that has simultaneously occurred. There are geographic differences in the incidence of hypertension as cause of ESRD, from 6% in Japan to 28.5% in the U.S., and 13% in Europe. Hypertension as cause of end-stage renal disease: lessons from international registries. 9870470: BACKGROUND: Hypertension is reported to be one of the most common causes of end-stage renal disease (ESRD) in Europe and in the United States. 9886902: During the last few years there has been a renewed interest in blood-pressure (BP)-induced kidney damage, owing to a progressive increase in the incidence and prevalence of hypertension and vascular diseases as a cause of end-stage renal disease (ESRD). 11116104: Therefore, to determine whether hypertension can directly induce endothelial dysfunction, we investigated the effect of increases in intra-arterial pressure on endothelium-dependent vasodilation of the human microvasculature. 11158948: These results demonstrate that conduit vessel endothelial dysfunction secondary to hypertension is not reversed by acute or chronic treatment with oral ascorbic acid. 11195397: These results suggest that exogenous NO from nipradilol reduces the endothelial dysfunction caused by hypertension without changing the blood pressure. Previous studies have shown that hypertension causes endothelial dysfunction. 11735092: Endothelial dysfunction such as caused by hypertension rather than metabolic dysregulation per se may underlie the elevated plasma vWF concentration found with insulin resistance. 11872376: And the question is whether endothelial dysfunction is a cause or consequence of hypertension. 11986897: Hypertension induces endothelial dysfunction, exacerbates the atherosclerotic process and it contributes to make the atherosclerotic plaque more unstable. 12570806: Following successful application in otherwise healthy animals, the approach resulted to be of therapeutic value in rats with endothelial dysfunction caused by arterial hypertension. 12877075: In this review, we present the possibility that endothelial dysfunction causes hypertension in diabetes mellitus. It is unclear that endothelial dysfunction is a cause or consequence of hypertension. 14678869: In patients with insulin resistance or type 2 diabetes mellitus, a set of metabolic insults--namely high plasma levels of glucose and free fatty acids, increased inflammation, dyslipidemia, and hypertension--cause endothelial dysfunction and a transition from an antiatherogenic endothelium to a proatherogenic endothelium. 15171338: [Mechanism of vascular endothelial dysfunction induced by hypertension]. 15212975: Our data suggest that protein kinase C plays a crucial role in the endothelial dysfunction induced by hypertension. 15510907: Aging, lipids (oxidized LDL), infective agents, inflammation, increased glucose level, hypertension, smoking, increased homocysteine level, oxidative stress etc. are recognized as factors which lead to endothelial dysfunction and cause atherosclerosis. 15790570: Pathological conditions such as hypertension and hyperglycemia as well as abrasions following balloon angioplasty all lead to endothelial dysfunction that impacts disease morbidity. 15884454: BACKGROUND: Hypertension is associated with functional and morphological alterations of the endothelium, which disturbs delicate balance of endothelium-derived factors resulting in endothelial dysfunction. 15956822: This review addresses recent developments in hypertension-induced endothelial dysfunction. 15976731: The mechanisms involved in the development of coronary artery disease (CAD) in the diabetic population are multifactorial, including hyperglycemia, hyperlipidemia, hypertension, and insulin resistance, ultimately leading to endothelial dysfunction and accelerated atherogenesis. 16335891: Thus, this case indicates that reversible posterior leukoencephalopathy syndrome is induced by cerebrovascular endothelial dysfunction, which is induced not only by high blood pressure but also hemostatic dysfunction. 16428344: Previous studies suggested that loss of tetrahydrobiopterin (BH(4)) may play an important role in the pathogenesis of vascular endothelial dysfunction induced by diabetes and hypertension. 16518526: It is assumed that endothelial dysfunction due to arterial hypertension could be improved or even normalized by antihypertensive treatment. 16715652: Hypertension causes endothelial dysfunction, which plays an important role in atherogenesis. 16736159: The study has been designed to investigate the effect of bis(maltolato) oxovanadium (BMOV), a protein tyrosine phosphatase inhibitor, on hypercholesterolemia and hypertension-induced vascular endothelial dysfunction. 17100143: Depression of endothelium-dependant vasodilatation is an early manifestation of endothelial dysfunction due to hypertension. Inshort, the endothelial dysfunction due to hypertension plays a role in a complex physiopathological process and is a marker of future cardiovascular events. 17653967: CONCLUSION: We demonstrate the impact of hypertension in IMA grafts producing increased endothelial dysfunction, reduced response to passive stretching, increased basal tone, and impaired responsiveness to exogenous vasoconstrictors and NO release. 17654441: Biomechanical forces on the endothelium, including low shear stress from disturbed blood flow and hypertension, are also important causes of endothelial dysfunction. 17878688: Cardiovascular disease (CVD) in ESRD patients with diabetes mellitus (DM) are implicated in the endothelial dysfunction caused by hyperglycemia, hyperlipidemia, and hypertension, and in the vascular calcification of intimal and medial arterial blood vessels caused by hyperphosphatemia. 17885259: METHODS: Pioglitazone (1 mg x kg(-1) x d(-1)) was orally administered to stroke-prone spontaneously hypertensive rats (SHRSP) to examine the effect on incidental stroke, cerebrovascular injury, brain inflammation, oxidative stress, and vascular endothelial dysfunction induced by hypertension. 17968002: Both hypertension and hypercholesterolemia induce endothelial dysfunction in the carotid artery. 18271765: CONCLUSIONS: PRES occurs as a result of disordered cerebral circulatory autoregulation and/or endothelial dysfunction, usually as a result of acute, intermittent hypertension. 18400490: In summary, aldosterone through mineralocorticoid receptors can participate in the vascular damage associated with different pathologies including hypertension through its prooxidant, pro-inflammatory and profibrotic effects that triggered endothelial dysfunction, an inflammatory process and vascular remodeling. 18497471: Hypertension and type 2 diabetes mellitus (T2DM) cause endothelial dysfunction probably through increased oxidant stress. 18729004: Traditional cardiovascular disease risk factors, such as hypertension, dyslipidemia and diabetes, cause endothelial dysfunction characterized by off-balanced vasodilation/vasoconstriction, increased oxidative stress and inflammation, deregulation of thrombosis and fibrinolysis, abnormal smooth muscle cell proliferation, and a deficient repair mechanism. 19633448: Data from the literature indicate that the age of the animal is a contributing factor and that endothelial dysfunction is likely to be a consequence of hypertension. 20349425: Cardiovascular risk factors such as hypertension may cause endothelial dysfunction and even disintegration, finally resulting in small vessel disappearance (vascular rarefaction) and tissue hypoxia. 21799161: BACKGROUND AND PURPOSE: It is well-established that hypertension leads to endothelial dysfunction in the cerebral artery. 21898987: ED and hypertension share some pathophysiologic pathways, such as oxidative stress-induced endothelial dysfunction and up-regulated RhoA/Rho kinase activity, and both are the diseases at different stages of the pathological process of vascular dysfunction. 21949627: Blood pressure (BP) reduction is the most effective way to reduce CV risk in patients with hypertension, but it is unknown whether endothelial dysfunction is a cause or consequence of hypertension. 22689073: Hypertension causes endothelial dysfunction which is considered an early sign for the development of CAD. 22819709: This study suggests that fasudil by inhibiting the Rho kinase activity normalizes the eNOS expression and phosphorylation and ameliorates the endothelial dysfunction induced by hypertension in the SHR model. 23289223: [Interaction of vasotonic bioeffectors in endothelial dysfunction pathogenesis due to arterial hypertension on aging]. 23971642: While endothelial dysfunction occurs early in ADPKD and precedes the onset of hypertension, the pathogenesis of endothelial dysfunction has not been extensively studied. 24043258: Cardiovascular risk factors such as hyperglycemia, hyperlipidemia, and arterial hypertension induce endothelial dysfunction with alterations in endothelial biosecretion and immune behavior. 25050356: Our study shows that superoxide radicals participate in haemodynamic control, but acute superoxide scavenging is ineffective in glomerular and tubular improvement, probably due to hypertension-induced strong endothelial dysfunction which neutralizes beneficial effects of O2(-) scavenging. 25659733: This study has been structured to investigate the role of agomelatine, a melatonergic MT1/MT2 agonist and nicorandil, a selective ATP sensitive potassium (KATP) channel opener in renal artery ligation (two-kidney-one-clip: 2K1C) hypertension induced endothelial dysfunction, brain damage and VaD. 27167462: CONCLUSIONS: Prediabetes and hypertension induce endothelial dysfunction and inflammation by elevating levels of soluble adhesion molecules and inflammatory cytokines. 27208157: In conclusion, chronic VNS prevents hypertension-induced endothelial dysfunction and aortic stiffening in an animal model of severe hypertension. 27627558: BACKGROUND: Hypertension-induced endothelial dysfunction is associated with an impaired bioavailability of nitric oxide regulated through interactions between nitric oxide synthase and heat shock protein-90 (Hsp-90). 29135307: The aim of this study was to examine whether a defective retinal vessels response is associated with HT-induced endothelial dysfunction. 29568075: Hypertension-induced endothelial dysfunction is associated with beta-amyloid (Abeta) deposition, a typical pathology of Alzheimer's disease (AD). In conclusion, eNOS downregulation contributed to hypertension-induced Alzheimer pathology and cognitive impairment. 29676873: Risk factors such as hypertension and dyslipidemia unbalance angiotensin II - bradykinin homeostasis, leading to endothelial dysfunction and changes in vascular structure that promote atherosclerosis and thrombosis. 30342074: It is evident that diseases such as diabetes, obesity, and hypertension disturb the normal endothelial functions in humans and lead to endothelial dysfunction, which may further precede to the development of atherosclerosis. 30571552: High Systolic Blood Pressure Induces Cerebral Microvascular Endothelial Dysfunction, Neurovascular Unit Damage, and Cognitive Decline in Mice. 30648528: These 2 disorders are associated with distinct etiologies including hypertension, atherogenic dyslipidemia, and significant vascular abnormalities that could lead to endothelial dysfunction. 31079531: Preeclampsia is a hypertensive pregnancy disease associated with a massive increase in sFlt-1 (soluble form of the vascular endothelial growth factor 1) in the maternal circulation, responsible for angiogenic imbalance and endothelial dysfunction. 31479151: KEY RESULTS: Relaxin treatment ameliorated hypertension-induced endothelial dysfunction by increasing NO-dependent relaxation and reducing endothelium-dependent contraction. 31610241: Nitrite abrogated both the decrease in intracavernosal pressure and endothelial dysfunction of the CC induced by hypertension. Given that nitrite is described to display antioxidant effects, we hypothesized that treatment with nitrite would exert antioxidant effects attenuating both reactive oxygen species (ROS) generation in the corpora cavernosa (CC) and ED induced by hypertension. 31745719: Mercury exposure accelerated the natural course of hypertension in young SHRs and increased oxidative stress associated with reduced participation of antioxidant enzymes, an activated COX-2 pathway, thereby producing endothelial dysfunction, which is a risk factor in prehypertensive individuals. 32536276: Increased Blood Pressure Causes Lymphatic Endothelial Dysfunction via Oxidative Stress in Spontaneously Hypertensive Rats.The lymphatic system is involved in the pathogenesis of edema, inflammation, and cancer metastasis. Increased Blood Pressure Causes Lymphatic Endothelial Dysfunction via Oxidative Stress in Spontaneously Hypertensive Rats. 32978495: High blood pressure is known increased inflammatory activity and to cause endothelial dysfunction has been showed in HT patients. 33808872: Among these, gasotransmitters such as nitric oxide (NO) and hydrogen sulfide (H 2 S) are very active molecules constitutively produced by endotheliocytes for the maintenance and control of vascular physiological functions, while their impairment is responsible for endothelial dysfunction and cardiovascular disorders such as hypertension, atherosclerosis, and impaired wound healing and vascularization due to diabetes, infections, and ischemia. 33858279: BACKGROUND: Arterial hypertension causes cardiovascular adverse events mainly through endothelial dysfunction, atherosclerosis, and inflammation. 34002299: Endothelial dysfunction, oxidative stress, and increased inflammatory activity are the main pathophysiological mechanisms responsible for cardiac remodeling secondary to hypertension. 34281445: CONCLUSION: In summary, the obtained results suggest that AELC can prevent and reverse the high blood pressure induced by fructose, probably by restoring nitric oxide level and by improving altered metabolic parameters. PURPOSE: Since metabolic abnormalities such as elevated glucose level and imbalanced lipid profiles increase the risk for hypertension and cause endothelial dysfunction, we evaluated the effect of aqueous extract of large cardamom (AELC) on fructose-induced metabolic hypertension and oxidative stress. 34368236: Conclusion: The dysregulations of lncRNA ENSMUST00000155383-associated genes might play crucial roles in hypertension-induced endothelial dysfunction through affecting calcium pathway. 35185772: Key end-organ pathological mechanisms, for which hypertension is proposed to be causative, include acute and covert cerebral ischemia and hemorrhage, accelerated brain atrophy, cerebral microvascular rarefaction and endothelial dysfunction, disruption of blood-brain barrier and neuroinflammation that affects amyloid pathologies. 35335911: In this review, we describe the relationship between OS and hypertension-induced endothelial dysfunction and the involvement and therapeutic potential of Nrf2 in HTN. 35396697: This study investigates the role of ulinastatin (UTI) and quercetin alone as well as in combination in hypertension-induced endothelial dysfunction and vascular dementia (VaD). Therefore, the utility of these agents might be studied further to understand their full potential in hypertension-induced VaD. METHOD: Two-kidney one-clip (2K1C) renovascular model was set up to induce hypertension in the Albino Wistar rats (males). 36332485: AIM: During hypertension-induced endothelial dysfunction, periodic mechanical stretching (MS) activates related inflammatory pathways and leads to endothelial damage, but the underlying mechanisms remain unknown. 36336162: Resveratrol, which has antiinflammatory and vasculoprotective properties, has been reported its beneficial effects on endothelial dysfunction induced by hypertension, diabetes and, aging. 37194678: OBEJECTIVE: We investigated the potential mechanism by which QQL improves hypertension-induced vascular endothelial dysfunction (VED). 38089998: Background: Previous study confirmed that both TaohongSiwu decoction (THSWD) and Dubosiella newyorkensis improved hypertension-induced endothelial dysfunction. Methods: Eight percent high-salt diet was applied to induce hypertension in a mouse model for 4 weeks. 38192137: Montelukast Ameliorates 2K1C-Hypertension Induced Endothelial Dysfunction and Associated Vascular Dementia. 38605139: Our data show that treatment with s(P)RR caused hypertension and growth restriction in vivo and caused marked endothelial dysfunction in vitro. 7731395: The influence of aging and/or hypertension caused no alterations of the alpha 1-agonist response provoked by phenylephrine in aortic rings. It is concluded that (1) the responsiveness of resistance arteries to adrenoceptor stimulation only changes with elevated blood pressure and (2) hypertension in combination with aging induces an endothelial dysfunction in conduit arteries but not in resistance vessels. 12806426: The prevalence of erectile dysfunction is increased with age and is often secondary to diseases such as depression, hypertension and diabetes. 15251486: Diabetes mellitus, hypertension, and tobacco abuse are the three most common causes of erectile dysfunction in men older than 50 years of age. 15843804: Although the function of penile erection might be affected by a secondary effect related to endothelial dysfunction of hypertension, these ultrastructural pathological changes of the penile cavernous tissue might also be one of the important mechanisms of erectile dysfunction caused by hypertension. 16687945: The pharmacologic management of hypertension has long been implicated in the genesis of erectile dysfunction; the latter is considered the main reason of nonadherence to antihypertensive therapy. 16900205: It is unclear whether high blood pressure per se or antihypertensive drug use causes erectile dysfunction (ED). 17151696: Phosphodiesterase-5 (PDE5) inhibitors are effective therapy in men with ED owing to hypertension who are taking antihypertensive medicines including those on multiple antihypertensive medicines. 17498098: Apparently, it takes years for HTN to cause ED. 19624788: Although the aetiology of ED is multifactorial, some of the associated comorbid conditions, including diabetes, cardiovascular disease and hypertension, can be a primary cause of ED. 20978287: Both small vessel disease, such as that in diabetes mellitus, and arteriosclerosis of bigger size arteries, as in hypertension, cause arterial insufficiency and erectile dysfunction. 22240443: Hypertension can lead to erectile dysfunction as a consequence of high blood pressure (BP) or due to antihypertensive treatment. 22750666: Although the etiology of hypertension-induced erectile dysfunction is multifactorial and still unknown, Rho-Rho kinase pathway is one of the key factors. 24132050: Non-diagnosed or silent DM, HT and ACVD can have roles in the etiology of arterial ED. 24930630: Hypertension, diabetes, hyperlipidemia and atherosclerosis are also linked to the etiology of lower urinary tract symptoms, benign prostatic hyperplasia/benign prostatic enlargement and erectile dysfunction. 26745574: INTRODUCTION: Stem cell therapy is thought to improve wound healing and promote vasculogenesis and has also been investigated as a treatment for patients with erectile dysfunction (ED), which is usually caused by a microvascular disease such as diabetes mellitus or hypertension. 26792698: CONCLUSIONS: High blood pressure can cause ED in rats, which could be mitigated by autologous SVF injection. 30152279: RESULTS: Hypertension can cause ED as a consequence of high blood pressure or antihypertensive treatment. 31610241: Nitrite abrogated both the decrease in intracavernosal pressure and endothelial dysfunction of the CC induced by hypertension. Given that nitrite is described to display antioxidant effects, we hypothesized that treatment with nitrite would exert antioxidant effects attenuating both reactive oxygen species (ROS) generation in the corpora cavernosa (CC) and ED induced by hypertension. 33118708: Dysregulation of NOS and alpha1AR, histological changes and oxidative stress in CC may be associated with the pathophysiology of hypertension-induced ED. 35019864: The novel NO donor, CCL5, was more efficient than L-arginine to improve diabetes and/or hypertension induced ED by the significant increase of ICP. 35752527: INTRODUCTION: Both hypertension and beta-blocker drugs used for treating hypertension (HT) can cause erectile dysfunction (ED). 10981140: Excess weight gain is a major cause of essential hypertension, and abnormal kidney function appears to be a cause as well as a consequence of obesity hypertension. 11510761: Many genes and environmental factors are involved in the pathogenesis of hypertension, but the exact cause of essential hypertension has not yet been clarified. 11791034: In the current study we tested whether young normotensive subjects with positive family history of arterial hypertension exhibit an increased sensitivity to Ang II, thereby potentially contributing to the pathogenesis of essential hypertension in these subjects. 15002004: This case demonstrates that hypertension could result in spite of the extremely decreased sodium reabsorption in Gitelman's syndrome and that essential hypertension is genetically heterogeneous, and abnormality of all genes may not be necessarily required to cause blood pressure rise. 15079793: OBJECTIVE: To investigate the genotype of Arg389Gly polymorphism in beta(1)-adrenergic receptor gene(beta(1)-AR), Arg16Gly polymorphism in beta(2)-adrenergic receptor gene (beta(2)-AR) and Trp64Arg polymorphism in beta(3)-adrenergic receptor gene (beta(3)-AR) in the high risk population of hypertension and analyze the role of the genes in the pathogenesis of essential hypertension. 15283761: Failure of these mechanisms predisposes the organism towards the development of hypertension, appears to underlie the development of some forms of experimental hypertension, and may even contribute to the pathogenesis of essential hypertension. 1735146: CONCLUSIONS: These data suggest that the impairment in baroreflex sensitivity in hypertension is in part genetically determined and may be an important hereditary component in the pathogenesis of essential hypertension. 18678361: UNLABELLED: High blood pressure (BP) is a major cause of cardiovascular disease and primary hypertension is a frequent pathological condition. 21309757: Dysregulation of thyroid hormones and prostaglandin E2 plays a role in the development of hypertension, suggesting that SLCO1B1 might contribute to the aetiology of essential hypertension (EH). 2446063: An involvement of peripheral serotonin in the genesis and maintenance of essential hypertension seems very unlikely, although vascular damage due to hypertension is probably enhanced by serotonin released from aggregating platelets. 30075114: Endothelial cells play a key role in the regulation of blood pressure; however, a Mendelian form of hypertension that is primarily due to endothelial dysfunction has not yet been described. Insights obtained from the study of rare Mendelian forms of hypertension have been invaluable in elucidating the mechanisms causing primary hypertension and development of antihypertensive therapies. 3054241: Alterations in the pattern of renal PG have been reported in hypertensive animals and in human essential hypertension, reflecting a primary causative defect or changes which are secondary to hypertension. 30894678: Despite the importance of hypertension, the pathogenesis of essential hypertension, which involves the complex interaction of several mechanisms, is still poorly understood. 30963979: Understanding the pathologies of these monogenic hypertensive disorders may provide insight into the causes of the more prevalent essential hypertension and new avenues to unravel the complexities of blood pressure regulation. 32504652: The association of higher BP with increased risk-taking behaviors may have relevance to the early pathogenesis of essential hypertension. 3385201: The geographic variations in blood pressure and hypertension in Great Britain provide a major opportunity for research into the causes of 'essential' hypertension. 3820528: Enhanced calcium-sensitivity of erythrocytes in hypertension--calcium-induced changes of erythrocyte osmotic fragility in essential hypertension. 7567973: To date, mutations in three genes have been implicated in the pathogenesis of human hypertension: mutations resulting in ectopic expression of aldosterone synthase enzymatic activity cause a mendelian form of hypertension known as glucocorticoid-remediable aldosteronism; mutations in the beta subunit of the amiloride-sensitive epithelial sodium channel cause constitutive activation of this channel and the mendelian form of hypertension known as Liddle syndrome; finally, common variants at the angiotensinogen locus have been implicated in the pathogenesis of essential hypertension in Caucasian subjects, although the nature of the functional variants and their mechanism of action remain uncertain. 8942392: Other interpretations are possible, but the evidence of this review suggests that further investigation of cerebral oxidative metabolism in hypertension and in related conditions may shed light on the still elusive aetiology of essential hypertension. 9821849: Mild hypertension does not appear to be associated with alterations of beta2-adrenoceptor sensitivity, and the findings do not support that adrenaline is involved in the pathogenesis of primary hypertension. 10367936: In conclusion, it was suggested that persistent distension of tumor vessels and the increase of diffusive extravasation of MAb caused by short-period-induced hypertension and inhibition of bradykinin degradation produced favorable effect for the MAb distribution in tumors. 20535647: In rodent models, activation of plasma kallikrein in vitreous increases retinal vascular permeability; whereas inhibition of the kallikrein kinin system reduces retinal leakage induced by diabetes and hypertension. 23478950: The eye signs are postulated to be due to two preeclamptic mechanisms involving disordered cerebral autoregulation: (1) hyperperfusion and breakdown of the blood-brain barrier that occurs with rising hypertension, causing fluid/blood product extravasation into brain parenchyma, or (2) focal reactive vasoconstriction and local hypoperfusion, contributed to by endothelial dysfunction. 30424161: The results show that dextran in 20 kDa and 70 kDa can penetrate the podocyte membrane, whereas dextran in 500 kDa was blocked until DeltaP >= 60 mmHg, which resembles the filtration function when DeltaP was in the range of a healthy kidney (DeltaP < 60 mmHg) as well as the hypertension-induced glomerular leakage (DeltaP >= 60 mmHg). 32078435: Inhibition of SREBP1 or VEGF-VEGFR2 signaling attenuates both Dll4 blockade-driven and hypertension-induced retinal leakage. 32765949: The latter might be the result of atherosclerosis, amyloid angiopathy, microbleeding and micro-strokes, together causing blood-brain barrier (BBB) dysfunction and vessel leakage, collectively originating from the consequence of hypertension, one of the main risk factors for VaD. 33307553: Dysfunctional tumor vasculature leads to the extravasation of blood to the interstitial space, hindering proper perfusion and causing interstitial hypertension. 33862471: The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). 34549626: Data indicated that within the PVN the transcytosis is the main mechanism governing both hypertension-induced BBB leakage as well as the exercise-induced correction. 36793787: Discussion: We conclude that endothelial cell TRPA1 channel activity increases cerebral blood flow during hypertension resulting in increased extravasation of blood during intracerebral hemorrhage events; however, this effect does not impact overall survival. 37533255: In the present study, histological analysis of human kidney samples revealed that hypertension induced mtDNA leakage and promoted the expression of stimulator of interferon genes (STING) in renal epithelial cells. 38239713: We hypothesized that genetic polymorphisms of junctional adhesion molecule-A (JAM-A) (which may result in compromised structure of tight junction proteins that form the BBB) in combination with cerebrovascular risk factors hypertension, lipid disorders, and type 2 diabetes may result in BBB leakage and increase the individual's risk of CSVD-related dementia. 16263593: CONCLUSION: We speculate that the model of pregnant SHR closely simulate human IUGR caused by hypertension in pregnancy and should enable investigation of mechanisms of hypertension-mediated placenta-vascular injury as well as provide a system for preclinical evaluations of future preventive neuroprotective treatments. 18696353: Hypertension is probably the most serious major complication that can develop, possibly leading to intrauterine growth retardation, maternal heart failure, and fetal haemorrhage. 2230413: Lupus nephropathy accompanied by diminished serum complement (CH50) and a rise in antibodies against dsDNA is a frequent clinical problem during pregnancy, which represents the adverse effect of hypertension or superimposed toxemia and causes fetal death or intrauterine fetal growth retardation. 25645738: In developed countries, chronic maternal diseases like hypertension, diabetes mellitus, renal disease or collagen vascular disease is the most common cause of intrauterine growth restriction (IUGR). 26655437: Hypertension is a common gestational complication, which can lead to foetal growth restriction (IUGR) and even to foetal or maternal death. 26974824: PE-associated pathologies, including thrombosis, hypertension, and impaired placental development, may result from imbalances between thromboxane A2 (TXA2) and prostacyclin. Preeclampsia (PE) is a potentially fatal pregnancy-related hypertensive disorder characterized by poor placenta development that can cause fetal growth restriction. 30660016: Blood pressure of 12-year-old children born after foetal growth restriction due to hypertensive disorders of pregnancy; relation to neonatal, life style, and family characteristics. 33140325: Hypertension and smoking may lead to FGR in different pathways as the two groups significantly differed in maternal characteristics, placental pathology, ultrasound findings, and neonatal outcomes. 34544755: Using a mouse model of the most common cause of IUGR, induced by hypertensive disease of pregnancy, we first assessed adult learning and memory function. 36635411: Preeclampsia is a hypertensive disorder of major concern in pregnancy than can lead to intrauterine growth restriction, placental abruption and stillbirth. 37062283: BACKGROUND: Hypertensive disorders of pregnancy cause fetal growth restriction and increased maternal morbidity and mortality, especially in women of African ancestry. 7072771: If hypertension causes intrauterine growth retardation only by means of reduced placental blood flow, this reduction in flow obviously must be considerable. 8937119: From this study, we conclude that measurement of uterine and fetal blood flow waveforms by pulsed Doppler ultrasonography is useful to assess fetal well-being in IUGR caused by hypertension during pregnancy. 9101251: Preeclampsia is a hypertensive disorder of human pregnancy that is a leading cause of premature delivery and fetal growth retardation. 9859861: Pre-eclampsia is a hypertensive disorder of human pregnancy that is a leading cause of premature delivery and fetal growth retardation. 10985691: These findings suggest that dysfunction of blood flow regulation due to increased arterial stiffness caused by hypertension-induced intimal fibrosis and loss of medial SMCs is an essential mechanism resulting in diffuse myelin loss of the cerebral white matter in BE, whereas luminal stenosis or occlusion and adventitial fibrosis are secondary. 1248080: Comparing those patients having severe (13), mild (10), or no (24) PSS myocardial lesions, and patent extramural coronary arteries, there were no major differences in age, sex, frequency and severity of pulmonary, renal or hypertensive disease which could account for the myocardial necrosis and fibrosis. 14581293: In the present study, we tested the hypothesis that Ac-SDKP reversal of hypertension-induced cardiac fibrosis involves a decrease in transforming growth factor-beta (TGF-beta) and/or connective tissue growth factor (CTGF). 15344302: A common pathophysiological mechanism for arrhythmia development is atrial distention and fibrosis induced by hypertension, coronary artery disease or ventricular dysfunction. 16043882: Hearts of normotensive angiotensin II type 2 receptor (AT2)-deficient mice do not develop fibrosis after angiotensin II-induced chronic hypertension. Thus, hypertension-induced fibrosis is probably triggered by other control mechanisms than fibrosis induced by MI. 16679404: Subendocardial fibrosis and impairment of subendocardial perfusion due to hypertension might change the transmural distribution of contractile myofiber function. 18178715: N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a tetrapeptide specifically degraded by angiotensin converting enzyme (ACE), reduces inflammation, fibrosis, and TOD induced by HBP. 18490734: Hypertension-induced cardiovascular hypertrophy and fibrosis are critical in the development of heart failure. We wondered whether vaccine bacillus Calmette-Guerin (BCG), which activated TLR4 to elicit immune responses, modulated the pressure overload-stimulated cardiovascular hypertrophy and cardiac fibrosis in the murine models of abdominal aortic constriction (AAC)-induced hypertension. 18793165: Elevated blood glucose over long periods together with glomerular hypertension leads to progressive glomerulosclerosis and tubulointerstitial fibrosis in susceptible individuals. 18948553: Chronic intake of a phytochemical-enriched diet reduces cardiac fibrosis and diastolic dysfunction caused by prolonged salt-sensitive hypertension. 19628782: CONCLUSIONS: MCPs partly mediate myocardial inflammation, fibrosis, vascular remodeling, and impaired vascular integrity induced by hypertension. 20542874: AIMS: Innate and adaptive immune responses are associated with the development of hypertension-induced myocardial hypertrophy and fibrosis. As a result, we investigated whether heat shock protein (HSP) 70, which is a molecule of damage-associated molecular patterns, could induce inflammation in the myocardium and promote the development of hypertension-induced cardiac hypertrophy and fibrosis. 20696682: OBJECTIVE: Hypertension may lead to left ventricular hypertrophy, fibrosis and degeneration of the conduction system. 21148624: Angiotensin-converting enzyme 2 activation protects against hypertension-induced cardiac fibrosis involving extracellular signal-regulated kinases. 21406596: CONCLUSION: We confirmed a positive effect of hemin on oxidative cardiac damage, apoptosis, and fibrosis induced by hypertension by modulating the NADPH oxidase activation through enhanced expression of the PI3K p85 regulatory subunit. 21530504: This study was designed to explore the role of IL-17 RA PLAD in hypertension-induced cardiac fibrosis. BACKGROUND: Hypertension causes cardiac fibrosis characterized by low-grade inflammation. 21610512: On the other hand, hypertension-induced fibrosis as well as macrophage infiltration in the heart was profoundly enhanced in PAI-1 mice. 22467306: Chronic ANG-(1-7) treatment significantly attenuated increases in myocyte diameter and cardiac fibrosis induced by hypertension in only trained 2K1C rats. 22556333: We investigated this process of regulating hypertension-induced cardiac fibrosis. 22681982: In order to explore this, we used RenTgKC mice overexpressing renin into the liver, leading to an increased plasma angiotensin II and thus induction of severe hypertension, and AS mice overexpressing aldosterone synthase (AS) in cardiomyocytes which have a doubled intracardiac aldosterone concentration. [Hypertension-induced fibrosis: a balance story]. 23032152: However, in situations of chronic injury or damage 5-HT signaling can have deleterious effects and promote aberrant wound healing resulting in tissue fibrosis and impaired organ regeneration. 23533637: Cardiac fibrosis is a deleterious consequence of hypertension which may further advance to heart failure and increased matrix metalloproteinase-9 (MMP-9) contributes to the underlying mechanism. 23615214: Lowering profilin-1 expression in SHRs significantly attenuated hypertension-induced cardiac hypertrophy and fibrosis and displayed a significant preservation of myofibrils, sarcolemmal caveolae, abundance of caveolin-3 protein, activity of eNOS and production of nitric oxide (NO). 23778187: BACKGROUND: Hypertension induces cardiovascular hypertrophy and fibrosis. 23887740: Inhibition of platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis. Taken together, our results indicate Ang II infusion-induced hypertension stimulated platelet activation and platelet-leukocyte conjugation, which initiated inflammatory responses that contributed to cardiac fibrosis. Inflammation promotes the development of cardiac fibrosis and heart failure induced by hypertension. 23942950: Pro-inflammatory role of platelets in hypertension-mediated end-organ damage : Editorial to: \Inhibition of Platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis\ by L.-X. 24171042: Treatment with SQ ameliorates cardial fibrosis induced by hypertension by attenuating the upregulation of ICAM-1, TNF- alpha , MCP-1, TGF- beta , Smad-3, P65, and P50 expression and improving PPAR alpha and PPAR gamma expression level. 24855831: Left ventricular (LV) fibrosis is one of the most prominent pathophysiological results of hypertension. 24899409: Moreover, pharmacological agents for the prophylaxis and treatment of hypertension-induced fibrosis in other organs may also be useful for keloids/HSs. 25308856: To investigate whether inhibition of miR-29a functioning prevents the hypertension-induced ventricular hypertrophy and fibrosis. 26063669: Prolonged hypertension led to increased cardiac stiffness, cardiac fibrosis, and thrombi formation. 27121797: The results from the present study suggest that activated platelets secrete P-selectin to promote cardiac inflammation and fibrosis in Ang II-induced hypertension. Platelet activation is important in hypertension-induced cardiac inflammation and fibrosis. 27349663: Complex diseases always involve some strait episode, such as myocardial hypertrophy and fibrosis caused by hypertension, microcirculation dysfunction and injury in heart, brain, lever, and intestine following ischemia and reperfusion, endotoxin induced multiorgan injury, and recovery after intestinal mucosa damage, for which intervention by a single medicine remains unsatisfied in clinic. 28336948: Our findings indicate that PAI-1 protects mice from hypertension-induced cardiac fibrosis by inhibiting the generation of active Pm. 28522072: It is either primary, related to myocardial inflammation and fibrosis, or secondary, due to pulmonary arterial hypertension (SSc-PAH) or systemic hypertension, in those patients with renal involvement. 28986310: Recently, a highly selective SGK1 inhibitor, EMD638683, was developed, though whether EMD638683 can prevent hypertension-induced cardiac fibrosis and the mechanisms by which this inhibitor may alter the disease process remain unknown. Using a murine Angiotension II (Ang II) infusion-induced hypertension model we found that EMD638683 treatment inhibited cardiac fibrosis and remodeling, with significant abatement of cardiac inflammation. 29671305: One of them?is hypertension induced left ventricular?hypertrophy and fibrosis, progressive?deterioration of left ventricular compliance,?increase in left ventricular enddiastolic?pressure which in turn lead to?left ventricular diastolic dysfunction.?The other pathomechanism of heart?failure associated to hypertension is?accelerated coronary artery atherosclerosis,?ischemia of the left ventricle?and its systolic dysfunction. Natural history of?hypertension leads to heart failure in?two main mechanisms. 30352200: Here, we detected the down-regulation of CGRP concomitant with senescence in fibrotic myocardium, both hypertension- induced left ventricular fibrosis in SHR rats and hypoxia-induced right ventricular fibrosis in pulmonary artery hypertension rats. 30541573: So, integrin alphanubeta5 might be considered a novel therapeutic target and cilengitide an effective pharmacological tool to limit the progression of hypertension-induced cardiac fibrosis. 30710427: Most importantly, we identify the efficacies of ATp300 inhibitors C646 and L002 in reversing hypertension-induced cardiac hypertrophy and fibrosis, and discover new anti-hypertrophic and anti-fibrotic candidates. Previously, we reported that acetyltransferase p300 (ATp300) inhibitor L002 prevents hypertension-induced cardiac hypertrophy and fibrosis in a murine model. Acetyltransferase p300 inhibitor reverses hypertension-induced cardiac fibrosis. In this short communication, we show that treatment of hypertensive mice with ATp300-specific small molecule inhibitor L002 or C646 reverses hypertension-induced left ventricular hypertrophy, cardiac fibrosis and diastolic dysfunction, without reducing elevated blood pressures. 31059021: Cardiac fibrosis secondary to long-term hypertension is known to promote cardiac dysfunction; however, few therapeutic agents are available for the treatment of this condition in clinical practice. Alamandine attenuates long-term hypertension-induced cardiac fibrosis independent of blood pressure. Collectively, the findings of the present study suggest that Ala is an effective anti-hypertensive peptide that can attenuate cardiac dysfunction and fibrosis induced by chronic hypertension, independent of BP. In the present study, the potential therapeutic effects of Ala on long-term hypertension-induced cardiac fibrosis were investigated in an aged, spontaneous hypertensive rat model. 31740371: CONCLUSIONS: Heart failure-related lung congestion was prevented when ACE-I was administered soon after LS impairment, accompanied by suppression of cardiac hypertrophy and fibrosis, thereby suggesting that the point of no return of myocardial remodeling due to hypertension was present after LS but before CS impairment. 32896627: Leech extract: a candidate cardioprotective against hypertension-induced cardiac hypertrophy and fibrosis. Leech extract: a candidate cardioprotective against hypertension-induced cardiac hypertrophy and fibrosis.ETHNOPHARMACOLOGICAL RELEVANCE: The prevalence of cardiovascular diseases (CVDs) has been increasing worldwide. Our findings imply that medicinal leach extract may be effective against hypertension-induced cardiac hypertrophy and fibrosis. 33175633: Whether hypertension-induced atrial fibrosis is mediated by platelets remains unknown. 35356999: Persistent arterial hypertension leads to structural and functional remodeling of the heart resulting in myocardial ischemia, fibrosis, hypertrophy, and eventually heart failure. 35370704: Dahl salt-sensitive (DSS) rats fed with a diet containing 8% NaCl AIN-76A developed left ventricular remodeling and diastolic dysfunction caused by hypertension. Conclusion: CANA can improve myocardial hypertrophy, fibrosis, and left ventricular diastolic dysfunction induced by hypertension in DSS rats, possibly through the activation of the AMPK/SIRT1/PGC-1a pathway to regulate energy metabolism and oxidative stress. 36206854: In this study, we investigated whether EPA mitigates the exacerbation of cardiac remodeling and fibrosis induced by established hypertension, a situation that closely recapitulates a clinical scenario. 3661718: To test the hypothesis that IHH may cause urinary sodium retention early in cirrhosis, we prepared cirrhotic dogs (chronic biliary obstruction) who underwent simultaneous hepatic denervation with end-side portacaval anastomoses. 36883469: However, its role in hypertension-induced renal inflammation and fibrosis remains unexplored. 37273847: Hypertension-induced inflammation and subsequent ventricular fibrosis are believed to underlie the development of HFpEF. 37348478: The aim of this study was to investigate the potential molecular mechanisms underlying the protective role of acacetin on hypertension-induced fibrosis in the heart. 37692038: Objectives: Arterial hypertension is associated with the triggering of the renin-angiotensin system, leading to left ventricle fibrosis and worse cardiovascular outcomes. 38019188: As an independent risk factor of atrial fibrillation (AF), hypertension (HTN) can induce atrial fibrosis through cyclic stretch and hydrostatic pressure. 8178541: Arterial hypertension causes myocardial hypertrophy and fibrosis, and affects coronary microcirculation by structural and functional changes of the small intramural resistance arteries, rarefiction of arterioles and capillaries and a distinct disturbance of endothelial vasomotion (i.e. 9532007: In the first 6 days, hypertension is not the only cause of fibrosis; the same level of adventitial fibrosis is detected in the nonhypertensive clipped kidney. 10981136: In hypertension, the increase in matrix deposition results in vascular stiffness and cardiac dysfunction. 11429340: Anesthesia for patients with Takayasu's arteritis is complicated by their severe uncontrolled hypertension, end-organ dysfunction resulting from hypertension, stenosis of major blood vessels affecting regional circulation, and difficulties encountered in monitoring arterial blood pressure. 11972549: Multiple organ dysfunction attributable to intra-abdominal hypertension has been called the abdominal compartment syndrome. Intra-abdominal hypertension did not necessarily lead to abdominal compartment syndrome, and often resolved without clinical sequelae. 12177607: CONCLUSIONS: An experimental model is presented that examines the influence of recipient hypertension in the pathogenesis of chronic dysfunction and injury developing in rat renal allografts over time. 12208718: Venous congestion and hypertension seem to cause the clinical dysfunction in this disorder. 12777568: The fetal pathophysiology of midaortic syndrome remains speculative, but likely includes fetal hypertension as the cause of cardiac dysfunction. 14566078: In hypertension quinapril, in spite of lowering of arterial blood pressure, is unable to display its beneficial effects on RBC aggregability possibly due to the hypertension-induced/accompanied dysfunction of vascular endothelium. 14758472: OBJECTIVE: Although intra-abdominal hypertension (IAH) can cause dysfunction of several organs and raise mortality, little information is available on the incidence and risk factors for IAH in critically ill patients. 15563577: We hypothesized that the greater number of high-blood pressure episodes associated with enhanced blood pressure variability causes cardiac hypertrophy and dysfunction by activation of mechanosensitive and autocrine pathways. 15694697: High-glycemic index nutrition is suggested to play a key role in the etiology of hypertension: The chronic stimulus of pancreatic beta-cells due to high-glycemic index nutrition may cause cell hypertrophy and dysfunction, resulting in postprandial hyperinsulinemia, and -- in susceptible subjects -- the development of EH. 15754152: Microvascular dysfunction may be secondary to hypertension, cardiomyopathy, infiltrative disease, valvular disease, or idiopathic. 16335185: Results demonstrated that the members, despite partially know renal physiopathology, they don't mean it as a consequence of high blood pressure. 16647348: PURPOSE: Renal allograft compartment syndrome (RACS) is early graft dysfunction secondary to retroperitoneal hypertension and resultant ischemia. 16788004: Thus our objective in the present study was to determine whether ACE2 gene transfer could decrease high blood pressure (BP) and would improve cardiac dysfunctions induced by hypertension in the spontaneously hypertensive rat (SHR) model. 17251496: CONCLUSIONS: These findings suggest that hypertension induces retinal dysfunction that is exacerbated with diabetes and ameliorated by treatment with an AT1-RB, and not just by normalizing BP. 17469698: INTRODUCTION: Intraabdominal hypertension (IAH) is increasingly appreciated by intensivists as an important cause of organ dysfunction, even at pressure levels which were previously thought to be harmless. 17469709: INTRODUCTION: Increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) is a cause of organ dysfunction in critically ill patients and is independently associated with mortality. The kidneys seem to be especially vulnerable to IAH induced dysfunction and renal failure is one of the most consistently described organ dysfunctions associated with IAH. CONCLUSION: IAH can cause renal dysfunction. 17469719: INTRODUCTION: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are increasingly recognised to be a contributing cause of organ dysfunction and mortality in critically ill patients. 17576536: MEASUREMENTS AND MAIN RESULTS: Prolonged IAH induced significant cardiopulmonary dysfunction and persistent abdominal organ injury. 18408835: CONCLUSIONS: The hypertensive patients presented significantly smaller oscillatory index than the normotensives, suggesting that arterial hypertension might cause dysfunction of the internal retina. 18487446: Hypertension induced by high-salt diet in Dahl salt-sensitive rats leads to compensatory cardiac hypertrophy by approximately 11 wk, cardiac dysfunction at approximately 17 wk, and death from cardiac dysfunction at approximately 21 wk. Alteration of gene expression during progression of hypertension-induced cardiac dysfunction in rats. 18577845: These results indicate that LV hypertrophy and dysfunction due to hypertension are more apparent in patients with cerebral hemorrhage than in those with cerebral infarction. Left ventricular (LV) hypertrophy and dysfunction due to hypertension have been established as risk markers for stroke in hypertensive patients. 19124682: We showed that a novel small molecule inhibitor of plasma kallikrein, 1-benzyl-1H-pyrazole-4-carboxylic acid 4-carbamimidoyl-benzylamide, delivered systemically via a subcutaneous pump, decreased Ang II-stimulated RVP by 70% (P<0.05) and ameliorates Ang II-induced hypertension, measured from the carotid artery by telemetry, but did not reduce Ang II-induced retinal leukostasis. These findings demonstrate that activation of the Ang II type 1 receptor increases RVP and suggest that systemic plasma kallikrein inhibition may provide a new therapeutic approach for ameliorating blood-retinal barrier dysfunction induced by hypertension. We investigated the effects of the Ang II type 1 receptor antagonist candesartan on retinal vascular permeability (RVP) in normotensive rats with streptozotocin-induced diabetes mellitus and in rats with Ang II-induced hypertension. 19332966: Hypertension and hyperglycemia directly damage the microvasculature, leading to small vessel dysfunction that manifests as the clinical disease states of diabetic retinopathy and nephropathy. 19770407: Our data demonstrate that biomechanical stress evoked by high blood pressure triggers an integrin-linked kinase 1/betaPIX/Rac-1 signaling, thus generating oxidative vascular dysfunction. 20156423: In spontaneously hypertensive rats (SHR) chronic hypertension may induce BBB dysfunction and pronounced defects in the integrity of the blood-CSF barrier. 20491359: INTRODUCTION: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) have been identified as a cause of organ dysfunction and mortality in critically ill patients. 20640215: Anaesthetising a child with Takayasu's arteritis for auto renal transplantation is a challenge as it is complicated by severe uncontrolled hypertension, end-organ dysfunction resulting from hypertension, stenosis of major blood vessels affecting regional circulation, and difficulties encountered in monitoring arterial blood pressure. 21233798: BACKGROUND: Hypertension (HTN) may lead to left ventricular hypertrophy and vascular dysfunction, which are independent factors for adverse cardiovascular outcomes. 21291889: There is ample evidence that regular exercise exerts beneficial effects on left ventricular (LV) hypertrophy, remodeling and dysfunction produced by ischemic heart disease or systemic hypertension. 21601166: Stroke patients of SVO are at higher risks of cardiac abnormalities, which might suggest an early cardiac dysfunction because of long-term hypertension. 21944444: It is remarkable to consider that two decades ago, IAH, the detrimental physiological effects of elevated IAP and ACS, the development of IAH-induced organ dysfunction and failure were essentially unrecognized as causes of morbidity and mortality among critically ill adult and pediatric patients. 22314211: Abdominal compartment syndrome (ACS) is defined as an organ dysfunction caused by intra-abdominal hypertension (IAH). 22731503: This study has been designed to investigate the role of phosphatidyl-inositol 3-kinase-gamma (PI3Kgamma) in deoxycorticosterone acetate salt (DOCA) hypertension induced vascular endothelium dysfunction. Wistar rats were uninephrectomised and DOCA (40 mg.(kg body mass)(-1), subcutaneous injection) was administered twice weekly for 6 weeks to produce hypertension. 22967989: Vascular remodeling-associated hypertension leads to left ventricular hypertrophy and contractile dysfunction in profilin-1 transgenic mice. 23127917: The present study aimed to investigate the protective effects of Ang-(1-7) on the physiopathologic changes caused by hypertension in brain of spontaneously hypertensive rats (SHRs). 23254193: These results show that cardiac remodeling induced by hypertension during pregnancy are improved in the postpartum period except fibrosis, whereas lactation induces cardiac contractile dysfunction in mice with a history of pregnancy-associated hypertension. 23608621: The significant increase of Nt-pro-BNP in response to high levels of IAP may reflect left ventricular strain and dysfunction due to the severe IAH and provide an alternative marker in the monitoring of IAH. 23881298: In this mini-review, we will highlight the role of immune regulatory T cells in hypertension-induced vascular dysfunction. 23944615: PURPOSE: Intra-abdominal hypertension (IAH) causes lung dysfunction in patients after hemorrhagic shock resuscitation. 24012160: BACKGROUND: Hypertension induces cardiac dysfunction, calcium (Ca(2+)) dysregulation, and arrhythmogenesis. 24238726: INTRODUCTION: Intra-abdominal hypertension is defined as a rise in intra-abdominal pressure leading to progressive dysfunction of the abdominal organs. 24500073: For more than 40 years, coronary artery disease and hypertension have been considered as the main causes of diabetes-related cardiac dysfunction. 24629670: We surmise that HT promotes aberrant regulation of cardiac Ca(2+), Cu(2+), Mg(2+) and Zn(2+), which does not necessarily result in cardiac dysfunction. The spontaneously hypertensive rat (SHR) has been studied extensively as a model of left ventricular hypertrophy (LVH) and associated cardiac dysfunction due to hypertension (HT). 24661554: In the present study, we investigated the development of hypertension in prenatally undernourished adult rats, including the mechanisms that culminate in dysfunctions of molecular signalling in the kidney. 24683264: BACKGROUND: Abdominal compartment syndrome (ACS) refers to organ dysfunction and ischemia resulting from intra-abdominal hypertension (IAH). 24727889: Aortic stiffening and arteriolar remodeling due to hypertension not only augment the central pressure by increasing the wave reflection but also may alter the central bidirectional flow, inducing hemodynamic damage/dysfunction in susceptible organs. 24740341: This phenomenon is similar to the well-described abdominal compartment syndrome, which is defined as new onset organ dysfunction or failure secondary to sustained intraabdominal hypertension and in which decompression is the standard treatment. 24881697: INTRODUCTION: Intraabdominal hypertension (IAH) is increasingly appreciated by intensivists as an important cause of organ dysfunction, even at pressure levels which were previously thought to be harmless. 24881708: INTRODUCTION: Increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) is a cause of organ dysfunction in critically ill patients and is independently associated with mortality. The kidneys seem to be especially vulnerable to IAH induced dysfunction and renal failure is one of the most consistently described organ dysfunctions associated with IAH. CONCLUSION: IAH can cause renal dysfunction. 24881718: INTRODUCTION: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are increasingly recognised to be a contributing cause of organ dysfunction and mortality in critically ill patients. 25224866: We found that increased changes in MBPS values in patients with prehypertension and Stage 1 hypertension seemed to cause microvascular dysfunction in the absence of obstructive coronary artery disease. 25437599: Renal allograft compartment syndrome (RACS) is graft dysfunction secondary to intracompartment hypertension. 25485905: These processes may contribute to the pathogenesis of hypertension-induced vascular dysfunction and organ injury. 25653998: INTRODUCTION: It is being increasingly recognized that intra-abdominal hypertension is an important cause of organ dysfunction. 26183483: The influence of long-term exercise on vascular dysfunction caused by hypertension remains unclear. 26273457: Organ dysfunctions caused by intraabdominal hypertension is named as abdominal compartment syndrome (ACS). 26708424: Hypertension causes cardiac hypertrophy, cardiac dysfunction and heart failure (HF). 26890576: A major cause of heart disease is the massive loss or dysfunction of cardiomyocytes caused by myocardial infarctions and hypertension. 26968123: BACKGROUND INFORMATION: Atherosclerosis is an inflammatory disease, in which risk factors such as hyperlipidemia and hypertension affect the arterial endothelium, resulting in dysfunction, cell damage or both. 27056: Reversibility of the blood-brain barrier dysfunction induced by acute hypertension. 27193439: L-NAME administration for 6 weeks elicited a significant increase in blood pressure which was corrected with MgO treatment; thereby cardiac hypertrophy developing secondary to hypertension was prevented. Hypertension significantly decreased the fractional shortening with slowing of shortening kinetics in left ventricular myocytes whereas magnesium treatment was capable of restoring hypertension-induced contractile dysfunction. 27432865: We revealed that GAS5 knockdown aggravated hypertension-induced microvascular dysfunction as shown by increased retinal neovascularization and capillary leakage. 27667708: While many systems contribute to blood pressure (BP) elevation, the vascular system is particularly important because vascular dysfunction is a cause and consequence of hypertension. 27841763: Hypertension disrupts these vital regulatory mechanisms, leading to the neuronal dysfunction and damage underlying cognitive impairment. 27903516: The maternal endothelium is targeted by placental and adipose tissue-derived factors like sFlt-1 and TNF-alpha that promote hypertension during pregnancy, resulting in vascular dysfunction and hypertension. 27924224: IAH-induced dysfunction of intestinal barriers is closely associated with oxidative imbalances, which are considered to provide a pathophysiological basis for subsequent gut-derived sepsis. Our results demonstrated that, to combat IAH-induced dysfunction of intestinal barriers, MICU1 undergoes a compensatory increase in expression, whereas 'mitochondrial calcium uniporter' (MCU) - a conserved Ca2+ transporter - becomes transcriptionally suppressed. 28041700: BACKGROUND: Hypertension-induced cardiac dysfunction is variable among different anti-hypertensive medications. 28293100: BACKGROUND: This work evaluated the hypothesis that 3,4-methylenedioxybenzoyl-2-thienylhydrazone (LASSBio-294), an agonist of adenosine A2A receptor, could be beneficial for preventing cardiac dysfunction due to hypertension associated with myocardial infarction (MI). 28374979: Matrix Metalloproteinase-2 Activity is Associated with Divergent Regulation of Calponin-1 in Conductance and Resistance Arteries in Hypertension-induced Early Vascular Dysfunction and Remodelling. 28429469: Older age, high weight, hypertension, and moderate kidney dysfunction might thus lead to peripheral nerve dysfunction in persons yet without symptoms or signs of polyneuropathy. 28703719: SSA patients may also suffer from cachexia and organ dysfunction resulting from tuberculosis, hepatitis B, and hypertension. 29309745: In conclusion, hypertension sustained for 4 weeks causes ophthalmic vascular dysfunction, retinal glial cell activation, oxidative stress, and neuroretinal impairment. 29337396: We evaluated whether aging and hypertension, which induce NO-related dilating dysfunction, are associated with decreased vascular GGT activity and modify the vasorelaxant effect of GSNO. 29357124: Pathophysiological situations, such as obesity, diabetes or hypertension, induce changes in its amount and in the expression pattern of vasoactive factors leading to a PVAT dysfunction in which the beneficial paracrine influence of PVAT is shifted to a pro-oxidant, proinflammatory, contractile, and trophic environment leading to functional and structural cardiovascular alterations and cardiovascular disease. 29505770: One example is long-standing hypertension leading to maternal cardiac dysfunction. 29788246: Hypertension-induced vascular dysfunction may present itself as a contributing, or consequential factor, to vascular remodeling caused by chronically elevated systemic arterial blood pressure. 29850631: Inflammasome infiltration has been identified to play a central role in the pathological progression of certain cardiovascular diseases, such as vascular damage spanning atherosclerosis, aneurysm, or arteritis; ischemic heart disease; and other nonischemic heart diseases including diabetic cardiomyopathy, chronic heart failure, and hypertension- or virus-induced cardiac dysfunction. 29981304: BACKGROUND: Hypertension promotes cardiac hypertrophy which finally leads to cardiac dysfunction. 30010004: CONCLUSIONS: Our data support an association between hypertension-induced vascular dysfunction and the sporadic occurrence of phosphorylated tau and cell death in the rat model, correlating with patient brain atrophy, which is relevant to vascular disease. 30276533: The main aim of the treatment of hypertensive crisis is the prevention or treatment of life-threatening complications of hypertension-induced organ dysfunction, including neurologic, ophthalmologic, renal, and cardiac complications. 30414897: We previously reported that CD4+CD25+ T regulatory cells (Treg) play an important preventive role in hypertension-induced vascular dysfunction. 30458302: ERS inhibition in DOCA-salt induced hypertension was observed to have reduced systolic blood pressure, improved endothelial dysfunction, enhanced plasma nitric oxide (NO) level, reduced protein expressions of phosphorylated-double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase (pPERK), 78 kDa glucose-regulated protein (GRP78), Inositol trisphosphate receptor1 (IP3R1) and Epidermal growth factor receptor (EGFR), increased expressions of endoplasmic reticulum Ca2+-ATPase2 (SERCA2) and B cell lymphoma2 (Bcl2) in vessels. Inhibition of endoplasmic reticulum stress protected DOCA-salt hypertension-induced vascular dysfunction. 3260581: Thus, a high K diet appears to protect the aortic endothelium from a hypertension-induced dysfunction. 7546504: Hypertension-induced dysfunction of circulation in hemorrhagic shock. 8252595: CONCLUSIONS: Genetically determined hypertension in combination with anaemia results in eccentric ventricular hypertrophy and cardiac dysfunction in spite of an increase in capillary luminal volume and limited structural damage. 10816725: PATHOPHYSIOLOGY: All these observations taken together suggest that activation of the RAS, which is necessary in certain circumstances to maintain glomerular filtration and tissue perfusion, can have a long-term deleterious effect on the heart, vessels, and kidneys, especially through glomerular hypertension which can lead to glomerulosclerosis. 12107734: Our data could also be relevant for e.g. hypertension-induced glomerulosclerosis. 1343284: By slowing mesangial cell proliferation, calcium antagonists also may slow the progression of hypertension-induced glomerular sclerosis. 1418851: Mechanisms involved in the progression to glomerular sclerosis induced by systemic hypertension during mild puromycin aminonucleoside nephrosis. 18701613: In addition, seven biopsies had underlying diabetic glomerulosclerosis and two had glomerulosclerosis attributable to obesity and hypertension. 1877649: Glomerular hypertension may be a key factor in the genesis of GS in this model in association with endothelial injury, intracapillary coagulation, and lipid accumulation. 18793165: Elevated blood glucose over long periods together with glomerular hypertension leads to progressive glomerulosclerosis and tubulointerstitial fibrosis in susceptible individuals. 1893609: Up to now, the pathogenetic mechanism underlying the development of glomerulosclerosis due to systemic hypertension has not completely been resolved. Basing on these results we presume that glomerular protein accumulation and concomitant glomerulosclerosis due to systemic hypertension might be a result of a synergistical interaction between hemodynamic factors and biochemical ones; we suggest one of the latter to be a decreased glomerular proteinase activity. 1928071: It has been proposed that once functioning renal mass has been reduced below a critical level, either as the result of disease, congenital absence of a kidney, or surgical ablation, that hyperfiltration and glomerular hypertension lead to progressive glomerular sclerosis and end-stage renal failure. 21136910: Diabetes mellitus and hypertension are the main causes of glomerulosclerosis and albuminuria in adults. 27070919: Matrix remodeling is a key feature of glomerulosclerosis secondary to diabetes or hypertension. 27558173: Glomerular hypertension is an important factor exacerbating glomerular diseases to end-stage renal diseases because, ultimately, it results in glomerular sclerosis (especially in hypertensive and diabetic nephropathy). The precise mechanism of glomerular sclerosis caused by glomerular hypertension is unclear, due partly to the absence of suitable in vitro or in vivo models capable of mimicking and regulating the complex mechanical forces and/or organ-level disease processes. 31822592: Our data revealed the metabolic aspects of hypertension-induced glomerular sclerosis, including lipid breakdown at early disease stages and activation of anaplerotic pathways to regenerate energy equivalents to counter stress. Overall, multilayered omics provides an overview of hypertensive kidney damage and suggests that metabolic or dietary interventions could prevent and treat glomerular disease and hypertension-induced nephropathy. 7756590: Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. 11903310: It has been suggested that the hypertension is due to induced growth in systemic resistance vessel walls by the AngII infusions. 17291198: To investigate whether substrate utilization influences cardiac growth and CHD risk, we examined the association between the functional LPL S447X (rs328) variant and hypertension-induced LV growth and CHD risk. The lipoprotein lipase gene serine 447 stop variant influences hypertension-induced left ventricular hypertrophy and risk of coronary heart disease. 1944790: Many cases of this long-term group were associated with hypertension or vascular abnormalities which would effect the aneurysmal growth. 23689903: CONCLUSION: Since chronic acidosis and hypertension associated with PHA-II can result in delayed growth and development in pediatric patients, genetic analysis to detect the CUL3 mutation and to enable intervention early in the disease course would be beneficial for infants with suspected PHA-II. 23753531: BACKGROUND: Hypertension or aortic stenosis causes pressure overload, which evokes hypertrophic myocardial growth. 28357400: Intra-Abdominal Hypertension Causes Bacterial Growth in Lungs: An Animal Study. 33677981: Chronic cardiac pressure overload, caused by conditions, such as hypertension, induces pathological hypertrophic growth of myocardium and vascular rarefaction, with largely unknown mechanisms. 36506065: One hypothesis is that changes in vascular supply to the adrenal cortex, due to phenomena of atherosclerosis or high blood pressure, may influence the morphology of the adrenal cortex, resulting in a compensatory growth and nodule formation in response to local hypoxia. 6295692: These studies suggest the participation of this nucleotide in the vascular growth induced by hypertension. 8494018: Interestingly, both hypertension and hyperlipidemia seem to evoke glomerular growth, a factor that has also been postulated to be involved in glomerular and tubular destruction. 1035833: Headaches due to psychic hypertension. 10759928: The most frequent etiologies of headaches secondary to systemic disorders were fever, acute hypertension, and sinusitis. 12131526: BACKGROUND: The notion that hypertension causes headache is widely accepted despite the absence of confirmation by well-designed studies. 13299645: [Headaches caused by hypertension]. 1360979: The most common chief complaints on admission were dyspnea, headache, palpitation, and edema which were due to hypertension and congestive heart failure. The majority of the patients required immediate medical treatment to control congestive heart failure due to hypertension at initial presentation. 16216977: The uncertainty over whether high blood pressure causes headache does not, however, detract from the practical benefits of the use of blood pressure-lowering drugs in preventing headaches and cardiovascular disease. This in turn indicates that high blood pressure is a cause of headache, but this conclusion is not supported by observational studies of blood pressure and headache. 16218388: Taking blood pressure is necessary, even though headache caused by hypertension is rare in children. 16450450: Could high blood pressure be causing your headache? 18259189: BACKGROUND: A 33-year-old woman was referred to the renal outpatient clinic with a headache caused by severe hypertension. 18402404: Headaches due to arterial hypertension, ENT problems or maxillofacial causes should not be forgotten. 18959167: Tension type headache (41% of those with headaches) and migraine without aura (10%) were most common in the primary headache group and headache due to arterial hypertension (7%) was the most prevalent among the secondary headaches. 21877593: The disease often presents with symptoms, such as headache and visual disturbances, resulting from arterial hypertension. 24907430: In Thai traditional medicine, leaves of Phyllanthus acidus (PA) have been used for many purposes including as an antihypertensive agent and to provide relief from a headache caused by hypertension. 2528790: The authors present the problem of vascular headache at children: headaches caused by high blood pressure, aneurysm and other intracranial vascular malformations of the intracranial venous sinuses thrombosis (here, the determining factors are the infectious and inflammatory factors). 25544906: This study describes a 26-year-old pregnant woman admitted with hypertension-induced headache. 26543560: One sibling presented with headache due to hypertension while the other two siblings were diagnosed with hypertension on a routine school check. 26703001: Of the medical conditions associated with pregnancy, hypothyroidism, anemia, and hypertension may have to be considered as possible causes of de novo headache. 28621587: We report a 14-year-old boy with recurrent episodes of headache caused by uncontrolled hypertension. 30900097: This fact makes difficult the clinical diagnosis of headache attributable to ICH in headache sufferers. 34148406: In Nepal, where hypertension is common and often untreated, we assessed the substance of this belief, hypothesising that, should hypertension be a significant cause of headache, a clear positive association between these disorders would exist. BACKGROUND: Hypertension and headache disorders are major contributors to public ill health, linked by a long-standing but questionable belief that hypertension is a conspicuous cause of headache. 35399063: The risk for obstructive sleep apnea was intermediate in 45.2% of the patients with hypertension-induced headache, but was lower in the majority of others. 35871790: The majority of secondary headaches are due to hypertensive disorders: preeclampsia-eclampsia, posterior reversible encephalopathy syndrome, and acute arterial hypertension. 37334325: In this report, we present a case of ES that presented with a constellation of neurological symptoms, including headache and visual disturbance, ultimately found to be due to cerebral sinus hypertension, exacerbated by certain movements, caused by an enlarged styloid process with calcification of the stylohyoid ligament, consistent with ES. 37637669: Hypertension was a rare cause of secondary headaches (2/26 patients). 3902676: Fenquizone showed also a significant decrease of symptoms (headache, dizziness) due to hypertension. 4387754: [The behavior of urinary elimination of catecholamines in headache caused by arterial hypertension]. 7606637: Headache may occasionally be caused by severe hypertension, which may also lead to the rare syndrome of acute hypertensive encephalopathy. 988703: Headaches due to psychic hypertension. 10551207: A greater proportion of women than men were aware of hypertension (19% v. 12%) and heredity (31% v. 17%) as major causes of heart disease. 10645696: Cerebrovascular disease (CVD) is the third leading cause of death in United States and hypertension is a leading cause of both stroke and heart disease. 11882568: Combined with the power of comparative genetics, these strategies will continue to improve the chances of finding candidate genes for cardiovascular traits such as susceptibility to heart diseases, hypertension, and hypertension-induced end-organ damage. 134136: Hypertension can be considered work-related and, therefore, compensable when it[occurs] causes cardiac disease in occupational groups for whom cardiac ailments are legislated as being work-incurred and in workers exposed to certain nitrate explosives. 15038235: Hypertension is the leading cause of heart disease in the United States. 15039815: Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. 15686326: Hypertension is a major cause of cardiac disease in patients on hemodialysis (HD) and is most commonly due to hypervolemia. 16227775: The devastating long-term consequences of high blood pressure include stroke, heart disease, atherosclerosis, renal disease, and other end-organ damage. 16429165: Hypertension is a leading cause of stroke, heart disease, and kidney failure. 19245692: BACKGROUND: Hypertension affects 29% of the adult U.S. population and is a leading cause of heart disease, stroke, and kidney failure. 21034543: CONCLUSIONS: Arrhythmia is the type of heart disease that has a highest incidence in patients with heart disease in pregnancy, while main types of heart disease that impair cardiac function are CHD and RHD; cardiac failure is more frequently caused by cardiopathy induced by hypertensive disorders complicating pregnancy and PPCM; impaired cardiac function increases perinatal morbidity; cardiac surgery before pregnancy could improve the cardiac function. RESULTS: In this study, main heart diseases in pregnancy were arrhythmia (n = 359, 31.4%), congenital heart disease (CHD; n = 291, 25.5%), and myocarditis and its sequelae (n = 284, 24.9%); based on the functional classification criteria of New York Heart Association (NYHA), more than half (n = 678, 59.4%) of patients were classified NYHA Class I; pregnant women in NHYA Class I-II (n = 951, 83.3%) commonly had arrhythmia, myocarditis and its sequelae, while those in NHYA Class III-IV (n = 191, 16.7%) mainly had CHD, rheumatic heart disease (RHD), cardiopathy induced by hypertensive disorders complicating pregnancy, and peripartum cardiomyopathy (PPCM). The incidence of cardiac failure in pregnant women with cardiopathy induced by hypertensive disorders complicating pregnancy and PPCM was relatively high, with a rate of 80% and 52.2%, respectively. 22096028: Interestingly, the pattern of dysregulation within the PGC-1 transcriptional regulatory circuit distinguishes the heart disease caused by hypertension from that caused by diabetes. 22701510: Hypertension is one of the major causes of heart cerebrovascular diseases. 23388090: Quantitative real-time polymerase chain reaction (PCR) analysis for a selected panel of miRNAs indicated that circulating levels of miR-16, miR-20b, miR-93, miR-106b, miR-223, and miR-423-5p were significantly increased in response to hypertension-induced heart failure, while this effect was blunted in response to treatment with antimiR-208a as well as an ACE inhibitor. The aim of this study is to determine if plasma miRNAs can be used as indicators of disease progression or therapeutic efficacy in hypertension-induced heart disease. Plasma microRNAs serve as biomarkers of therapeutic efficacy and disease progression in hypertension-induced heart failure. 2394006: The importance of hypertension in the pathogenesis of severe diabetic heart disease is discussed. 24139520: CONCLUSION: Hypertension is the leading cause of cardiac disease among the elderly in our setting, emphasizing the necessity to strengthen the preventive strategies against hypertension in Cameroon. 24600247: More than 60% reported that untreated hypertension may cause heart disease or stroke. 25211544: BACKGROUND: A national health objective is to reduce average U.S. sodium intake to 2,300 mg daily to help prevent high blood pressure, a major cause of heart disease and stroke. 25932893: Hypertension is a chronic condition that can lead to heart disease, stroke, and other diseases that can result in premature death. 25984322: METHODS: We studied heart samples from human organ donors: 10 healthy donors, 16 with hypertension, 23 with chronic alcohol consumption and 7 with other causes of cardiac disease. 26619661: Abstract Hypertension is the major cause of cardiovascular disease. Persistent hypertension leads to cardiovascular remodeling and resulted in heart diseases such as coronary artery disease, heart failure, and arrhythmia. 27072344: BACKGROUND: Hypertension is the leading cause for heart disease and stroke, for mortality and morbidity worldwide, and a high sodium-to-potassium intake ratio is considered a stronger risk factor for hypertension than sodium alone. 27842710: Hypertension is the most important preventable cause of heart disease and stroke worldwide. 28507654: BACKGROUND: More than half of all heart disease and stroke are attributable to hypertension, which is associated with approximately 10% of direct medical costs globally. 28634521: Background: Heart disease as a result of Hypertension is known to occur. 28906541: CONCLUSIONS: Hypertension affects millions of people in SSA and if left untreated, is a major cause of heart disease and stroke. 29042191: CONCLUSIONS: Hypertension affects millions of people in SSA and if left untreated, is a major cause of heart disease and stroke. 30168608: Significant correlations were found between ECD and mortality due to coronary heart disease (r = -0.39, P = 0.011), hypertension (r = -0.33, P = 0.033), and all-cause cardiac disease (r = -0.36, P = 0.019). 30395142: CONCLUSIONS: Hypertension affects millions of people in Africa and if left untreated is a major cause of heart disease, kidney disease and stroke. 30586432: CONCLUSION: Hypertension is the leading etiology of heart diseases in rural Tanzania. 31123838: PURPOSE OF REVIEW: Despite enhanced screening and therapeutic management, hypertension remains the most prevalent chronic disease in the United States and the leading cause of heart disease, chronic kidney disease, and stroke in both men and women. 32161893: These include hypertension that causes fatal cardiac disorders, such as angina pectoris, ischemic heart diseases, and myocardial infarction, and also cerebrovascular diseases; congestive heart failure; infective endocarditis, valvular diseases, and carrying pacemakers; and the use of antiplatelet and anticoagulant drugs that are commonly prescribed for patients who have experienced heart stroke. 32317757: Among them, hypertension is a leading cause for stroke, heart disease and kidney failure. 34269398: Current guidelines do not support the use of specific vasodilator treatment in group II - due to heart disease and group III-due to lung disease pulmonary hypertension, unless the patient presents with severe pulmonary hypertension (mean pulmonary artery pressure>35 mm Hg or cardiac index < 2.0 L/min) with right ventricular dysfunction and is treated in an expert center and preferably in the context of a randomized control trial. 34466545: CONCLUSION: The results of this study showed that using 2D conventional echocardiography as a noninvasive method if performed in prestigious centers can evaluate systolic and diastolic function Tissue Doppler parameters very well in the early stages of heart disease caused by HTN. 34527077: This research is aimed at studying the effect of Angelica sinensis polysaccharide (ASP) extracted from the Lixinshui prescription on cardiac disease induced by hypertension in rats. 35372607: CONCLUSION: Patients with heart disease caused by high blood pressure in Iran have poorer diet and physical activity compared to healthy people. 37995049: INTRODUCTION: Hypertension is the leading cause of heart disease in the world, and discontinuation or nonadherence of antihypertensive medication constitutes a significant global health concern. 38505582: Background: The incidence of hypertension is increasing significantly on a global scale, and it is considered the leading cause of heart disease and death. 7496053: Considerable evidence--both in experimental animal models and in humans--points to hypertension as of critical importance in the pathogenesis of severe diabetic heart disease. 8026350: Hypertension (38.1%) was the second most common cause of heart disease. 8705323: Elevated Lp(a) serum levels did not correlate with the stage of the heart ischemic disease and aortosclerosis, but they correlate with the stage of functional CNS defect due to arteriosclerosis and arterial hypertension, hence the increase in Lp(a) serum level as an indicator of arteriosclerotic evolution of cerebral arteries is significant. 9119541: Similar changes occur in other types of heart disease due to arterial hypertension or inflammation processes. 9301656: High blood pressure causes heart disease and remains a major public health issue. 9411586: Considerable evidence, both in experimental animal models and in humans, points to hypertension as of critical importance in the pathogenesis of severe diabetic heart disease. 9632091: Although hypertension and possibly amyloidosis were thought to be the cause of her cardiac disease, cardiac and skeletal muscle changes characteristic of chloroquine toxicity were observed. 9883063: Considerable evidence, both in experimental animal models and in humans, points to hypertension as being of critical importance in the pathogenesis of severe diabetic heart disease. 10081616: We studied the effects of BDF 9148 on the action potentials and contractions of left ventricles from 5-week-old prehypertensive, 14-week-old hypertensive, 6- and 12-month-old hypertension-associated hypertrophy and 18-month-old hypertension-induced heart failure SHR and age-matched Wistar-Kyoto normotensive (WKY) rats. 10193711: Heart failure is a clinical syndrome that is predominantly caused by cardiovascular disorders such as coronary heart disease and hypertension. 10228470: Hypertension and coronary heart disease are the main causes of heart failure. 10551712: CONCLUSIONS: Hypertension remains a common etiologic factor for the development of heart failure but was the primary cause of heart failure in a minority of study patients. Association of body mass, gender and race with heart failure primarily due to hypertension. 10652967: Patients with hypertension are at increased risk of developing heart failure (HF), but the mechanisms by which hypertension leads to HF have not been clarified [although left ventricular hypertrophy (LVH) is clearly a predictor of an increased risk of HF]. 10760631: Hypertension and coronary disease remain the leading causes of the disease, and heart failure due to myocardial infarction has increased in prevalence. 10918642: Hypertension and coronary artery disease are the leading causes of heart failure. 11028347: [Therapeutic strategies of heart failure due to hypertension]. 11113719: Uncontrolled hypertension is known to be a primary cause of heart failure and is also known to be very prevalent and frequently uncontrolled in the Polish population. Isolated hypertension was a further cause of heart failure in 8% of men and 13% of women. 11416576: Clinical manifestations of specific cardiovascular diseases, e.g., atherosclerosis and hypertension, that lead to heart failure and stroke likely become altered in older persons of advanced age because interactions occur between age-associated cardiovascular changes in health and specific pathophysiologic mechanisms that underlie cardiovascular diseases. 11578717: Hypertension is an important cause of heart failure especially in the African and African-American population. 11761828: Heart failure is a clinical syndrome caused mainly by cardiovascular diseases such as coronary heart disease, hypertension and valvular disease, but several categories of drugs may potentially induce heart failure in patients without previous heart disease or precipitate revealing of heart failure symptoms in patients with preexisting left ventricle impairment. 11790921: In the United States, cardiovascular disease, e.g., atherosclerosis and hypertension, that lead to heart failure and stroke, is the leading cause of mortality, accounting for over 40 percent of deaths in those aged 65 years and above. 11799429: CONCLUSION - Patients with serious cardiac failure and ventricular dysfunction caused by hypertension, alcoholism, or myocarditis can experience marked improvement in ventricular dysfunction after undergoing appropriate therapy within the venue of the doctor's office. 12028912: Hypertension was the most frequent cause of heart failure. 12034159: The principal causes of heart failure included dilated cardiomyopathy due to coronary arterial disease (30%), valvular disease (28%) and heart failure secondary to hypertension (25%). 12131643: We describe the case of a 56-year-old man who developed acute hypertension leading to cardiac insufficiency, arrhythmia, severe heart failure and death. 12133028: Coronary artery disease and hypertension are the two major underlying causes of heart failure. 12151871: Heart failure is one of the most common causes of cardiovascular morbidity and mortality, and hypertension is the most common cause of cardiac failure. 12534856: With the aging of the population and effective treatment of hypertension and coronary artery disease, the two major underlying causes of HF, the number of older Americans with HF is expected to rise significantly in the coming decades. 12623300: Our results suggest the possibility that the Gq-Rho kinase pathway plays an important role in the process of hypertension-induced LV hypertrophy leading to contractile dysfunction. Chronic inhibition of Rho kinase blunts the process of left ventricular hypertrophy leading to cardiac contractile dysfunction in hypertension-induced heart failure. 12641877: Increased vascular volume causes hypertension, which in turn causes LVH, cardiac failure, and ischemic heart disease (IHD). 12797915: Ischemic heart disease is a more frequent cause of in the patients seen by cardiologists than in those seen by Primary Care physicians, and hypertension is the leading cause of heart failure in these patients. 1285608: The upper body hypertension resulted in generalised convulsions and cardiac failure with pulmonary oedema. 12890915: Using a model of heart failure induced by hypertension in Dahl salt-sensitive (DS) rats, the mechanisms by which ACE inhibitors (ACEI) exert a beneficial effect on myocardial contractility were studied. 13020927: [Results of thoracolumbar sympathectomy in the treatment of cardiac insufficiency due to arterial hypertension]. 13066612: [Treatment of cardiac insufficiency due to arterial hypertension by thoracolumbar sympathectomy]. 1331961: Several authors have reported on the association between arterial hypertension and nephroblastoma as being the result of hyperreninism due to hilar compression; however severe hypertension was uncommon. Within 48 h, cardiac failure secondary to systemic arterial hypertension occurred, requiring intensive care. 14511898: In most cases, HF develops as a result of either long-standing hypertension or a myocardial infarction (MI). 14626517: Heart failure is a common, costly, and generally fatal condition that most often results from coronary artery disease or hypertension. 14967113: The control of risk factors for hypertension and ischemic heart disease, the main causes of heart failure in Spain, is the only method to halt the foreseeable increase in heart failure in the near future. 15039815: Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. 15114770: [Remodeling in cardiac failure of functional class I due to arterial hypertension associated with ischemic heart disease]. 15253329: Arterial hypertension is the commonest cause of heart failure in the Savannah region of Nigeria. 15254965: Excessive fibrosis, which has been associated with certain forms of hemodynamic overload such as hypertension, is thought to result in increased ventricular chamber stiffness, and eventual heart failure. 15521474: It was higher in the young patients, less symptomatic, and in patients with heart failure due to hypertension. 15570901: Case 2 had heart failure due to hypertension. 15700394: If left unchecked and untreated, uncontrolled high blood pressure can lead to heart failure, kidney failure, heart attack and stroke. 15779167: Anemia, hypertension and rheumatic fever were the causes of heart failure in these 3 patients, but they were not apparent when the initial diagnosis was made. 15956824: PURPOSE OF REVIEW: Hypertension leads to left ventricular hypertrophy, diastolic dysfunction, and eventually clinical heart failure (hypertensive heart disease). 16004861: Hypertension is most often cited as the sole etiology of heart failure in African Americans. 16190566: Complications of CDS have functional nature and comprise: renal failure (hepatorenal syndrome), respiratory failure in context of hepatopulmonary syndrome, cardiac insufficiency produced by portopulmonary hypertension or portal cardiomyopathy, hemorrhages from digestive tract caused by hypertensive portal gastropathy or derangements of brain perfusion. 16290968: Our findings are consistent with the increased risk older women have of developing heart failure because of hypertension. BACKGROUND: Epidemiologic studies suggest that women are at increased risk of developing heart failure secondary to hypertension. 1655265: It would now seem logical to determine whether cardioreparation can be achieved with lisinopril in patients with hypertension and left ventricular hypertrophy, in whom pathologic remodelling of the myocardium is responsible for symptomatic heart failure. 16651474: BACKGROUND: Hypertension is a major cause of heart failure (HF) and is antecedent in 91% of cases. 16699305: Progressive dyspnea, palpitations, and paroxysmal attacks of severe hypertension leading to cardiac failure had developed in a 25-yr-old woman. 16766638: Hypertension is a common cause of heart failure, and ventricular arrhythmias are a major cause of death in heart failure. 16782803: The intact KCNJ11-encoded K(ATP) channel is thus a required safety element preventing hypertension-induced heart failure, with channel dysfunction a molecular substrate for stress-associated channelopathy in cardiovascular disease. 16880252: BACKGROUND: Systemic hypertension is a rare but important cause of neonatal heart failure. 17013566: The interplay between Ang II and TGF-beta1 causes continued activation that may result in chronic hypertension and progressive myocardial fibrosis, leading to heart failure. 17210842: METHODS AND RESULTS: To explore the effect of an ameliorated mitochondrial ATP/ADP transportation on cardiac dysfunction, we generated transgenic rats overexpressing ANT1 in the heart (ANT rats) and crossed them with renin-overexpressing rats (REN rats) suffering from hypertension-induced cardiac insufficiency. Hypertension-induced cardiac hypertrophy in the REN rats was prevented by parallel ANT1 overexpression, however, and left ventricular function remarkably improved. 17266625: Hypertension plays major causative roles in development of cardiac failure and end-stage renal disease (ESRD). 17378995: There is growing evidence that nitric oxide (NO)-mediated endothelial dysfunction occurs in hypertension and may represent the earliest stage of target organ damage, which ultimately leads to hypertensive heart disease and heart failure (HF). 17487241: Heart failure secondary to ischemic heart disease, hypertension, and myocardial infarction is a common cause of death in developed countries. 17630346: As a critical step toward understanding the role of abnormal intracellular Ca(2+) release via the ryanodine receptor (RyR(2)) during the development of hypertension-induced cardiac hypertrophy and heart failure, this study examines two questions: 1) At what stage, if ever, in the development of hypertrophy and heart failure is RyR(2) hyperphosphorylated at Ser(2808)? 17667868: Consequently, blacks have a 1.3 times greater rate of nonfatal stroke, 1.8 times greater rate of fatal stroke, 1.5 times greater rate of heart disease death, 4.2 times greater rate of end-stage kidney disease, and a 50% higher frequency of heart failure; overall, mortality due to hypertension and its consequences is 4 to 5 times more likely in African Americans than in whites. 17713747: Arterial hypertension is the leading cause of coronary artery disease and cardiac failure, and coronary artery disease is the cause of heart failure in 50% of cases. 17910144: CONCLUSION: Hypertension was the major aetiology of heart failure followed by IHD. 17957325: Hypertension was the commonest cause of AHF. 18280594: OBJECTIVES: The aim of the present study was to investigate the effect of chronic treatment with a TNFalpha antagonist in a rat model of the early stage of heart failure due to hypertension. 18413490: Pharmacological inhibition of epsilon-protein kinase C attenuates cardiac fibrosis and dysfunction in hypertension-induced heart failure. 18607681: A 51-year-old woman developed heart failure due to severe hypertension of the upper half of the body caused by coarctation of the aorta. 18647880: We followed cardiac function and metabolic changes during 2 wk of angiotensin II (ANG II)-induced hypertension in control and heart-specific lipoprotein lipase knockout (hLpL0) mice. Both ANG II and deoxycorticosterone acetate-salt induced hypertension caused heart failure only in hLpL0 mice. 18651438: BACKGROUND: Despite effective repair of coarctation of the aorta (CoAo), arterial hypertension (AH) and early coronary artery disease that may result in heart failure. 18655459: This rare congenital autosomal recessive condition is characterized by progressive cone-rod retinal dystrophy associated with obesity, sensorineural deafness, type 2 diabetes, congenital cardiac insufficiency secondary to dilated cardiomyopathy, systemic hypertension and kidney failure. 18696353: Hypertension is probably the most serious major complication that can develop, possibly leading to intrauterine growth retardation, maternal heart failure, and fetal haemorrhage. 18804478: We recently found that inhibition of epsilonPKC slows down the progression of hypertension-induced HF in salt-sensitive Dahl rats fed a high-salt diet. Six week-old male Dahl rats were fed with a high-salt diet to induce systemic hypertension, which resulted in concentric left ventricular hypertrophy at the age of 11 weeks, followed by myocardial dilatation and HF at the age of 17 weeks. Mast cells and epsilonPKC: a role in cardiac remodeling in hypertension-induced heart failure. Together, our data suggest that epsilonPKC inhibition attenuates pathological remodeling in hypertension-induced HF, at least in part, by preventing cardiac MC degranulation. 19041574: We sought to investigate left ventricular (LV) systolic function in patients with heart failure caused by hypertension using a 2-D strain approach and to validate this method against Doppler strain measurements. 19210213: Hypertension, cardiomyopathy, rheumatic heart disease, chronic lung disease and pericardial disease are the main contributors to the etiology of cardiac failure in sub-Saharan Africa, accounting for over 90% of cases. 19253285: Despite equivalent systemic HTN produced by chronic hyperaldosteronism, 114 unique proteins were altered in Kir6.2-KO compared to WT hearts. KCNJ11 null mutants, lacking Kir6.2 ATP-sensitive K(+) (K(ATP)) channels, exhibit a marked susceptibility towards hypertension (HTN)-induced heart failure. 19340531: Endogenous angiotensin II has fewer effects but neuronal nitric oxide synthase has excitatory effects on renal sympathetic nerve activity in salt-sensitive hypertension-induced heart failure. The effects of endogenous angiotensin II (Ang II) and neuronal nitric oxide synthase (nNOS) on tonic sympathetic activity were studied in salt-sensitive hypertension-induced heart failure. These results suggest that endogenous Ang II has fewer effects, but nNOS has excitatory effects on tonic RSNA in salt-sensitive hypertension-induced heart failure. 19615312: Hypertension in elderly patients is a common and frequent disease which could cause stroke, heart failure and renal dysfunction. 19645208: Beta blockers seem not to be superior to other medication in reducing the development of heart failure due to hypertension. 19766467: It has been demonstrated that hypertension can lead to coronary heart disease, heart failure, stroke, and memory loss. 19809991: Hypertension may provoke de novo left ventricular hypertrophy and cardiac failure in dialysis patients and is also associated with a higher risk of stroke. 19853610: Increased expression of NCAM was also found during the remodeling period in a rat model of hypertension-induced heart failure. 2000773: Hypertension and coronary disease were the predominant causes for heart failure and accounted for more than 80% of all clinical events. 20019604: In the Chinese, hypertension remains an important cause of heart failure and recent data suggest that heart failure with preserved systolic function is common. 20024475: CONCLUSIONS: Untreated hypertension has been identified as the leading cause of heart failure in Abuja, Nigeria, which is similar to that in many other parts of sub-Saharan Africa. 20083682: BACKGROUND: Heart failure with preserved ejection fraction is 1 consequence of hypertension and is caused by impaired cardiac diastolic relaxation. 20102951: Diabetics were also more likely to be women, have a history of hypertension, ischemic cause for HF, and were more likely to be treated with diuretics. 20231522: Prolonged hypertension is the leading cause of heart failure. 20383902: Treating hypertension is one of the best ways to help avoid diastolic problems that can lead to heart failure. 20388649: AIMS: To test acute effects of the corticotropin-releasing factor-related peptide urocortin 2 (Ucn2) on left ventricular (LV) function and the propensity for ventricular arrhythmias in the isolated heart of an animal model of hypertension-induced heart failure. Acute effects of urocortin 2 on cardiac function and propensity for arrhythmias in an animal model of hypertension-induced left ventricular hypertrophy and heart failure. 20577843: However, disease-related stresses, such as hypertension or myocardial infarction, provoke a series of changes that culminate in heart failure and/or sudden death. 20599008: Previous work suggested that their use could increase heart failure (HF), which is 1 of the consequences of uncontrolled hypertension. 20735508: BACKGROUND: Heart failure is a common consequence of hypertension, with Doppler echocardiography being the gold-standard tool to evaluate left ventricular function, mainly hypertension-induced left ventricular damage. 20888832: Increasing evidence implicates dysregulation of this transcriptional regulatory circuit in the metabolic and functional disturbances that presage heart failure due to common diseases such as hypertension and diabetes. 21034543: CONCLUSIONS: Arrhythmia is the type of heart disease that has a highest incidence in patients with heart disease in pregnancy, while main types of heart disease that impair cardiac function are CHD and RHD; cardiac failure is more frequently caused by cardiopathy induced by hypertensive disorders complicating pregnancy and PPCM; impaired cardiac function increases perinatal morbidity; cardiac surgery before pregnancy could improve the cardiac function. RESULTS: In this study, main heart diseases in pregnancy were arrhythmia (n = 359, 31.4%), congenital heart disease (CHD; n = 291, 25.5%), and myocarditis and its sequelae (n = 284, 24.9%); based on the functional classification criteria of New York Heart Association (NYHA), more than half (n = 678, 59.4%) of patients were classified NYHA Class I; pregnant women in NHYA Class I-II (n = 951, 83.3%) commonly had arrhythmia, myocarditis and its sequelae, while those in NHYA Class III-IV (n = 191, 16.7%) mainly had CHD, rheumatic heart disease (RHD), cardiopathy induced by hypertensive disorders complicating pregnancy, and peripartum cardiomyopathy (PPCM). The incidence of cardiac failure in pregnant women with cardiopathy induced by hypertensive disorders complicating pregnancy and PPCM was relatively high, with a rate of 80% and 52.2%, respectively. 21250584: Based on disease-specific estimates of prevalence and incidence rates of heart failure, we conservatively estimate the prevalence of heart failure in India due to coronary heart disease, hypertension, obesity, diabetes and rheumatic heart disease to range from 1.3 to 4.6 million, with an annual incidence of 491 600-1.8 million. 2150343: Medical history and clinical and laboratory investigation showed that the heart failure was due exclusively to arterial hypertension. 21566223: Recent unbiased studies using genome-wide single nucleotide polymorphism microarrays have shown fewer positive results than when these platforms were applied to hypertension, myocardial infarction, or diabetes, possibly reflecting the complex etiology of heart failure. 21850540: Although several risk factors including hypertension, cardiac hypertrophy, coronary artery disease, and diabetes are known to result in heart failure, elderly subjects are more susceptible to myocardial infarction and more likely to develop heart failure. 21900086: Therapeutic inhibition of miR-208a by subcutaneous delivery of antimiR-208a during hypertension-induced heart failure in Dahl hypertensive rats dose-dependently prevents pathological myosin switching and cardiac remodeling while improving cardiac function, overall health, and survival. 21937860: Chronic left ventricular (LV) pressure overload induced by hypertension is one of the most common causes of heart failure. 22028869: Resveratrol improves survival, hemodynamics and energetics in a rat model of hypertension leading to heart failure. 22072105: Cardiac hypertrophy occurs as an adaptation to hypertension but a sustained hypertrophic response can ultimately lead to heart failure. 22304758: Of these, 84% had hypertension, and hypertensive heart disease was the most common aetiology of HF (39.2%). 22405664: This article focuses on the potential role of mineralocorticoid receptor antagonists (MRAs) in patients with stage B heart failure (HF) due to hypertension, diabetes mellitus, and/or visceral obesity with the metabolic syndrome. 22500284: Involvement of the thoracic and abdominal aortas, although rare, causes marked hypertension and may lead to severe heart failure. 2254567: Factors predictive of an increased probability of readmission included a prior history of heart failure, four or more admissions within the preceding 8 years, and heart failure precipitated by an acute myocardial infarction or uncontrolled hypertension (all P less than .05). 22945249: Heart failure was most commonly due to hypertension (n = 453 [45.4%]) and rheumatic heart disease (n = 143 [14.3%]). 23064369: In this issue of the JCI, Young et al. show that endoplasmic reticulum (ER) stress is an essential signaling event for angiotensin II-induced hypertension in cells of the central nervous system. Hypertension occurs in approximately 30% of individuals in Western populations and is known to be a major cause of stroke, heart failure, and myocardial infarction. 23388090: Quantitative real-time polymerase chain reaction (PCR) analysis for a selected panel of miRNAs indicated that circulating levels of miR-16, miR-20b, miR-93, miR-106b, miR-223, and miR-423-5p were significantly increased in response to hypertension-induced heart failure, while this effect was blunted in response to treatment with antimiR-208a as well as an ACE inhibitor. The aim of this study is to determine if plasma miRNAs can be used as indicators of disease progression or therapeutic efficacy in hypertension-induced heart disease. Plasma microRNAs serve as biomarkers of therapeutic efficacy and disease progression in hypertension-induced heart failure. 23436107: Hypertension is identified as the main precursor of left ventricular hypertrophy and therefore can lead to diastolic dysfunction and heart failure. 23625274: Hypertension and coronary heart disease are the leading causes of HF in China, as they are in many Western nations, potentially highlighting the improvement in socioeconomic conditions in China. 23887740: Inhibition of platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis. Taken together, our results indicate Ang II infusion-induced hypertension stimulated platelet activation and platelet-leukocyte conjugation, which initiated inflammatory responses that contributed to cardiac fibrosis. Inflammation promotes the development of cardiac fibrosis and heart failure induced by hypertension. 23894332: These findings demonstrate the anti-oxidant potential of APN in oxidative stress-associated cardiovascular diseases, such as hypertension-induced HF-preserved EF. 23929067: Hypertension and cardiomyopathies share maladaptive changes of cardiac morphology, eventually leading to heart failure. 23956210: BACKGROUND: Cardiac hypertrophy and subsequent heart failure triggered by chronic hypertension represent major challenges for cardiovascular research. 2400227: Three children who presented with heart failure in infancy caused by severe hypertension as a result of unilateral renal arterial disease are described. 24131668: Hypertension and obesity each are well known to result in heart failure with preserved ejection fraction. 24371501: Arterial hypertension is one of the most prevalent cardiovascular diseases and one of the most important causes of heart failure with low or preserved ejection fraction. 24550138: These findings suggest that the ATF3 activator tBHQ may have therapeutic potential for the treatment of pressure-overload heart failure induced by chronic hypertension or other pressure overload mechanisms. 24786443: In Africa, hypertension is the leading cause of heart failure; whereas at global levels, hypertension is responsible for more than half of deaths from stroke, just less than half of deaths from coronary artery disease, and for more than one-tenth of all global deaths. 24962957: Heart failure was most commonly a result of hypertension (n = 363, 39.5%) and only 7.8% had ischaemic heart failure. 25014216: It is known that activation of poly(ADP-ribose) polymerase enzyme (PARP) plays an important role in the development of postinfarction as well as long-term hypertension induced heart failure. 25245534: Pulmonary effects of chronic elevation in microvascular pressure differ between hypertension and myocardial infarct induced heart failure. 25598183: This arises from the increase in cardiovascular disease and associated risk factors such as hypertension and diabetes, as well as causes of heart failure which are particular to sub-Saharan Africa, such as endomyocardial fibrosis. 25618515: BACKGROUND: Hypertension has been established as one of the commonest causes of heart failure especially in sub-Saharan Africa. 25702467: The objective of study was to determine LV IRT in normally developing embryos and embryos with early UM of chromosomal and cardiac abnormalities and to test the hypothesis of embryonic hypertension as a cause of transient heart failure. 25767287: Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke. 25803693: Therefore, we determined the efficacy of ET and HIIT to alter cardiac muscle characteristics involved in the development of diastolic dysfunction, such as ventricular hypertrophy, fibrosis and angiogenesis, in a well-established rodent model of hypertension-induced heart failure before the development of overt heart failure. 25828108: BACKGROUND: The development of heart failure (HF) secondary to hypertension is a complex process related to a series of physiological and molecular factors including glucose dysregulation. 26248278: The effects of chronic blockade of vasopressin type 1a receptors (V1aR) and the additive effects of a type 2 receptor (V2R) antagonist on the treatment of hypertension-induced heart failure and renal injury remain to be unknown. 26259287: Obesity is associated with numerous comorbidities, including hypertension, lipid disorders and type II diabetes, and is also a major cause of cardiovascular disease, coronary disease, heart failure, atrial fibrillation, and sudden death. 26567492: Cancer drugs can cause cardiotoxicity by effects on heart cells, thromboembolic events, and/or hypertension that can lead to heart failure. 26619661: Abstract Hypertension is the major cause of cardiovascular disease. Persistent hypertension leads to cardiovascular remodeling and resulted in heart diseases such as coronary artery disease, heart failure, and arrhythmia. 26702612: Hypertension, diabetes mellitus and hyperlipidemia are the major causes of heart failure. 26708424: Hypertension causes cardiac hypertrophy, cardiac dysfunction and heart failure (HF). 26883434: Myocardial infarction or sustained overload as a result of pathological causes such as hypertension or valve insufficiency may result in progressive remodeling and finally lead to heart failure (HF). 26937528: More effort should go into preventing rheumatic heart disease and hypertension which result in heart failure in women. 26995439: Hyperactive sympathetic nervous system aggravates hypertension and it can cause complications like left ventricular hypertrophy, heart failure, arrhythmias and atherogenesis. 27080145: Hypertension was the commonest cause of heart failure (70; 48.6%). 27122686: UNLABELLED: Hypertension is the leading cause of heart failure and cardiovascular comorbidities in developed countries. 27132712: It may have an acute presentation in the form of heart failure in the neonate or may be discovered incidentally in adult because of severe treatment-resistant hypertension. 27133203: Endoplasmic reticulum (ER) stress has been reported to be involved in many cardiovascular diseases such as atherosclerosis, diabetes, myocardial ischemia, and hypertension that ultimately result in heart failure. 27524216: Diseases such as diabetes mellitus, hypertension and ischemic heart disease continue to be the leading causes of HF. 27528985: It may be due to any of a wide variety of causes - in Malawi, cardiomyopathies, hypertension and rheumatic heart disease are probably the commonest causes of heart failure. 28229901: Hypertension is an important cause of HF. 28430843: BACKGROUND: Hypertension is a major cause of heart failure. 28502640: Cardiac failure is most commonly secondary to uncontrolled arterial hypertension or myocardial ischaemia. 28568509: Heart failure in African cohorts occurs at a younger age than in North America and Europe and is more likely to be due to hypertension. 28581677: Extracellular fluid volume overload and its inevitable consequence, hypertension, increases cardiovascular mortality in the long term by leading to left ventricular hypertrophy, heart failure, and ischemic heart disease in dialysis patients. 28711447: Longstanding hypertension ultimately leads to heart failure (HF), and, as a consequence most patients with HF have a history of hypertension. 28748885: Although hypertension is the most common cause of cardiac failure, the role of primary myocardial dysfunction should also be considered. 28796250: p53-mediated miR-18 repression activates HSF2 for IGF-IIR-dependent myocyte hypertrophy in hypertension-induced heart failure. Transgenic overexpression of miR-18 in cardiomyocytes is sufficient to protect against dilated cardiomyopathy during hypertension-induced heart failure. Hypertension-induced cardiac hypertrophy and attenuated cardiac function are the major characteristics of early stage heart failure. Our results demonstrated that the p53-miR-18-HSF2-IGF-IIR axis was a critical regulatory pathway of cardiomyocyte hypertrophy in vitro and in vivo, suggesting that miR-18 could be a therapeutic target for the control of cardiac functions and the alleviation of cardiomyopathy during hypertension-induced heart failure. 29180262: Thus, our study uncovered a novel MEL18-SUMO-1-HSF2-IGF-IIR pathway in the heart that profoundly influences cardiac hypertrophy for hypertension-induced heart failure. In this study, we found that heat shock transcription factor 2 (HSF2) activated IGF-IIR to induce cardiac hypertrophy for hypertension-induced heart failure. However, the detailed mechanism by which HSFs regulates IGF-IIR during hypertension-induced cardiac hypertrophy remains elusive. Inhibition of HSF2 SUMOylation via MEL18 upregulates IGF-IIR and leads to hypertension-induced cardiac hypertrophy. 29286090: However, inhibition of galectin-3 by intravenous tail vein injection of a galectin-3-targeting short hairpin RNA-expressing vector during hypertension-induced heart failure in Dahl hypertensive rats increased rat survival and body weight. 29449707: Uncontrolled hypertension leads to cardiac hypertrophy, followed by cardiac failure. 29493835: BACKGROUND: Hypertension is the leading cause of morbidity, the identified cause of heart failure in 45% of patients and is associated with more than 70% of cardiovascular disease-related hospital admissions in Haiti. 29593530: Sirt1/p53/Drp1dependent mitochondrial fission may be a valuable therapeutic target for hypertension induced heart failure. 29649151: Systemic hypertension, which eventually results in heart failure, renal failure or stroke, is a common chronic human disorder that particularly affects elders. 29671305: One of them?is hypertension induced left ventricular?hypertrophy and fibrosis, progressive?deterioration of left ventricular compliance,?increase in left ventricular enddiastolic?pressure which in turn lead to?left ventricular diastolic dysfunction.?The other pathomechanism of heart?failure associated to hypertension is?accelerated coronary artery atherosclerosis,?ischemia of the left ventricle?and its systolic dysfunction. Natural history of?hypertension leads to heart failure in?two main mechanisms. 29857545: Myocardial apoptosis and fibrosis represent important contributing factors for development of hypertension-induced heart failure. 30158213: This study suggests that ENPP1 enzyme replacement therapy could be a more effective GACI therapeutic than bisphosphonates, treating not just the vascular calcification, but also the hypertension that eventually leads to cardiac failure in GACI patients. 30159417: We previously demonstrated that in a murine model of pressure overload, a model of heart failure secondary to aortic stenosis or chronic high blood pressure, elevated myocardial expression of miR-199b-5p is sufficient to activate calcineurin/NFAT signaling, leading to exaggerated cardiac pathological remodeling and dysfunction. 30359575: Type 2 diabetes mellitus (DM2) follows impaired glucose tolerance in obesity and is frequently associated with hypertension, causing adverse myocardial remodelling and leading to heart failure. 30560138: The clinical phenotype was secondary to resistant hypertension due to bilateral renal artery stenosis, and her blood pressure and heart failure resolved after successful renal artery angioplasty. In this article, we describe a case of resistant hypertension in a 63-year-old woman leading to heart failure and marked morbidity. Resistant hypertension remains an important cause of heart failure. 30581101: OBJECTIVE: Sustained hypertension is a major cause of heart failure in aging hypertensive patients. We therefore hypothesized that central knockdown of salusin beta might be effective for hypertension-induced heart failure treatment. 30670148: Inhibition of ETS-1 could be a potential therapeutic strategy for treatment of heart failure secondary to chronic hypertension. 30703746: Our systemic study clearly supports the modulation of CSRP3 by a polyphenol-rich berries diet as an efficient cardioprotective strategy in hypertension-induced heart failure. The capacity of a polyphenol-enriched diet (i.e., blueberries, blackberries, raspberries, strawberry tree fruits and Portuguese crowberries berries mixture) to promote animal survival and protect cardiovascular function from salt-induced hypertension was evaluated in a chronic salt-sensitive Dahl rat model. 3120215: Hypertension, when severe, damages small blood vessels, causing kidney failure, hemorrhage, strokes, and heart failure; when the condition is mild to moderate, it produces atherosclerosis. 31234877: CONCLUSIONS: The co-morbidity of hypertension and inhaled nanoparticles induces irreversible hemodynamic impairment associated with cardiac structural damage potentially leading to heart failure. 31653505: The aim of this study was to analyze the changes in stress and strain in the left ventricle (LV) in hypertension-induced HFpEF rats. Cardiac wall mechanics analysis in hypertension-induced heart failure rats with preserved ejection fraction. 31656497: Methodology: Seventy-six subjects with heart failure secondary to hypertension and 92 normal controls underwent clinical, electrocardiographic and echocardiographic evaluation. 31747542: The risk of heart failure attributable to hypertension was two-fold higher in heart failure with preserved ejection fraction (38.7%) than heart failure with reduced ejection fraction (17.8%). 31771489: Arterial hypertension is by far the most common cause of heart failure, followed by cardiomyopathies and rheumatic heart diseases. 31840653: Long Noncoding RNA FTX Reduces Hypertrophy of Neonatal Mouse Cardiac Myocytes and Regulates the PTEN/PI3K/Akt Signaling Pathway by Sponging MicroRNA-22.BACKGROUND Cardiac myocyte hypertrophy results from clinical conditions that include hypertension and valvular heart disease, and can result in heart failure. 31890481: Of patients admitted for heart failure, uncontrolled hypertension was the most commonly identified etiology of heart failure, cited in 124 (42.2%) cases. 32039239: Cardiotoxicity induced by anti-cancer treatments compromise vasospastic and thromboembolic ischemia, dysrhythmia, hypertension, myocarditis, and cardiac dysfunction that can result in heart failure. 32079284: However, chronic stresses such as hypertension or cancer cachexia cause irreversible remodeling of the heart, leading to heart failure. 32265349: Established hypertension is a causative factor of heart failure, which is characterized by increased vascular resistance and intractable uncontrolled blood pressure. 32270083: Conclusion: While hypertension does not result in as long leaves and costs, it should be prevented for being a significant cause of stroke and HF, both of which account for longer sick leaves and higher social security costs. 32393064: Hypertension, or elevated blood pressure, if left untreated can result in myocardial hypertrophy leading to heart failure (HF). 32524327: These risk factors act individually or more commonly in groups, directly or indirectly (hypertension, obesity, and T2DM may lead to HF through an intervening myocardial infarction). 32527992: Relationship Between Ubiquitin-Specific Peptidase 18 and Hypertension in Polish Adult Male Subjects: A Cross-Sectional Pilot Study.BACKGROUND Arterial hypertension (HT) is a leading cause of cardiac hypertrophy and heart failure. 32820187: Effects of empagliflozin and target-organ damage in a novel rodent model of heart failure induced by combined hypertension and diabetes. 32890260: Established hypertension is a causative factor of heart failure, which is characterized by increased vascular resistance and intractable uncontrolled blood pressure. 32928542: Hypertension (HT) and ischemic heart disease (IHD) are the leading causes of HF. 33035444: Sympathetic hyperactivity and diminished parasympathetic activity are the characteristic features of many cardiovascular disease states including hypertension, myocardial ischemia, and arrhythmias that result in heart failure. 33493215: AIM: Hypertension is the leading cause of heart failure (HF) in sub-Saharan Africa. 33597461: He was provisionally diagnosed with decompensated heart failure precipitated by cellulitis and uncontrolled hypertension. 33876316: Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. 34290289: In heart failure (HF) caused by hypertension, the myocyte size increases, and the cardiac wall thickens. 34359440: Hypertension, causing cardiovascular disease, stroke, and heart failure, has been a rising health issue worldwide. 34525837: The Black patient cohort was younger, more obese and with a history of hypertension, and more nonischemic cause of heart failure, relative to the White patient group. 34548653: Therapy-resistant hypertension is a serious medical problem, causing end-organ damage, stroke, and heart failure if untreated. 34567228: Purpose: Hypertension is an important cause of nonischemic heart failure. 35083170: In Asia, HT is the most common cause of HF after ischemic heart disease. 35174479: A significant cardiac complication of diabetes is cardiomyopathy, a form of ventricular dysfunction that develops independently of coronary artery disease, hypertension and valvular diseases, which may subsequently lead to heart failure. 35269958: This review summarizes common cardiotoxic effects of KIs, including hypertension, arrhythmias with bradycardia and QTc prolongation, and cardiomyopathy that can lead to heart failure, as well as less common effects such as fluid retention, ischemic heart disease, and elevated risk of thromboembolic events. 35310970: Diabetic cardiomyopathy (DbCM) occurs independently of cardiovascular diseases or hypertension, leading to heart failure and increased risk for death in diabetic patients. 35345276: CONCLUSIONS: The results can improve our understanding of the macrophages-associated molecular mechanisms in heart failure induced by dilated cardiomyopathy, ischemic cardiomyopathy or hypertension and 5 hub DEMRGs may help prevent the adverse left ventricular remodeling to decrease mortality and morbidity. 35356999: Persistent arterial hypertension leads to structural and functional remodeling of the heart resulting in myocardial ischemia, fibrosis, hypertrophy, and eventually heart failure. 35409698: Most importantly, uncontrolled HPT can lead to severe complications (stroke, heart attack, kidney disease, and heart failure), mainly ignoring the signs in nascent stages. 35555894: Hypertension and cardiac hypertrophy initiate molecular pathways that can result in heart failure (HF). 36044874: HTN can lead to heart failure (HF) by causing hypertensive left ventricular hypertrophy (HTN LVH). 36405687: The diabetic population has been increasing in the past decades and diabetic cardiomyopathy (DCM), a pathology that is defined by the presence of cardiac remodeling and dysfunction without conventional cardiac risk factors such as hypertension and coronary heart diseases, would eventually lead to fatal heart failure in the absence of effective treatment. 36483558: Aims: Cardiac fibrosis is central to heart failure (HF), especially HF with preserved ejection fraction (HFpEF), often caused by hypertension. 36604473: Hypertension is a leading cause of heart failure and other cardiovascular diseases. 36825182: Salvianolic acid D: A potent molecule that protects against heart failure induced by hypertension via Ras signalling pathway and PI3K/Akt signalling pathway. 37156668: BACKGROUND AND AIMS: Heart failure (HF) is often triggered by hypertension and can benefit from antihypertensive treatment. 37468902: It is unrelated to hypertension and coronary artery disease and can lead to heart insufficiency, heart failure and even death. 37568493: Further, HF development in obesity or DM is rare in the absence of HTN or coronary artery disease (CAD), whereas HTN often causes HF per se. 37696999: Ventricular remodeling is one of the main causes of mortality from heart failure due to hypertension. 37881391: CONCLUSIONS: A large sector of the general population did not know that uncontrolled HTN may cause HF, especially those free from both conditions. Of the responders, 50% knew that uncontrolled HTN can lead to HF. 37892623: Erroneously, HTN, which is the leading cause of cardiovascular disease and premature death worldwide and is present in more than 90% of HF patients, is tightly linked with SNS overactivity. In contrast, it has been undermined in HF with preserved LVEF (HFpEF), which is due to hypertension (HTN) in the vast majority of the cases. 38048979: Myocardial remodeling, which occurs in the final stage of cardiovascular diseases such as hypertension, can ultimately result in heart failure. 38056241: Inhibiting the MAPK pathway improves heart failure with preserved ejection fraction induced by salt-sensitive hypertension. 38148348: The goal of the study are to define the energy metabolic profile in heart failure induced by obesity and hypertension in aged female mice, and to attempt to lessen the severity of heart failure by stimulating myocardial glucose oxidation. The primary energy metabolic change in heart failure induced by obesity and hypertension in aged female mice is a dramatic decrease in glucose oxidation. 13-Month-old C57BL/6 female mice were subjected to 10 weeks of a 60% high-fat diet (HFD) with 0.5 g/L of Nomega-nitro-L-arginine methyl ester (L-NAME) administered via drinking water to induce obesity and hypertension. 38232920: Pulmonary hypertension, a condition marked by high blood pressure in the lungs, can lead to heart failure and other complications. 38242833: Cardiovascular toxicities caused by cancer therapies include different severities of cardiomyopathy, arrhythmia, myocardial ischaemia, hypertension, and thrombosis, which may lead to left ventricular dysfunction and heart failure. 38636400: Diabetic cardiomyopathy (DCM) is a common severe complication of diabetes that occurs independently of hypertension, coronary artery disease, and valvular cardiomyopathy, eventually leading to heart failure. 4568098: [Heart failure caused by sclerotic coronary diseases and hypertension and its management]. 6314794: It is concluded that there are other factors, besides hypertension, which precipitate heart failure in Nigerian hypertensives. 6458936: Hypertension, iodopathic cardiomegaly and pulmonary heart disease were major causes of cardiac failure. 6723181: Heart failure secondary to latrogenic systemic hypertension in an infant with congenital adrenal hyperplasia. 7212468: In the obstructive group, they had severe cyanosis, heart failure, small heart and pulmonary fields with a \ground glass\ or mottled appearance on chest X-ray due to hypertension and edema. 7574363: Heart failure was of an ichaemic origin in 37% of cases, idiopathic in 25% and due to hypertension in 25%. 7614719: Responses to high vascular pressure after induction of pacing-induced heart failure in dogs. 7720745: Two newborn infants developed cardiac failure due to severe hypertension which was recognised as the heart failure was treated. 7758051: Hypertension is a potentially life-threatening condition that can lead to heart failure, stroke, and kidney disease. 7808691: Heart failure, arrhythmia, or chest pain can be a consequence of diabetes independent of coronary disease or hypertension. 7954535: In each group there were similar numbers of patients in whom heart failure was due to coronary heart disease, high blood pressure, or idiopathic dilated cardiac myopathy. 7981482: Heart disease in older individuals can be characterised as the result of 2 processes, hypertension and atherosclerosis, which are the major causes of heart failure in the elderly population. 8279451: Of the group, five patients had cardiac failure due to systemic hypertension (4 patients), valvular disease (4 patients), or coronary atherosclerosis (4 patients). 8960492: The heart failure was secondary to severe hypertension from hyperreninemia. 9115206: Cardiac hypertrophy and heart failure caused by high blood pressure were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart failure. 9140785: Hypertension is regarded as the most common cause of heart failure in Nigeria and other Black African countries. How common is heart failure due to systemic hypertension alone in hospitalised Nigerians? A few reports suggest that heart failure due to hypertension hardly occurs without the presence of an extra burden on the heart from the presence of other cardiac risk factors. 9583454: The patient was admitted to Tenri Hospital because of heart failure, which was thought to be caused by moderate aortic regurgitation, moderate hypertension, and mild chronic renal failure. 9692655: PATIENTS: Twelve men with stable New York Heart Association class II or III heart failure secondary to ischemic heart disease or hypertension. 9752888: Hypertension is a major cause of heart failure, evolving from left ventricular hypertrophy to systolic and diastolic dysfunction. 9789465: The case report describes a 50-years-old patient with left ventricular hypertrophy, severe heart failure and ischemic chest pain due to untreated arterial hypertension. 9931137: A relatively new model of HF, the spontaneously hypertensive heart failure (SHHF) rat spontaneously and reproducibly develops left ventricular hypertrophy (LVH) and progresses to HF, thus enabling longitudinal studies to examine the cellular and molecular bases for hypertension-induced cardiac hypertrophy and subsequent HF. 12669921: Self-reported stress and subsequent hospital admissions as a result of hypertension, varicose veins and haemorrhoids. 18212446: Hypertension is the fourth common cause of end-stage renal disease. Hypertension was responsible for 935 hospital admissions in 1997. 21240595: BACKGROUND: Treatment-resistant hypertension is a common problem in an outpatient setting and often results in hospital admission. 24005922: Particulate matter and hospital admission due to arterial hypertension in a medium-sized Brazilian city. This study aims to assess the effects air pollution on hospitalization due to hypertension. A significant association between exposure to particulate matter and hospitalization due to hypertension was identified using Poisson regression with lags of up to four days. An ecological study was conducted using data regarding hospitalizations due to hypertension in Sao Jose dos Campos, State of Sao Paulo, Brazil between January 1, 2007 and December 31, 2010. 26286805: We aimed to understand and to provide evidence on relationships of the weather as biometeorological and hospital admissions due to hypertension, angina, myocardial infarction and ischemic heart disease in a national setting in recent years that might help indicate when to expect more admissions for health professionals and the general public. 28845316: Acute heart failure is a common reason for hospital admission and is usually caused by decreased cardiac output either as a result of an intrinsic cardiac issue or as a result of severe hypertension with elevated afterload. 29637415: Although TIH affects only a minority of patients exposed to thiazides, the high prevalence of hypertension leads to TIH being the most common cause of drug-induced hyponatremia requiring hospital admission in the UK. 30281763: RESULTS: We recorded 493,299 hospitalizations due to arterial hypertension from 2010 to 2015, with an average annual progressive cost decrease of -7.76% and -24.21%. CONCLUSION: Hospital admissions due to arterial hypertension have an impact on the percentage of admissions due to primary care- sensitive conditions. Factors associated with hospital admissions due to hypertension. OBJECTIVE: To study the temporality of hospital admissions due to arterial hypertension and its associated factors. 32410189: The ever increasing hospital admission and mortality due to heart failure, diabetes, hypertension, and cancer could be due to long-term exposure to particles in different countries. 33667277: BACKGROUND: Hypertension is a major health problem in Ghana, being a leading cause of admissions and deaths in the country. 37156576: CONCLUSION: This study provides the first comprehensive assessment of factors influencing hospitalisation duration of admissions due to hypertension in Ghana. 37217123: Of this total: 13 164 (95%CI: 9930-16 398) admissions were attributable to exposure to O 3 , the only pollutant to show a statistically significant (p < 0.05) association with admissions due to hypertensive disorders; and 10 575 (95%CI: 3573-17 566) admissions were attributable to daytime noise levels, while admissions due to hyperemesis gravidarum and vomiting were related to exposure to night noise. 15132714: METHODS: Domestic (US) cases of apparently unconfounded, acute hypertension leading to hospitalisation were collected and reviewed from the spontaneous adverse events database of the FDA for rofecoxib, celecoxib, nabumetone and oxaprozin for the initial 3 years of marketing. Spontaneous reports of hypertension leading to hospitalisation in association with rofecoxib, celecoxib, nabumetone and oxaprozin. 16114768: The greatest burden and the largest increase in the rate of hospitalisation will be due to hypertensive disease. CONCLUSIONS: There will be an exponential increase in hospitalisation due to diabetes, hypertension and ischaemic heart disease. DESIGN: Morbidity data, maintained at the Medical Statistics Unit of the Ministry of Health, from 1981 to 2000, were used to model trends of hospitalisation due to diabetes mellitus, hypertensive disease and ischaemic heart disease. An increase is estimated in the incidence of hospitalisation by 36%, 40% and 29% due to diabetes mellitus, hypertensive disease and ischaemic heart disease, respectively, in 2010 as compared to 2005. 16796409: The above mentioned hospitalization is attributable directly to the HT in the half of the cases. 17089198: Threatened preterm labour, antenatal hemorrhage, hypertensive disorders, severe vomiting and diabetes remained the five most common causes for antenatal hospitalization, although the trends for the first four declined dramatically from 1991/92 to 2002/03. 17167523: The adjusted difference in hospitalization incidence attributable to hypertension was significantly higher for the lower education group than the higher education group, and such a pattern tended to be more pronounced among diabetic people. 17288240: In the analyzed years the count of hospitalizations caused by angina pectoris, heart failure, hypertension, atherosclerosis and strokes has dropped, minor changes were visible in frequency of hospital admissions because of acute myocardial infarction and the count of cerebral infarction cases slightly increased. ln the analyzed years in the Lower Silesia region there was visible slight improvement in the area of most main circulatory system diseases. 18709492: Hospitalization due to arterial hypertension was more frequent in women, whereas those for COPD and psoriasis were more frequent in men. 20064067: Congestive heart failure, chronic obstructive pulmonary disease, diabetes, and hypertension are common causes of hospitalization in the elderly. 20414531: BACKGROUND: In Curitiba, systemic hypertension (SH) is the second leading cause of hospitalization and the leading cause of death from cardiovascular diseases. 23449017: These categories were used to compare the risk of undergoing hospitalization in the 1 year after the baseline survey and to examine the percentage of inpatient medical expenditure attributable to overall hypertension relative to total medical expenditure in the study population. 23726180: In conclusion, the prevalence of hospitalization due to hypertensive disease significantly increased in the United States from 1980 to 2007. Trends in the prevalence of hospitalization attributable to hypertensive diseases among United States adults aged 35 and older from 1980 to 2007. We aimed to examine the trend in the prevalence of hospitalization attributable to hypertensive disease and its subtypes among United States adults aged >=35 years from 1980 to 2007. 24005922: Particulate matter and hospital admission due to arterial hypertension in a medium-sized Brazilian city. This study aims to assess the effects air pollution on hospitalization due to hypertension. A significant association between exposure to particulate matter and hospitalization due to hypertension was identified using Poisson regression with lags of up to four days. An ecological study was conducted using data regarding hospitalizations due to hypertension in Sao Jose dos Campos, State of Sao Paulo, Brazil between January 1, 2007 and December 31, 2010. 24823931: The number of disease-specific hospitalizations, the length of hospital stay, and the number of visits to family physicians and medical specialists due to HYP or DM2 in 2005-2008 were evaluated. 26216517: Heart failure (HF) is the end result of a diverse set of causes such as genetic cardiomyopathies, coronary artery disease, and hypertension and represents the primary cause of hospitalization in Europe. 2657954: Hospitalization was most often due to hypertension and threatened premature labour and lasted on average longer among nulliparae. 27461237: RESULTS: There were 0.92, 0.97 and 1.04 million ED visits (0.71-0.77 % of all ED visits) with hypertension as the primary diagnosis in 2009, 2010 and 2012, respectively; 23 % resulted in hospitalization. 27776558: BACKGROUND AND AIMS: Arterial hypertension is a major cause of death worldwide. Characterization and history of arterial hypertension leading to inpatient treatment. 29229570: RESULTS: Most healers believed that hypertension was caused by the disorder of fire and wind elements in the body. In Thailand, illness and hospitalisation in the modern public health system due to high blood pressure is increasing. 30281763: RESULTS: We recorded 493,299 hospitalizations due to arterial hypertension from 2010 to 2015, with an average annual progressive cost decrease of -7.76% and -24.21%. CONCLUSION: Hospital admissions due to arterial hypertension have an impact on the percentage of admissions due to primary care- sensitive conditions. Factors associated with hospital admissions due to hypertension. OBJECTIVE: To study the temporality of hospital admissions due to arterial hypertension and its associated factors. 33319027: We found no evidence that the MDP led to reductions in hospitalizations due to hypertension. In this paper, we study the impact of Brazil's More Doctors Program (MDP) on hospitalizations due to cerebrovascular disease and hypertension. 33629868: METHODS AND RESULTS We used the best available estimates of independent associations of cardiometabolic conditions with a risk of COVID-19 hospitalization; nationally representative data on cardiometabolic conditions from the National Health and Nutrition Examination Survey 2015 to 2018; and US COVID-19 hospitalizations stratified by age, sex, and race/ethnicity from the Centers for Disease Control and Prevention's Coronavirus Disease 2019-Associated Hospitalization Surveillance Network database and from the COVID Tracking Project to estimate the numbers and proportions of COVID-19 hospitalizations attributable to diabetes mellitus, obesity, hypertension, and heart failure. 36027359: There were zero re-hospitalizations due to high blood pressure. 36402355: Our primary outcome was composite maternal morbidity defined as: severe hypertension (BP >= 160/110 mmHg) or preeclampsia with severe features, the need for a second antihypertensive agent, postpartum hospitalization > 4 days, and maternal adverse outcome secondary to hypertension as evidenced by pulmonary edema, acute kidney injury (creatinine level >= 1.1 mg/dl), cardiac dysfunction (e.g. elevated brain natriuretic peptide level) or cardiomyopathy, posterior reversible encephalopathy syndrome (PRES), cerebrovascular accident, or admission to an intensive care unit. 36604756: There were no serious ocular adverse events in either group; however, there were three serious systemic events in the combination group, including hospitalizations due to pancreatitis, pneumonia, and worsening hypertension. 14342045: [PATHOLOGICAL ANATOMY AND PATHOGENESIS OF PULMONARY HYPERTENSION IN CHRONIC INSUFFICIENCY OF THE LEFT VENTRICLE CAUSED BY ARTERIOSCLEROSIS AND HYPERTENSION]. 16778983: Based on the research of the three gasotransmitters in hypoxic and high pulmonary blood flow-induced pulmonary hypertension, it was found that the dysfunction of the gasotransmitter pathways was involved in the pathogenesis of pulmonary hypertension and the supplement of gasotransmitters could alleviate pulmonary hypertension and pulmonary vascular remodeling. 17048411: In contrast, POPH has a prevalence of 2-16% and is only considered proven, if other causes of the pulmonary hypertension than the high portal pressure are excluded. 20522577: Inflammation is likely a critical underlying etiology in many forms of severe pulmonary hypertension (PH), and schistosomiasis-associated PH, one of the most common causes of PH worldwide, is likely driven by the host response to parasite antigens. 20671265: The mechanisms underlying schistosomiasis-induced pulmonary hypertension (PH), one of the most common causes of PH worldwide, remain unclear. 21955237: The prevalence of schistosomiasis is so overwhelming that schistosomiasis-associated pulmonary hypertension (Sch-PH) may be the most prevalent cause of pulmonary hypertension around the world. 25735576: Other causes include PH secondary to left heart disease, interstitial lung disease-related PH, chronic thromboembolic PH and pulmonary veno-occlusive disease. 25882070: Differentiation of POPH from other causes of pulmonary hypertension, such as volume overload or a hyperdynamic high flow state, is critical because a diagnosis of POPH has significant implications for liver transplant risk stratification, Model for End Stage Liver Disease exception points, and the use of pulmonary arterial hypertension-(PAH) specific therapy. 30294198: In this review, we discuss the pathophysiology of SAPH, which may resemble pulmonary arterial hypertension as well as secondary causes of PH. We offer a screening algorithm for SAPH, and advocate for detailed assessment of the cause of PH in each patient prior to choice of an individualized treatment plan. 8329411: These hemodynamic factors include pulmonary hypertension, perioperative ischemia, reperfusion injury, and changes in both blood pressure and loading conditions caused by hypertension and its treatment. 907433: The possibly associated cardiac malformations, the persistance of fetal obstructive hypertension due to the increase of the flow in the left pulmonary artery, the left to right shunt induced by the abnormal venous return and predominantly by the systemic blood supply to the right lung, are responsible, at various degrees, for pulmonary hypertension. 9117101: This pulmonary hypertension involved a post-capillary mechanism, secondary to the left ventricular haemodynamic effects of the acute increase of left ventricular after-load induced by systemic hypertension. 10396707: A 47-year-old man with hypertensive heart disease and left heart failure due to left ventricular diastolic dysfunction was admitted to our hospital because of emergent hypertension. 17378995: There is growing evidence that nitric oxide (NO)-mediated endothelial dysfunction occurs in hypertension and may represent the earliest stage of target organ damage, which ultimately leads to hypertensive heart disease and heart failure (HF). 20937450: Hypertensive heart disease (HHD), a result of long-standing hypertension, is characterized by changes in the myocardial structure and function in the absence of other primary cardiovascular abnormalities. 22658278: CONCLUSION: In our largely black cohort of ED patients with elevated blood pressure, subclinical hypertensive heart disease was highly prevalent, suggesting the need for coordinated efforts to reduce cardiac consequences of hypertension in such inner-city communities. 24639061: Hypertensive heart disease (HHD) defines the complex and diverse perturbations of cardiac structure and function occurring secondary to hypertension. 28285801: Hypertension (HTN) is the most common cause of hypertensive heart disease, which comprises of left ventricular hypertrophy (LVH), left atrial enlargement, diastolic dysfunction, functional mitral regurgitation and neurohormonal changes. 30637533: RECENT FINDINGS: HHD results from long-standing hypertension and is characterized by the development of left ventricular hypertrophy and diffuse interstitial fibrosis. 31193675: This case shows that habitual methamphetamine use may cause hypertensive heart disease because of chronic hypertension. 7494927: Arterial hypertension can cause left ventricular hypertrophy and consequent hypertensive cardiopathy, a condition that is associated with the development of heart failure, arrhythmia and ischemia. 7634285: Several studies, performed during the past 20 years in different experimental animal models of hypertension and in men, have allowed to clarify important pathophysiological and clinical aspects of the hypertensive cardiovascular disease, i.e. the pathological condition characterized by marked structural and functional alterations of the heart induced by arterial hypertension. 11177307: We performed morphological assay of the myocardium in Wistar rats with anthracycline cardiomyopathy and SHR rats with genetically determined arterial hypertension causing hypertrophic cardiomyopathy. 125353: These cardiac features in type III, which are quite similar to those in hypertrophic cardiomyopathy, seemed to be a secondary change induced by systemic hypertension on the basis of some predisposition. 15105787: IN A PATHOLOGICAL CONTEXT: The Doppler echocardiography also detects the various cardiovascular affections related to ageing: valvulopathies, notably calcified aortic stenosis and mitral failure due to mitral anulus calcification or prolapsus of the valve; primary hypertrophic cardiomyopathy or secondary to arterial hypertension or an amyloidosis, and possibly leading to heart failure with spared systolic function, frequent in elderly patients; ischemic cardiopathies that have benefited, as in younger patient, from new echographical stress testing techniques, which safely study the variability in myocardial ischemia. 15220895: Differences in regional systolic and diastolic function by Doppler tissue imaging in patients with hypertrophic cardiomyopathy and hypertrophy caused by hypertension. METHODS: A total of 62 participants were studied: 21 with HCM; 22 with LVH secondary to hypertension; and 19 control subjects. We evaluated DT differences for patients with LVH caused by hypertension and patients with HCM, assessing regional systolic and diastolic function. 17579564: BACKGROUND: The clinical phenotype of both hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) induced by hypertension is heterogeneous. 18177389: The aim of this study was to investigate differences in MA motion between hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) patients due to hypertension or aortic stenosis using real time three-dimensional echocardiography (RT3DE). 19771749: Echocardiography is the tool of choice for the assessment of the athlete's heart and also for the differentiation of physiologic and pathologic LVH (hypertrophic cardiomyopathy and LVH due to arterial hypertension). 2137778: Quantitative 2-D echocardiography is useful to differentiate patients with hypertrophic cardiomyopathy from those with secondary myocardial hypertrophy due to hypertension. 21911172: Our patient suffered from hypertrophic cardiomyopathy due to long-standing hypertension with Dana Point Classification Group 2 pulmonary hypertension from the underlying cardiac disease, along with renal failure necessitating renal replacement therapy. 2424266: It is speculated whether hypertrophic cardiomyopathy and hypertension are both caused by systemic disorders of calcium channels and calcium uptake and binding by cardiac and smooth muscle membranes, respectively. 26659373: BACKGROUND: The differential diagnosis of left ventricular (LV) hypertrophy remains challenging in clinical practice, in particular, between hypertrophic cardiomyopathy (HCM) and increased LV wall thickness because of systemic hypertension. 27757525: We analyzed the waveform of systolic strain and strain-rate curves to find a characteristic left ventricular (LV) myocardial contraction pattern in patients with hypertrophic cardiomyopathy (HCM), and evaluated the utility of these parameters for the differentiation of HCM and LV hypertrophy secondary to hypertension (HT). 31345016: Effect of MiR-34a on hypertension-induced hypertrophic cardiomyopathy in rats via the TGF-beta1/smads signaling pathway. 34817008: BACKGROUND: Hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) secondary to systemic hypertension (HTN) may be associated with left atrial (LA) functional abnormalities. 35195213: BACKGROUND: Hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) secondary to systemic hypertension (HTN) may be associated with left atrial (LA) functional abnormalities. 36997815: Sacubitril/valsartan reverses cardiac structure and function in experimental model of hypertension-induced hypertrophic cardiomyopathy. This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Thirty Wistar Kyoto rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM), were used for this study. 6685744: The cases examined consisted of 24 cases of hypertrophic cardiomyopathy (HCM), 10 cases of left ventricular hypertrophy (LVH) due to hypertension or aortic valvular stenosis and 23 healthy subjects. 7495208: It is not clear how frequently hypertrophic cardiomyopathy coexists with essential hypertension or whether chronic hypertension per se, induces hypertrophic cardiomyopathy (hypertensive hypertrophic cardiomyopathy). 8034891: Analysis of transmural trend of myocardial integrated ultrasound backscatter for differentiation of hypertrophic cardiomyopathy and ventricular hypertrophy due to hypertension. CONCLUSIONS: Hypertrophic cardiomyopathy and ventricular hypertrophy due to hypertension can be differentiated on the basis of quantitative analysis of the transmural gradient in integrated backscatter. 1000982: The most frequent form of cardiac lesion, however, is myocardial hypertrophy resulting from systemic hypertension. 10093576: Autopsy revealed high-grade myocardial hypertrophy caused by the hypertension, contracted kidney of vascular cause, hyperplasia of the parathyroid and calcification of the renal parenchyma as a sign of secondary parathyroidism. 10323483: The objective was to test the hypothesis that the effects of the sodium channel blockers lignocaine and tetrodotoxin are modified in the presence of hypertension-induced hypertrophy. 10426844: QT dispersion is also increased in myocardial hypertrophy secondary to systemic hypertension. 10472076: The structural and functional changes in arterial wall material associated with hypertension-induced hypertrophy may explain why medium-sized arteries maintain their distensibility characteristics despite a distending pressure increase; these changes may not be associated with an intrinsic (isobaric) decrease in the distensibility of large arteries. The purpose of this article is to review the relations between hypertension-induced hypertrophy and stiffness of the arterial wall. 10779123: Hypertension leads to ventricular hypertrophy and, eventually, to heart failure. These results show that cardiac responses are only minimally affected during the development of DOCA-salt hypertension-induced hypertrophy, despite the reported decreases in adenylate cyclase activity, in these rats. 10899071: GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. 10972671: BACKGROUND: In vivo, intraglomerular hypertension results in resident cell hypertrophy, proliferation and matrix protein production, leading to glomerulosclerosis. 11411317: Arterial hypertension causes myocardial hypertrophy and affects coronary circulation through structural and functional changes of the coronaries. 11436209: Cardiac remodeling in case of hypertension induces hypertrophy of myocytes and elevated collagen content and, subsequently, impaired diastolic filling of the left ventricle. 11524061: The disparity between midwall and endocardial shortening suggests reduced myofibril function in patients with hypertension-induced hypertrophy. 11827997: Myocardial hypertrophy resulting from hypertension often precedes heart failure. 12630091: It was established that hypertension induced hypertrophy and polyploidy of leimoyocytes of the circular muscular layer in the tunica media of the cerebral arteries, that was manifested as the increase in their nuclear DNA content and in the numbers of binuclear cells. 1266969: Hypertension, in turn, induced hypertrophy of the tunica media of the aorta. 12920136: A high salt diet significantly elevated blood pressure only in the beta3-null mice and resulted in hypertrophic changes in the aortic smooth muscle layer and cardiac enlargement. 130205: Augmented right ventricular function in systemic hypertension-induced hypertrophy. 1343288: Regression of hypertension-induced vascular hypertrophy by an ACE inhibitor and calcium antagonist in the spontaneously hypertensive rat. These results show that delapril and manidipine caused regression of hypertension-induced vascular hypertrophy in SHR. 1360561: It is possible that hypertension causes glomerular enlargement, proteinuria, and segmental glomerular lesions because of loss of functioning glomeruli due to ischaemia. 138750: Lysosomal enzymes in the development and regression of myocardial hypertrophy induced by systemic hypertension. 140280: Uncontrolled hypertension increases the workload of the left ventricle causing the development of hypertrophy and an increase in myocardial oxygen consumption that may precipitate ischemia because of inadequate oxygen delivery related to accelerated coronary atherosclerosis. 14504689: In addition, in separate preclinical studies, the NHE-1 inhibitor cariporide also prevented and/or caused regression of age-related and hypertension-induced myocardial fibrosis and hypertrophy. 14570285: Morphometrically, the arachnoid artery in control cats had a significantly thinner media than the renal artery, and the medial hypertrophy of the arachnoid artery resulting from HT occurred significantly less frequently than that of the renal artery. 15220895: Differences in regional systolic and diastolic function by Doppler tissue imaging in patients with hypertrophic cardiomyopathy and hypertrophy caused by hypertension. METHODS: A total of 62 participants were studied: 21 with HCM; 22 with LVH secondary to hypertension; and 19 control subjects. We evaluated DT differences for patients with LVH caused by hypertension and patients with HCM, assessing regional systolic and diastolic function. 1535028: Thus, there is a greater transmural resistance to microvascular perfusion in hearts with myocardial hypertrophy secondary to hypertension. 15501680: Chronic hypertension also causes hypertrophy, but in addition it causes an excessive increase in fibroblasts and extracellular matrix (fibrosis), death of cardiomyocytes and ultimately heart failure. 15694697: High-glycemic index nutrition is suggested to play a key role in the etiology of hypertension: The chronic stimulus of pancreatic beta-cells due to high-glycemic index nutrition may cause cell hypertrophy and dysfunction, resulting in postprandial hyperinsulinemia, and -- in susceptible subjects -- the development of EH. 16128371: QTd is increased in myocardial hypertrophy secondary to systemic hypertension. 16132109: In addition, in natural hypertension-induced hypertrophic hearts in genetically hypertensive rats, the COX protein was significantly lower than in normotensive rats. 16223983: Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. 16331818: CONCLUSION: The activation of ERK may play an important role in the development of myocardial hypertrophy caused by hypertension. 16412184: Severe uncontrolled hypertension may lead to severe hypertrophy of the left ventricle and produce systolic anterior motion of the mitral valve and an outflow gradient. 16472143: Second, most patients who undergo such surgery have myocardial hypertrophy due to hypertension, pressure or volume overload mediated by valve disease, or myocardial infarction. 16672836: PURPOSE: We tested how hypertension-induced compensated hypertrophy, both alone and coupled with exercise training, affects left ventricular (LV) Ca(2+) responsiveness during acidosis. 16982960: These results suggest that cathepsin S participates in pathological LV remodeling associated with hypertension-induced HF. 17009742: [Caveolin-3 and myocardial hypertrophy caused by hypertension]. 1721986: Also, systemic hypertension leads to hypertrophy, resulting in systolic and diastolic function abnormalities. 17382525: Hypertrophy, which may be induced by hypertension among other factors, is characterized by an increase in left ventricular mass and an associated increase in force production capacity. 17658497: Smoking accelerates the progression of hypertension-induced myocardial hypertrophy to heart failure in spontaneously hypertensive rats. 1773526: Structural changes in the cardiovascular musculature of the SHR during the development of hypertension appears to involve both prehypertensive hyperplastic cellular growth and hypertension induced cellular hypertrophy. 17873027: We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. 18032575: Exercise training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. Severe hypertension increased systolic blood pressure to 202 +/- 9 mmHg and induced pathological hypertrophy (LV hypertrophy index was 0.34 +/- 0.02 vs. 0.44 +/- 0.02 in Ctl-Sed and HT-Sed groups, respectively) with LV relaxation alteration (early-to-atrial wave ratio = 2.02 +/- 0.11 vs. 1.63 +/- 0.12). 18070810: The presence of left ventricule hypertrophy (LVH) due to arterial hypertension may impair atrial function. 18490734: Hypertension-induced cardiovascular hypertrophy and fibrosis are critical in the development of heart failure. We wondered whether vaccine bacillus Calmette-Guerin (BCG), which activated TLR4 to elicit immune responses, modulated the pressure overload-stimulated cardiovascular hypertrophy and cardiac fibrosis in the murine models of abdominal aortic constriction (AAC)-induced hypertension. 18634778: While hypertension-induced significant aortic wall hypertrophy and approximately 9-fold increases in the ratio of MMP-2/TIMP-2 mRNA expression (both P<0.05), lercandipine did not affect these changes. 18758513: SIM reverses these abnormalities and prevents the development of primary cardiac hypertrophy as well as hypertrophy secondary to L-NAME-induced hypertension. 18838620: AMP activated protein kinase 2 protection during hypertension-induced hypertrophy: a common mediator in the signaling crossroads. 19442329: The high blood pressure induces vascular hypertrophy, which in turn leads to increased vascular resistance. 19689927: Thus, sustained high BP may have caused progressive medial hypertrophy, increased aortic rigidity, and enlarged hearts with left ventricular dilation. 1981491: The apparent incidence of regression of hypertrophy was lower in the thiazide-alone group (group 1) than in the thiazide + beta-blocker group (group 2), most likely due to mild hypertension in group 1. 19858409: Using smooth muscle-targeted receptor activity-modifying protein 2 transgenic mice with increased vascular density of functional AM1 receptors, we demonstrate that receptor activity-modifying protein 2 transgenic mice are not protected against angiotensin II-induced hypertension or cardiac hypertrophy. The finding that the vascular smooth muscle AM1 receptor acts at a local level to protect against hypertension-induced vascular hypertrophy and inflammation provides evidence that targeting this receptor may be a beneficial therapeutic approach. 20198856: This result suggest implication of mitochondrial DNA in hypertension-induced left venticular hypertrophy. 2021114: The high blood pressure induces vascular hypertrophy, which in turn leads to increased vascular resistance. 2044440: High blood pressure causes vascular hypertrophy, and hypertrophic vessels are hyperresponsive to vasoconstriction. 20542874: AIMS: Innate and adaptive immune responses are associated with the development of hypertension-induced myocardial hypertrophy and fibrosis. As a result, we investigated whether heat shock protein (HSP) 70, which is a molecule of damage-associated molecular patterns, could induce inflammation in the myocardium and promote the development of hypertension-induced cardiac hypertrophy and fibrosis. 20972511: This was an echocardiographic study intended to describe the impact of left ventricular pressure overload and hypertrophy due to hypertension on right ventricular morphology and function. 2143634: Isoproterenol and myocardial O2 supply/consumption in hypertension-induced myocardial hypertrophy. 2159693: Similarly, local converting enzyme inhibition in the vascular wall may not only constitute a mechanism involved in the antihypertensive effects of converting enzyme inhibitors, but may also contribute to the regression of hypertension-induced vascular hypertrophy. 2258776: It is likely that prolonged stress-induced hypertension is the result of neurohormonal trophic factors which cause vascular hypertrophy or atherosclerosis. 23778187: BACKGROUND: Hypertension induces cardiovascular hypertrophy and fibrosis. 24065618: This approach has not been evaluated in humans or large animals with hypertension-induced pathological hypertrophy. Evaluation of docosahexaenoic acid in a dog model of hypertension induced left ventricular hypertrophy. 24114660: However, the antihypertensive effects were not associated with significant reversal of hypertension-induced vascular hypertrophy. 24189624: CONCLUSION: These results indicate that activation of aortic vascular ATRAP partially inhibits the Nox4/p22(phox)-ROS-p38MAPK/JNK pathway and pathological aortic hypertrophy provoked by Ang II-mediated hypertension, thereby suggesting ATRAP as a novel receptor-binding modulator of vascular pathophysiology. 24416343: CONCLUSIONS: Collectively, the present findings indicate that type 2 diabetes in its early stage is not yet associated with adverse cardiac structural changes, but already renders the heart more susceptible to hypertension-induced hypertrophic remodeling. METHODS: Thereto, 14-wks-old male db/db mice and non-diabetic db/+ mice received vehicle or angiotensin II (AngII) for 4 wks to induce mild hypertension (n = 9-10 per group). 24523346: Reactivation of fetal genes is commonly observed in hypertension-induced hypertrophy; however, this response is blunted in diabetic hearts, partially due to upregulation of the posttranslational modification O-linked-beta-N-acetylglucosamine (O-GlcNAc) to proteins by O-GlcNAc transferase (OGT). 24603314: Retinoid X receptor agonists inhibit hypertension-induced myocardial hypertrophy by modulating LKB1/AMPK/p70S6K signaling pathway. 2481172: High blood pressure (BP) leads to myocardial hypertrophy, a process in which catecholamines, and probably other hormones, are involved. 24930630: Hypertension, diabetes, hyperlipidemia and atherosclerosis are also linked to the etiology of lower urinary tract symptoms, benign prostatic hyperplasia/benign prostatic enlargement and erectile dysfunction. 25052897: Subgroup analysis revealed CT-1 levels to be highest in patients with hypertension-induced hypertrophy with HF, followed by patients with hypertension-induced left ventricular hypertrophy without HF (SMD, 0.52; 95% CI, 0.30-0.75 fmol/mL), patients with hypertension without left ventricular hypertrophy (SMD, 0.67; 95% CI, 0.46-0.88 fmol/mL) as compared with normotensive patients (SMD, 0.74; 95% CI, 10.45-1.04 fmol/mL). 25132960: UNLABELLED: Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. 2522298: This study examined myocardial O2 supply and O2 consumption in hypertension-induced myocardial hypertrophy. 2524290: These studies suggest that significant alterations in myocardial and coronary vascular structure and function occur in hypertension-induced cardiac hypertrophy. The purpose of these studies was to evaluate cardiovascular structural and functional changes in a model of hypertension-induced myocardial hypertrophy in which vasodilator therapy decreased blood pressure to normal levels. 25712288: Hypertension may cause myocardial hypertrophy even at a young age. 25770244: Proliferation and hypertrophy of vascular smooth muscle cells represent hallmark features of vessel remodeling secondary to hypertension. 26093301: Hypertension induced hypertrophy and diastolic dysfunction and is associated with cardiac oxidation and reduced NO production. 27262674: In contrast, pathological hypertrophy is induced by factors such as prolonged and abnormal hemodynamic stress, due to hypertension, myocardial infarction etc. 27349663: Complex diseases always involve some strait episode, such as myocardial hypertrophy and fibrosis caused by hypertension, microcirculation dysfunction and injury in heart, brain, lever, and intestine following ischemia and reperfusion, endotoxin induced multiorgan injury, and recovery after intestinal mucosa damage, for which intervention by a single medicine remains unsatisfied in clinic. 27514538: Oxidative stress is an important contributory factor for the development of cardiovascular diseases like hypertension-induced hypertrophy. 28009703: OBJECTIVE: Hypertension (increased afterload) results in cardiomyocyte hypertrophy leading to left ventricular hypertrophy and subsequently, heart failure with preserved ejection fraction. 28383811: HSF1 phosphorylation by ERK/GSK3 suppresses RNF126 to sustain IGF-IIR expression for hypertension-induced cardiomyocyte hypertrophy. Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure (HF). 28447711: The results revealed that GSPE alleviated hypertension-induced hypertrophic vascular remodeling in the small arteries of SHR, which was independent of blood pressure. 29032314: Systemic HT was induced by the constriction of one of the renal arteries (Goldblatt HT), while BF in the CCA was reduced and increased by the constriction of the ipsilateral CCA and the ligation of the contralateral CCA, respectively. However, only in HT/lower BF group, WSS and vascular smooth muscle-activated vascular contraction were smaller than in the other groups, possibly because of wall hypertrophy induced by HT. 2932919: The purpose of this study was to determine 1) whether a severe hypoxic stimulus could produce an increase in coronary and collateral vascularization and 2) whether minimal coronary resistance, which increases with hypertension-induced hypertrophy, decreases when hypoxia is superimposed on volume load hypertrophy. 2935604: The therapeutic effect can be assessed at various levels of aim, such as: (1) a reduction in cardiovascular morbidity and mortality, (2) a normalization of hypertension-induced cardiovascular hypertrophy or renal damage or (3) simply a fall in blood pressure. 2963794: This suggests that these changes are the result of hypertrophy per se, rather than due to a generalised mechanism secondary to hypertension and operating on all tissues. In association with left ventricular hypertrophy (secondary to hypertension), left ventricular pHi became significantly alkaline in all experimental hypertensive groups compared with control values; pHi control (in response to an acidosis) was also significantly improved. 2964946: Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). 2969734: Nevertheless, not in all cases of SCD was myocardial hypertrophy caused by AH. 2970842: ECG, systolic blood pressure (BP), the ratio (R) of grams of myocardial mass/100 g of body mass, total lipids, cholesterol, triglycerides and phospholipids in blood plasma and the left ventricular myocardium, as well as the plasma free fatty acids, were investigated in 58 male Wistar rats 3, 30 and 180 days after operation, in a model of myocardial hypertrophy (MH) induced by experimental coarctation hypertension, after the method of Selye. 2973462: Conditions known to affect cardiac myosin composition, such as hypothyroidism and hypertrophy secondary to systemic hypertension, do not change the troponin T isoform profile of adult rat ventricles. 2987125: Moderate left ventricular hypertrophy induced by long-term aortic banding in dogs resulted in elevations in beta-adrenergic receptor density (115 +/- 14 fmol/mg) and decreases in affinity (10.4 +/- 2.2 nM) similar to those observed in the dogs with left ventricular hypertrophy induced by hypertension. beta-Adrenergic and cholinergic receptors in hypertension-induced hypertrophy. 30860808: The ciliopathic hearts displayed hypertrophy with compromised functions in left ventricle pressure, stroke volume, ejection fraction, and overall cardiac output because of prolonged hypertension. 3157434: In contrast, the hypertension-induced hypertrophy of the left ventricle was further increased in a dose-dependent fashion by minoxidil. 31830479: Verapamil decreases calpain-1 and matrix metalloproteinase-2 activities and improves hypertension-induced hypertrophic cardiac remodeling in rats. 32566092: Hypertension induces vascular hypertrophy, which changes blood vessels structurally and functionally, leading to reduced tissue perfusion and further hypertension. 33240671: Herein, the effect of miR-26a-5p on cardiac hypertrophy was investigated using phenylephrine (PE)-induced cardiac hypertrophy in vitro and in a rat model of hypertension-induced hypertrophy in vivo. 33611212: Small Molecule Compound Nerolidol attenuates Hypertension induced hypertrophy in spontaneously hypertensive rats through modulation of Mel-18-IGF-IIR signalling. However, their effects on hypertension induced cardiac complications are not completely understood. CONCLUSION: Collectively, the data reveals that the cardioprotective effect of nerolidol against hypertension induced hypertrophy involves reduction in blood pressure and regulation of the cardiac Mel-18-IGFIIR signalling cascade. 34259984: PURPOSE: Systemic hypertension may induce adverse hypertrophy of the left cardiac ventricle. 34816004: However, the apoE-/- mice presented signs of diastolic dysfunction by hypertrophic changes in left ventricle, due probably to arterial hypertension. 35356999: Persistent arterial hypertension leads to structural and functional remodeling of the heart resulting in myocardial ischemia, fibrosis, hypertrophy, and eventually heart failure. 36527481: Quercetin ameliorated hypertension-induced coronary arterial hypertrophic remodeling, although it did not reduce cardiac hypertrophic remodeling and dysfunction. 36577600: We discuss recent preclinical studies that use targeted antagomir delivery systems to treat three major cardiovascular diseases (atherosclerosis, myocardial infarction, and cardiac hypertrophy, including hypertrophy caused by hypertension), highlighting therapeutic results and discussing challenges that limit clinical applicability. 37116729: CONCLUSION: Compound Qidan Formula, composed of traditional Chinese herbs, can significantly improve cardiac function, improve atrial and ventricular remodeling, and prevent myocardial fibrosis and hypertrophy in rats with HFpEF induced by hypertension and diabetes mellitus. 3955449: It is known that hypertension results in hypertrophy of vascular smooth muscle. 4093618: In addition, apical hypertrophy in ASH-HT with the NH form of septal configuration seemed to be caused by hypertension. 4767260: Hypertension induces hypertrophy and increased turnover of aortic smooth muscle cells along with an accumulation of connective tissue in the aortic wall. 6197373: Mechanisms of vascular hypertrophy induced by hypertension were studied in cultured aortic smooth muscle cells from spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) and compared with those from normotensive Wistar-Kyoto (WKY) rats. Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats. 6867318: Hypertension leads to hypertrophy of the left ventricle through enlargement of individual muscle fibres, but numeric hyperplasia also occurs. 7097402: Carotid body hyperplasia occurred in cases of myocardial hypertrophy secondary to both hypoxaemia and systemic hypertension. 7115983: In both these experiments although BAPN lowered blood pressure it did not affect the hypertension-induced hypertrophy of the aorta. BAPN suppressed the rise in blood pressure during the developing phase of deoxycorticosterone acetate-salt-induced hypertension and in this model the compound also prevented the accompanying aortic hypertrophy. 7449279: These results indicate that hypertrophy of the media is a consequence of high blood pressure rather than a genetically determined pathogenetic factor for the development of hypertension in spontaneously hypertensive rats. The increased peripheral resistance observed in established hypertension has been attributed to structural changes in the resistance vessels, which are considered to be due mainly to medial hypertrophy. 7512481: These long term benefits include protection of the vasculature, an attenuation of hypertension-induced hypertrophy and improved left ventricular diastolic function. 7635546: The purpose of this article is to review some clinical and fundamental evidence that hypertension-induced arterial wall hypertrophy at the site of large and medium-sized arteries is not necessarily associated with a decreased arterial distensibility and increased elastic modulus, and to demonstrate the opposing effects of aging and hypertension-induced hypertrophy on the arterial mechanics in vivo. in the studies reported here, the elastic properties of large and medium-sized arteries were noninvasively assessed from the simultaneous measurement of internal diameter and blood pressure inside the systolic-diastolic range. 7774863: Nevertheless the differences in the expression of the fetal forms of FN mRNA observed among the various models of hypertension-induced hypertrophy indicate that the process of FN pre-mRNA splicing in the adult myocardium is specifically regulated and depends on the pathological situations and the type of cell. 8038754: These results indicate that medial hypertrophy is a late consequence of chronic hypertension in this model and is confined primarily to the abdominal aorta. 8178541: Arterial hypertension causes myocardial hypertrophy and fibrosis, and affects coronary microcirculation by structural and functional changes of the small intramural resistance arteries, rarefiction of arterioles and capillaries and a distinct disturbance of endothelial vasomotion (i.e. 8281955: Hypertension produces myocyte hypertrophy and increases the extracellular matrix. 888910: Morphometric analysis of hypertension-induced hypertrophy of rat thoracic aorta. 8913533: This abnormal growth occurs during hypertension-induced vascular hypertrophy, during the development of an atherosclerotic lesion, and during the development of a restenotic lesion following angioplasty. 8946071: The structural and functional changes of the arterial wall material that are associated with the hypertension-induced hypertrophy could be a means by which medium-sized arteries maintain their distensibility characteristics despite increased distending pressure, and large arteries compensate for the age-induced decrease in arterial compliance. 8949371: This preliminary study shows that, like in humans, high fat diet in dogs induced abdominal obesity with systemic hypertension but failed to provoke left cardiovascular hypertrophy after 20 weeks. [Experimental hypertension induced by hypercaloric diet]. 9196540: The mechanism by which hypertension produces hypertrophy is unclear, but our results suggest that this structural modification is not related to the activities of some peptidases, e.g. protein and peptide hydrolases. 9278778: This study has shown that there are no differences in the cardiac responses to isoprenaline at beta(1)-adrenoceptors, isoprenaline KA values or the beta(1)-adrenoceptor reserve for isoprenaline on the SHR left ventricle in prehypertension or in the early stages of hypertension-induced hypertrophy. 9299358: Therefore, we studied the expression of TnT isoforms (SDS-PAGE, Western blots), myosin isoforms, myofibrillar ATPase activity, and left ventricular (LV) mechanoenergetics (rbc perfused, isovolumically contracting isolated heart) in a rabbit model of mild hypertrophy (LVH) due to gradual hypertension caused by 12 weeks of cellophane wrap of the kidneys (n=12). 9351439: To determine the involvement of proinflammatory cytokine in cardiac hypertrophy and CHF induced by mechanical overload, we investigated the expression of interleukin (IL)-1 beta and monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein-1 (MCP-1) in the left ventricle (LV) of Dahl salt-sensitive (DS) rats that showed hypertrophy of the LV induced by hypertension and subsequently developed CHF. 9384495: Long-term hypertension induced myocardial hypertrophy and an abnormal response to NA. We sought to examine whether myocardial hypertrophy induced by long-term hypertension changes the effects of NO on myocardial contractility. These results suggests that positive inotropic effects of exogenous and endogenous NO are not changed in hypertension induced myocardial hypertrophy. 9403566: Decreased tissue HGF in target organs of hypertension may be due to increased tissue angiotensin II. In contrast, tissue HGF concentrations in heart, aorta, and kidney were significantly decreased in SHR as compared with WKY at 25 weeks of age, when these organs showed hypertrophic changes induced by hypertension (P<.01). 9412636: Systemic hypertension also causes vascular hypertrophy. 9488198: In both atherosclerosis and arterial hypertension, structural and functional abnormalities result in vascular hypertrophy that is associated with an increased ratio of vascular media thickness to lumen diameter and hyperreactivity of vascular smooth muscle cells (VSMCs), resulting in uncontrolled cell migration and growth in vivo. 9546036: Also acute hypertension may produce less hypertrophy in the elderly and therefore place more hemodynamic stress on the left ventricle than in young adults. This is typical of what occurs in hypertension induced hypertrophy as well. 9574484: The predominance of fiber bundles arranged in an approximately transverse direction with regard to the arterial cone axis suggests a resistance to enlargement resulting from high aortic blood pressure. 9693501: Both combinations of the antihypertensive drugs prevented development and progression of myocardial hypertrophy due to hypertension. 9812770: It indicates that amlodipine is of great significance on regression of genesis and development of cardiovascular hypertrophy due to hypertension. The effect of anti-hypertensive drug amlodipine on regression of cardiovascular hypertrophy due to hypertension was studied by using cultured smooth muscle cells derived from arteries of spontaneously hypertensive rats (SHR) and measuring [3H]-TdR and [3H]-Leucine binding. 10147590: Patients were selected from echocardiographic criteria and specific history of disease and divided into the following groups: compensated moderate to severe aortic regurgitation; compensated LV hypertrophy caused by systemic hypertension; and dilated congestive cardiomyopathy. 10337348: UNLABELLED: DETECTION OF LEFT VENTRICULAR HYPERTROPHY: High blood pressure can lead to left ventricular hypertrophy and is an independent risk factor of cardiovascular disease. 10435057: Although arterial hypertension is regarded as the principal factor, the pathogenesis of LV hypertrophy in PHPT is complex and not completely defined, moreover the effects of successful parathyroidectomy (PTX) are not fully elucidated. 10773237: OBJECTIVE: In left ventricular hypertrophy (LVH) due to systemic hypertension, myocardial fibrosis is an important determinant of pathologic hypertrophy. 10818082: We conclude that in Dahl rats, LVH secondary to hypertension protects against ischemia-induced diastolic dysfunction by minimizing the size of the region of severe acidosis. Accordingly, we studied isolated hearts from 3 groups of Dahl salt-sensitive rats, controls, and hearts with matched amounts of LVH secondary to either hypertension or aortic constriction. 10886571: Inadequate diagnosis and therapy of arterial hypertension as causes of left ventricular hypertrophy in uremic dialysis patients. 10993775: We used an LV time-varying elastance model coupled to an arterial four-element lumped-parameter model to study ventricular-arterial interaction in hypertension-induced LVH. 11033114: METHODS: LVH was secondary to perinephritis-induced hypertension. 11045938: High blood pressure is the leading cause of left ventricular hypertrophy (LVH); however, not all hypertensive patients develop LVH. 11230273: We conclude that ventricular stretch and other mechanisms (eg, cardiac vagal activity) in rats appear to be more potent than hypertension-induced left ventricular hypertrophy in predisposing for lethal arrhythmias in the setting of acute ischemia. 11413864: The results showed that 6 weeks of hypertension resulted in left ventricle myocardial hypertrophy, documented by weight, morphometry and morphological changes. 11433216: This report reviews the connective tissue matrix of the normal human myocardial tissue and the pathological myocardial fibrosis in left ventricular hypertrophy due to chronic arterial hypertension in humans and in human chronic chagasic myocarditis. 11447089: CONCLUSIONS: Systemic HTN induces LV hypertrophy, myocardial fibrosis, and isolated diastolic dysfunction in the absence of local or systemic activation of Ang II or ET. 11477918: [Progress in the treatment of hypertension-induced left ventricular hypertrophy with Chinese traditional medicine]. 11686913: The groups included patients with: dilated cardiomyopathy (n = 29), myocardial infarction (n = 90), established coronary artery disease without a myocardial infarction (n = 11), or hypertension induced left ventricular hypertrophy (n = 15). 11812909: In ESRD patients, hypertension is also a leading cause of LVH, but structural LV changes and myocardial fibrosis may also be due to non-haemodynamic factors such as angiotensin II, parathyroid hormone, endothelin, aldosterone, increased sympathetic nerve discharge and increased plasma catecholamines. 11827687: OBJECTIVE: To characterize the cardiac angiotensin and endothelin (ET) system in compensated left ventricular hypertrophy due to long standing arterial hypertension and to assess the role of angiotensin and ET converting enzymes in mediating the observed changes of angiotensin and ET levels, respectively. 11910313: RESULTS: Hypertension induced compensatory left ventricular (LV) hypertrophy at 13 weeks in six untreated rats. 11993020: Thus, LV hypertrophy, probably secondary to hypertension, is the most frequent echocardiographic finding, with LV dysfunction (such as seen in coronary artery disease) seen less often. 12074352: METHODS: We examined 49 athletes with left ventricular (LV) hypertrophy due to endurance training, 49 patients with LV hypertrophy due to arterial hypertension, and 26 untrained healthy control subjects by conventional echocardiography. 12122615: Similar effects were seen in hearts with left ventricular hypertrophy secondary to perinephritis-induced hypertension. 12189324: Drug-induced regression of left ventricular hypertrophy (LVH) due to arterial hypertension is generally accompanied by improved cavity filling because of changes in the structural and functional determinants of diastolic efficiency. 12204500: CONCLUSIONS: Myocardial perfusion reserve and maximal coronary flow improved in asymptomatic patients with hypertension-induced LVH after long-term treatment with lisinopril but not with losartan. 12355999: In patients with type 2 diabetes, left ventricular hypertrophy is mainly due to high blood pressure, but also to reduced elasticity of the large vessels, defective vasomotricity and dysfunction of the arterial endothelium. 12372679: CONCLUSIONS: Diminished functional capacity in patients with hypertension-induced LVH is related to the impairment in MPR and left ventricular diastolic function. 12398877: METHODS: The one-kidney, one-clip model (1K1C) of hypertension was used to produce LVH. 12489796: Although kinins have been associated with the regulation of cardiovascular function in left ventricular hypertrophy (LVH) as a consequence of hypertension, myocardial infarction (MI), and/or diabetic cardiomyopathy, less is known about their receptor regulation under these conditions. 12620705: BACKGROUND: The aim of this study was to identify the best correlate of myocardial oxygen demand (MVO(2)) in patients with hypertension induced left ventricular hypertrophy (LVH), and to examine whether relationships between these surrogates and MVO(2) differed between patients with LVH and control subjects. CONCLUSIONS: The best correlate of resting MVO(2) in the patients with hypertension induced LVH was the stress-mass-heart rate product. 12623300: Our results suggest the possibility that the Gq-Rho kinase pathway plays an important role in the process of hypertension-induced LV hypertrophy leading to contractile dysfunction. Chronic inhibition of Rho kinase blunts the process of left ventricular hypertrophy leading to cardiac contractile dysfunction in hypertension-induced heart failure. 12623952: We used the Dahl salt-sensitive (DS) rat model, in which systemic hypertension causes LVH at the age of 11 weeks, followed by HF at the age of 18 weeks. 12631088: CONCLUSION: Young adult patients with pediatric ESRD are at risk for LVH caused by hypertension and for aortic valve calcification. 12641877: Increased vascular volume causes hypertension, which in turn causes LVH, cardiac failure, and ischemic heart disease (IHD). 135571: There was no hypertensive subject with both signs of left ventricular hypertrophy on orthogonal electrocardiography and either an a/H ratio over 15 per cent or an abnormal atrial sound, indicating two different forms of cardiac involvement as the result of hypertension. 1363074: The LV diastolic dysfunction seen in 8/11 cases may have been related to LV hypertrophy caused by long-term hypertension or chronic persistent ischemia. 1414167: The main early pathophysiological disturbance is left ventricular hypertrophy, resulting from hypertension, coronary artery disease, increasing age and obesity. 14295381: [ELECTROVECTOCARDIOGRAPHIC STUDY OF 25 PATIENTS WITH LEFT VENTRICULAR HYPERTROPHY CAUSED BY ARTERIAL HYPERTENSION]. 1438089: The close relationship between urinary albumin excretion and Sokolow index observed in this study suggests that left ventricular hypertrophy due to hypertension may account for the increased cardiovascular mortality observed in non diabetic subjects with microalbuminuria. 145228: Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. 14587651: The short-term (three months) effects of rilmenidine on systemic hypertension induced left ventricular hypertrophy (LVH) and left ventricular systolic and diastolic functions in comparison with those of perindopril and nifedipine-slow release (SR) formulation were studied. 14621181: However, it is not clear whether there is any difference between the coronary blood flow increase in LVH caused by hypertension (HTH) and that caused by hypertrophic cardiomyopathy (HCM) when the heart rate increases. Different coronary blood flow increase in left ventricular hypertrophy due to hypertension compared to hypertrophic cardiomyopathy at elevated heart rate. 15039815: Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. 15110903: METHODS: Study subjects comprised 16 patients with hypertension-induced left ventricular hypertrophy and 10 normotensive controls. 15189524: Our findings, also supported by preliminary results on patients affected by hypertension induced LV hypertrophy, suggest a potential role of MCG in the evaluation of early electrophysiological alterations due to LV concentric remodeling. 15220895: Differences in regional systolic and diastolic function by Doppler tissue imaging in patients with hypertrophic cardiomyopathy and hypertrophy caused by hypertension. METHODS: A total of 62 participants were studied: 21 with HCM; 22 with LVH secondary to hypertension; and 19 control subjects. We evaluated DT differences for patients with LVH caused by hypertension and patients with HCM, assessing regional systolic and diastolic function. 15272237: Hypertension and anemia may be causes of left ventricular hypertrophy (LVH) in uremia but the molecular mechanism is not known. 1530791: CONCLUSIONS: Left ventricular hypertrophy caused by hypertension or other cardiovascular disease is not only a marker for but also a contributor to cardiovascular morbidity and mortality in elderly and young patients. 1530994: Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia. 15522574: In patients with coronary artery disease, the presence of left ventricular hypertrophy secondary to hypertension is associated with an increased collateral development. 15549413: In transplanted patients a concentric LVH as a result of chronic hypertension is mostly observed; in dialysis patients a more asymmetric septal LVH is found as a result of chronic volume overload. 158962: However, coronary vascular resistance is greatly increased when hypertension is the cause of left ventricular hypertrophy. Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation. 15913489: Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. 15956824: PURPOSE OF REVIEW: Hypertension leads to left ventricular hypertrophy, diastolic dysfunction, and eventually clinical heart failure (hypertensive heart disease). 15976793: METHODS: We sought to evaluate the differences in coronary flow velocity using conventional transthoracic Doppler echocardiography, measuring both the left anterior descending and such intramural (IM) coronary arteries' flow, among the following 4 categories of patients with myocardial hypertrophy: group A, obstructive hypertrophic cardiomyopathy (n = 12); group B, nonobstructive hypertrophic cardiomyopathy (n = 10); group C, left ventricular hypertrophy (LVH) due to hypertension (n = 10); and group D, LVH due to aortic valve stenosis (n = 10). 16053992: BACKGROUND: Left ventricular (LV) hypertrophy and diastolic dysfunction, which are common cardiac consequences of hypertension, are modified by insulin resistance. 16132238: In contrast to men, hypertension and diabetes represent the major risk factors for development of HF in women and hypertension is also the major cause of left ventricular hypertrophy and stroke. 16243920: We conclude from these data that HT alone is an insufficient descriptor of the cause of LV hypertrophy and diminished LV cardiomyocyte function in the SHR rat. 16439828: BACKGROUND: Left ventricular (LV) hypertrophy is a common consequence of systemic hypertension (SH) and obstructive sleep apnea (OSA). 16457607: Comparison of the protein profile of established and regressed hypertension-induced left ventricular hypertrophy. The main finding of this work was to identify proteins differently expressed in hypertension-induced LVH and the fact that after regression of LVH (histologically determined), the proteome still maintains a number of expressed proteins characteristic of the hypertrophied heart. 1655265: It would now seem logical to determine whether cardioreparation can be achieved with lisinopril in patients with hypertension and left ventricular hypertrophy, in whom pathologic remodelling of the myocardium is responsible for symptomatic heart failure. 16627048: Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. 16750782: BACKGROUND: Hypertension-induced left ventricular hypertrophy (LVH) is associated with an increased risk of cardiovascular morbidity and death by mechanisms not well characterized. 16849902: In conclusion, these agents are efficacious in antihypertensive therapy and can play an important role in the prevention or regression of left ventricular hypertrophy due to hypertension. 16955278: We report on three cases of hypertension-induced LVH in the pediatric population and its regression after treatment with antihypertensive medications. 16955820: Left ventricular hypertrophy (LVH), estimated by echocardiography, was the most frequently observed systemic consequence of hypertension, being present in 32 (91.4%) of the hypertensive dogs. 17082376: Beta-adrenergic receptor (beta-AR) responsiveness is downregulated in left ventricular (LV) hypertrophy induced by chronic hypertension. 17130255: Proteomic analysis of early left ventricular hypertrophy secondary to hypertension: modulation by antihypertensive therapies. Further investigations are necessary to elucidate the exact role of CS-1 and ubiquinone biosynthesis protein COQ7 in the setting of hypertension-induced LVH. Untreated or poorly controlled arterial hypertension induced development of pathologic left ventricular hypertrophy (LVH), a common finding in hypertensive patients and a strong predictor of cardiovascular morbidity and mortality. An experimental model of hypertension-induced early LVH was performed in spontaneously hypertensive rats, and the cardiac protein pattern compared with the normotensive Wistar Kyoto counterpart was analyzed. 17172276: Three geometric patterns of LVH can be induced by hypertension: concentric remodeling, concentric hypertrophy, and eccentric hypertrophy. 17178264: CONCLUSIONS: The Glu27 variant of beta(2)AR enhances hypertension-induced left ventricular hypertrophy. 17291198: To investigate whether substrate utilization influences cardiac growth and CHD risk, we examined the association between the functional LPL S447X (rs328) variant and hypertension-induced LV growth and CHD risk. The lipoprotein lipase gene serine 447 stop variant influences hypertension-induced left ventricular hypertrophy and risk of coronary heart disease. 17579564: BACKGROUND: The clinical phenotype of both hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) induced by hypertension is heterogeneous. 17585473: Uncontrolled hypertension induces left ventricular hypertrophy, heart failure and death, but also promotes deterioration of allograft function. 17637792: Echocardiographic characterization of the geometry in hypertension-induced LV hypertrophy might become an important step in the selection of optimal antihypertensive therapy. 1777585: Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. 17827797: Hypertension causes left ventricular hypertrophy and increases in large artery stiffness with ageing, both of which are cardiovascular risks. 17885545: Left ventricular hypertrophy is a major cardiac sequel of hypertension. 17895567: The pattern of LVH is distinctive in hypertrophic or metabolic cardiomyopathy and differs from that seen in LVH caused by hypertension or aortic stenosis. 17979778: Hypertension-induced left ventricular hypertrophy (LVH), along with ischemic heart disease, result in LV remodeling as part of a continuum that often leads to congestive heart failure. 18177389: The aim of this study was to investigate differences in MA motion between hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) patients due to hypertension or aortic stenosis using real time three-dimensional echocardiography (RT3DE). 1827058: Early after the onset of left ventricular hypertrophy secondary to hypertension, coronary vasodilator reserve is significantly impaired. During cardiac hypertrophy secondary to hypertension, the coronary arteries fail to enlarge in concert with ventricular enlargement. 1832414: This LVH resulting from hypertensive disease conveys an independent risk of premature cardiovascular morbidity and mortality. 1833986: These data support several important conclusions regarding long-term hypertension-induced LVH in dogs. 1834553: We measured left ventricular blood flow with radioactive microspheres during aortic pressure reduction in 10 open-chest, anesthetized dogs with left ventricular hypertrophy due to chronic hypertension and in 10 matched normotensive dogs. 1837564: Left ventricular hypertrophy due to hypertension was used as an index of the severity of hypertension. 1838767: We have shown that these reflexes are markedly depressed in subjects with left ventricular hypertrophy (LVH) due to hypertension and that this is also the case when, in normotensive subjects, LVH is caused by prolonged physical training. 1839825: Left ventricular hypertrophy is the most important cardiovascular consequence of chronic systemic hypertension. Left ventricular hypertrophy resulting from systemic hypertension: adaptive advantage and adverse consequences. 1839891: STUDY OBJECTIVE: The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. Effect of left ventricular hypertrophy secondary to systemic hypertension on left coronary artery flow dynamics. 1841924: [Left ventricular hypertrophy secondary to systemic hypertension: its effect on coronary hemodynamics]. 18471464: Functional differences of left ventricular hypertrophy induced by either arterial hypertension or aortic valve stenosis. The aim of this study was to reveal functional differences of left ventricular (LV) hypertrophy induced by either aortic stenosis (AS) or arterial hypertension (AH) assessed by strain-rate imaging. 18577845: These results indicate that LV hypertrophy and dysfunction due to hypertension are more apparent in patients with cerebral hemorrhage than in those with cerebral infarction. Left ventricular (LV) hypertrophy and dysfunction due to hypertension have been established as risk markers for stroke in hypertensive patients. 18754816: These results demonstrated that PPARalpha activator fenofibrate may exert a protective effect on cardiac remodelling in SHRs by decreasing the expression of c-fos and c-jun and suppressing the formation of c-fos/c-jun heterodimers, which may further inhibit transcription of the downstream genes involved in the pathogenesis of left ventricular hypertrophy induced by hypertension. 18764802: Left ventricular hypertrophy (LVH), present in 70-80% of patients at the start of dialysis, results from chronic high blood pressure, volume overload, or both, in association with a number of metabolic and neurohumoral alterations. 18804478: We recently found that inhibition of epsilonPKC slows down the progression of hypertension-induced HF in salt-sensitive Dahl rats fed a high-salt diet. Six week-old male Dahl rats were fed with a high-salt diet to induce systemic hypertension, which resulted in concentric left ventricular hypertrophy at the age of 11 weeks, followed by myocardial dilatation and HF at the age of 17 weeks. Mast cells and epsilonPKC: a role in cardiac remodeling in hypertension-induced heart failure. Together, our data suggest that epsilonPKC inhibition attenuates pathological remodeling in hypertension-induced HF, at least in part, by preventing cardiac MC degranulation. 18806901: There is an abnormal accumulation of fibrillar collagen accompanying the hypertension-induced LV hypertrophy, which is also associated with decreased compliance and LV diastolic dysfunction. 19018687: In-keeping with this, it has been observed that hypertension-induced LVH increases the risk of sudden cardiac death. 19166699: Hypertension is the most common cause of left ventricular (LV) hypertrophy. 19204182: Long-term urocortin 2 treatment in hypertensive rats induced sustained blood pressure reduction and diminished the development of hypertension-induced left ventricular hypertrophy and the deterioration of left ventricular contractile function. 19325563: Therefore, regression of hypertension-induced LVH is associated with a distinct gene expression profile, suggesting the effect of both treatment and a previously unknown specific myocardial physiology after regression of LVH. Transcriptome of hypertension-induced left ventricular hypertrophy and its regression by antihypertensive therapies. Left ventricular hypertrophy (LVH), a common consequence of systemic hypertension associated with poor clinical outcome, is also a potentially reversible condition. 19367002: This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. 19427502: Obesity hypertension through metabolic, endocrinic, and systemic hemodynamic alteration causes structural vascular and cardiac adaptations that trigger concentric, eccentric left ventricular hypertrophy and electrophysiological changes, which may increase the risk for congestive heart failure and sudden cardiac death as a result of arrhythmias. 19561308: Left ventricular (LV) hypertrophy (LVH) is an independent risk factor for cardiovascular mortality and is commonly caused by hypertension. 19620510: Hypertension also induces left ventricular (LV) hypertrophy. 19771749: Echocardiography is the tool of choice for the assessment of the athlete's heart and also for the differentiation of physiologic and pathologic LVH (hypertrophic cardiomyopathy and LVH due to arterial hypertension). 19809991: Hypertension may provoke de novo left ventricular hypertrophy and cardiac failure in dialysis patients and is also associated with a higher risk of stroke. 19815660: AIMS: Chronic hypertension may cause left ventricular hypertrophy (LVH). 19844185: OBJECTIVE: Both hypertension and aortic valve stenosis induce left ventricular hypertrophy. 19917781: Hypertension leads to LVH in adults, but its role in the pathogenesis of LVH in children is not as well established. 20042874: OBJECTIVE: Left ventricular hypertrophy (LVH) is a major cardiac sequel of hypertension and a powerful predictor of cardiovascular morbidity and mortality. 20070154: Left ventricular hypertrophy (LVH) is a complication that may result from chronic hypertension. 20087555: The aim of this study was to examine the relationship between HTN-induced LVH and TOD (retinopathy and renal failure). 20226627: LA enlargement on echocardiography has been documented in HCM and moderate or severe HT, both conditions causing LV hypertrophy. 20388649: AIMS: To test acute effects of the corticotropin-releasing factor-related peptide urocortin 2 (Ucn2) on left ventricular (LV) function and the propensity for ventricular arrhythmias in the isolated heart of an animal model of hypertension-induced heart failure. Acute effects of urocortin 2 on cardiac function and propensity for arrhythmias in an animal model of hypertension-induced left ventricular hypertrophy and heart failure. 20480263: Structural remodelling of the heart, known as left ventricular hypertrophy (LVH), is a consequence of systemic hypertension, and is associated with an increased risk of cardiovascular morbidity and mortality. 20563545: Substantial consequences of hypertension are microangiopathy, interstitial fibrosis and left ventricular hypertrophy. Arterial hypertension often leads to diseases of kidneys, vessels and brain. 20635566: Left ventricular hypertrophy is the most prominent evidence of target organ damage caused by hypertension in children and adolescents. 20696682: OBJECTIVE: Hypertension may lead to left ventricular hypertrophy, fibrosis and degeneration of the conduction system. 21066891: CONCLUSIONS: Changes in RAS in the hypertrophied myocardium of SHR may be one of the molecular mechanisms for hypertension leading to left ventricular hypertrophy. 21233798: BACKGROUND: Hypertension (HTN) may lead to left ventricular hypertrophy and vascular dysfunction, which are independent factors for adverse cardiovascular outcomes. 21274714: LV mass index was not discriminant between patients with HCM and those with LVH due to hypertension. 21320507: Left ventricular hypertrophy due to hypertension represents a major risk factor for adverse cardiovascular events and death. 2139976: Left ventricular hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. 2150470: Its contribution to global cardiovascular risk is three times greater than that of hypertension which is the principal cause of LVH. 2150476: Left ventricular hypertrophy secondary to hypertension has been associated with a reduction of maximum coronary flow per unit mass as shown by the increase in the minimal threshold of coronary vascular resistance per gramme. 22015318: Left ventricular hypertrophy (LVH) induced by systemic hypertension (SH) represents a maladaptive response to the increased overload. 22093163: The myocardial ischemia was due to severe resistant hypertension complicated with concentric left ventricular hypertrophy and increased arterial stiffness. 22113443: Our analysis calls for a more aggressive treatment of hypertension and related CV risk factors leading to LVH. 22252479: BACKGROUND: Hypertension-induced left-ventricular hypertrophy (LVH) is generally accompanied with coronary neovascularization. 22340460: Hypertension is the major cause of LVH. 22380695: Cardiac remodelling is defined as changes in the size, shape, and function of the heart, which are most commonly caused by hypertension-induced left ventricular hypertrophy and myocardial infarction. 22666973: Diagnostic dilemma occurs when this type of HCM is newly discovered in a patient previously diagnosed with left ventricular hypertrophy (LVH) secondary to hypertension. 22730392: We sought to determine if interferon-gamma (IFNgamma) plays a role in mediating the transition from hypertension-induced LVH to diastolic HF. 22967989: Vascular remodeling-associated hypertension leads to left ventricular hypertrophy and contractile dysfunction in profilin-1 transgenic mice. 23072794: BACKGROUND: Systemic Hypertension (SH) is the main cause of left ventricular (LV) hypertrophy in the general population, but only scanty data are available on LV geometric remodeling (LVGR) in hypertensive patients with GH deficiency (GHD). 23073243: 2K1C hypertension induced LV hypertrophy associated with augmented gelatinolytic activity at an early phase of hypertension and further increased after 75 days of hypertension. 23140764: Hypertension can induce left ventricular hypertrophy (LVH), and the nitric oxide (NO) pathway plays an important role in the pathogenesis of cardiac hypertrophy. 23169928: Sustained hypertension resulted in worsening left ventricular hypertrophy and he died suddenly at a tragically young age several years after presentation. 23192734: Clinical value of carotid wave intensity analysis for differentiating nonobstructive hypertrophic cardiomyopathy from left ventricular hypertrophy secondary to systemic hypertension. 23213108: METHODS AND RESULTS: LV tissue samples were procured from normal dogs (CTRL) and old dogs with hypertension-induced LV hypertrophy and diastolic dysfunction (OHT/HFpEF). 23363940: Arterial stiffness (AS) and central (aortic) blood pressures play a significant role in end-organ damage such as LV hypertrophy caused by hypertension. 23671437: Non-dipping blood pressure pattern may be responsible for the development of left ventricular concentric hypertrophy secondary to hypertension. INTRODUCTION: Long-lasting arterial hypertension causes left ventricular hypertrophy (LVH) and impairs left ventricular diastolic function. 23673471: The results from the present study suggest that the dephosphorylation of Src tyrosine kinase 529, the phosphorylation of tyrosine 418 and their subnuclear redistribution are involved in endonuclear signal transduction in cardiac myocytes, which regulates the development and progression of LV eccentric hypertrophy induced by hypertension. 23747907: Similar to clinical echocardiographic observations, hypertension in rats results in left ventricular hypertrophy (LVH) and diastolic dysfunction and aldosterone receptor blockade reduces LVH in SHR. 23865125: OBJECTIVE: To explore the pattern of left ventricular hypertrophy caused by hypertension and to compare it with idiopathic hypertrophiccardiomyopathy. 24023472: BACKGROUND: Left ventricular hypertrophy (LVH) is a common pathophysiological consequence of hypertension. 24065618: This approach has not been evaluated in humans or large animals with hypertension-induced pathological hypertrophy. Evaluation of docosahexaenoic acid in a dog model of hypertension induced left ventricular hypertrophy. 24139053: Secondary objectives were to determine geometric alterations of the left ventricle and to analyze the interdependence of hypertension and obesity to induce LVH. 24337854: Multivariate analysis showed that hypertension and acute rejection history were the risk factors that resulted in left ventricular hypertrophy. 24412709: Left ventricular hypertrophy is a common consequence of hypertension. 24629670: We surmise that HT promotes aberrant regulation of cardiac Ca(2+), Cu(2+), Mg(2+) and Zn(2+), which does not necessarily result in cardiac dysfunction. The spontaneously hypertensive rat (SHR) has been studied extensively as a model of left ventricular hypertrophy (LVH) and associated cardiac dysfunction due to hypertension (HT). 24640942: BACKGROUND: Left ventricular (LV) twist is usually influenced by LV hypertrophy resulting from hypertension or vascular stiffness. 24647357: However, in hypertension-induced left ventricular hypertrophy (H-LVH), the signaling pathways of tanshinone IIA in inhibition of remodeling and cardiac dysfunction remain unclear. The complex regulation of tanshinone IIA in rats with hypertension-induced left ventricular hypertrophy. 24728428: BACKGROUND: High blood pressure causes left ventricular hypertrophy, which is a negative prognostic factor among hypertensive patients. 24933619: In conclusion, we found evidence that two beta1-blockers with different properties attenuate hypertension-induced LV hypertrophy and cardiac collagen deposition in association with significant cardiac antioxidant effects and MMP-2 downregulation, thus suggesting a critical role for beta1-adrenergic receptors in mediating those effects. Hypertension induces left-ventricular hypertrophy (LVH) by mechanisms involving oxidative stress and unbalanced cardiac matrix metalloproteinase (MMP) activity. 25052897: Subgroup analysis revealed CT-1 levels to be highest in patients with hypertension-induced hypertrophy with HF, followed by patients with hypertension-induced left ventricular hypertrophy without HF (SMD, 0.52; 95% CI, 0.30-0.75 fmol/mL), patients with hypertension without left ventricular hypertrophy (SMD, 0.67; 95% CI, 0.46-0.88 fmol/mL) as compared with normotensive patients (SMD, 0.74; 95% CI, 10.45-1.04 fmol/mL). 2521543: Left ventricular hypertrophy is a common consequence of chronic hypertension. 2521791: Although hypertension is the major cause of left ventricular hypertrophy (LVH), numerous studies failed to demonstrate a close correlation between resting blood pressure (BP) and degree of LVH. 2524524: Left ventricular hypertrophy due to hypertension is associated with a decrease of coronary vascular reserve. 2530619: Ventricular arrhythmias and left ventricular hypertrophy secondary to hypertension: a brief review. 2530923: The present case shows that an impending myocardial infarction may occur in patients having normal coronary arteriogram but with left ventricular hypertrophy secondary to arterial hypertension. 2532080: Left ventricular hypertrophy (LVH) is a structural adaptation of the heart and is a response to increased hemodynamic and metabolic demands, which are most commonly caused by systemic hypertension. LVH induced by hypertension is associated with reduced myocardial compliance, structural alterations, and changes in coronary perfusion. Effects of calcium entry blockade on hypertension-induced left ventricular hypertrophy. 2533528: Importance of abnormalities in coronary flow reserve to the pathophysiology of left ventricular hypertrophy secondary to hypertension. 25413328: Our data suggest that in hypertension-induced left-ventricular hypertrophy, the mechanical performance of the tissue is compromised such that myocardial efficiency is reduced. 25593786: However, earlier stages of disease may be causally related or contribute to peripheral or cerebral embolism, pre-hypertension and hypertension, and increased left ventricular afterload resulting in left ventricular hypertrophy and diastolic dysfunction. 25691541: CONCLUSIONS: In SHR, hypertension induces early subcellular LA myocyte Ca2+ remodelling during compensated LV hypertrophy. 25791172: In conclusion, we propose that metabolic imaging with FDG PET may provide a novel approach to guide the treatment of patients with hypertension-induced LVH. 26594908: OBJECTIVES: Hypertension (HTN) is a common cause of left ventricular hypertrophy (LVH). In this study, we tested the hypothesis that metabolic remodeling, characterized by increased myocardial glucose uptake, precedes structural and functional remodeling in HTN-induced LVH. 26995439: Hyperactive sympathetic nervous system aggravates hypertension and it can cause complications like left ventricular hypertrophy, heart failure, arrhythmias and atherogenesis. 27168169: PURPOSE OF REVIEW: Left ventricular hypertrophy (LVH), an important consequence of hypertension, is traditionally classified as either concentric or eccentric based on the presence or absence of increased relative wall thickness. 2735090: Five frequently used hemodynamic oxygen consumption parameters were compared with the directly measured myocardial oxygen consumption (MVO2) in 28 patients with different heart diseases (4 without heart disease, 2 with mitral valve prolapse, 20 with coronary artery disease with or without left ventricular dysfunction, 2 with mitral regurgitation, 1 with hypertrophic obstructive cardiomyopathy and 3 with left ventricular hypertrophy due to hypertension). 27757525: We analyzed the waveform of systolic strain and strain-rate curves to find a characteristic left ventricular (LV) myocardial contraction pattern in patients with hypertrophic cardiomyopathy (HCM), and evaluated the utility of these parameters for the differentiation of HCM and LV hypertrophy secondary to hypertension (HT). 27816525: Arterial hypertension causes left ventricular (LV) myocyte hypertrophy. 27861330: High blood pressure is the primary cause of left ventricular hypertrophy (LVH), which represents a strong predictor of future heart failure and cardiovascular mortality. Increased mean aliphatic lipid chain length in left ventricular hypertrophy secondary to arterial hypertension: A cross-sectional study. 27872872: Systemic hypertension is a causative factor in left ventricular hypertrophy (LVH). 28062414: A novel complex I inhibitor protects against hypertension-induced left ventricular hypertrophy. 28099129: Using a limit of LVMI ?38 g/m2.7 in evaluating LVH secondary to HT in obese individuals may lead to an overestimated diagnosis rate of LVH. 28123181: Reverse electrical remodeling following pressure unloading in a rat model of hypertension-induced left ventricular myocardial hypertrophy. 28410843: BACKGROUND: Left ventricular hypertrophy (LVH) secondary to hypertension has been accepted to prevent heart failure (HF) while paradoxically increasing cardiovascular morbi-mortality. 2842021: Correlation of left ventricular hypertrophy and its regression by lisinopril with salt-induced hypertension. The interaction of salt with hypertension-induced left ventricular hypertrophy and its reversal by inhibition of angiotensin converting enzyme were studied in salt sensitive and salt resistant Dahl rats. 28448842: The stronger association with BP in women may relate to more severe hypertension-induced left ventricular hypertrophy. 28553631: With multiple definitions, prevalence of pediatric HTN-induced LVH is difficult to ascertain. 28581677: Extracellular fluid volume overload and its inevitable consequence, hypertension, increases cardiovascular mortality in the long term by leading to left ventricular hypertrophy, heart failure, and ischemic heart disease in dialysis patients. 28627693: In the present study, utilizing a model of hypertension-induced cardiac hypertrophy in spontaneous hypertensive rats, it was demonstrated that RD was significantly associated with a reduction in LV hypertrophy. In addition, RD in hypertension-induced LV hypertrophy rats was associated with the attenuation of cellular autophagic response over activation at a physiological level. 28757483: BACKGROUND: Left ventricular (LV) hypertrophy and subclinical cerebrovascular disease are early manifestations of cardiac and brain target organ damage caused by hypertension. 28799247: Hypertension-induced left ventricular hypertrophy (LVH) is an independent risk factor for heart failure. 2889345: It is now generally accepted that hypertension-induced left ventricular hypertrophy (LVH) represents a phenomenon of multifactorial origin. 29156835: Indonesian herbal medicine prevents hypertension-induced left ventricular hypertrophy by diminishing NADPH oxidase-dependent oxidative stress. 29161309: CONCLUSION: The results suggest by three alternative and complementary ways (analysis of anatomy and cardiac function, metabolism and histological structure) that dronedarone has the potential to reverse the LVH induced by arterial hypertension in the SHR model of compensated ventricular hypertrophy. 29249587: Correlations of Serum Cyclophilin A and Melatonin Concentrations with Hypertension-induced Left Ventricular Hypertrophy. 2926037: Routine clinical echocardiographic data were obtained on 34 subjects at the Mayo Clinic (10 normal subjects, 10 patients with amyloid heart disease, 8 patients with hypertrophic cardiomyopathy and 6 patients with left ventricular hypertrophy due to hypertension). 2945675: Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors. 2948470: [Effects of exercise on coronary circulation in left ventricular hypertrophy caused by hypertension]. 2954450: Left ventricular (LV) filling was examined by Doppler and M-mode echocardiography in 24 patients with LV hypertrophy (five with aortic stenosis, six with hypertrophic cardiomyopathy, and 13 with LV hypertrophy secondary to systemic hypertension) and in 18 normal subjects. 2960623: After treatment with alpha-methyldopa a regression of left ventricular hypertrophy, due to hypertension, has been reported in spontaneously hypertensive rats. 2961249: Overall risk of left ventricular hypertrophy secondary to systemic hypertension. 29626209: The aims of this study were to determine the impact of the XRCC3 polymorphism on the incidence of hypertension-induced left ventricular hypertrophy (LVH) and to investigate the mechanisms underlying any potential relationship. 2963527: These findings indicate that celiprolol can be used for the successful long-term treatment of essential hypertension, and that such treatment reduces left ventricular hypertrophy induced by high blood pressure. 2963794: This suggests that these changes are the result of hypertrophy per se, rather than due to a generalised mechanism secondary to hypertension and operating on all tissues. In association with left ventricular hypertrophy (secondary to hypertension), left ventricular pHi became significantly alkaline in all experimental hypertensive groups compared with control values; pHi control (in response to an acidosis) was also significantly improved. 2964945: Accordingly, this study was undertaken in a nonhuman primate model of left ventricular hypertrophy caused by gradual onset experimental hypertension. 2964946: Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). 29671305: One of them?is hypertension induced left ventricular?hypertrophy and fibrosis, progressive?deterioration of left ventricular compliance,?increase in left ventricular enddiastolic?pressure which in turn lead to?left ventricular diastolic dysfunction.?The other pathomechanism of heart?failure associated to hypertension is?accelerated coronary artery atherosclerosis,?ischemia of the left ventricle?and its systolic dysfunction. Natural history of?hypertension leads to heart failure in?two main mechanisms. 2968038: Left ventricular (LV) hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. 2969742: Left ventricular hypertrophy secondary to systemic hypertension is associated with altered autoregulation of myocardial perfusion; 4. 2987125: Moderate left ventricular hypertrophy induced by long-term aortic banding in dogs resulted in elevations in beta-adrenergic receptor density (115 +/- 14 fmol/mg) and decreases in affinity (10.4 +/- 2.2 nM) similar to those observed in the dogs with left ventricular hypertrophy induced by hypertension. beta-Adrenergic and cholinergic receptors in hypertension-induced hypertrophy. 29958714: It is unknown whether left ventricular hypertrophy (LVH) as a consequence of hypertension is also a risk factor for both these end points. 29968754: Extracellular volume (ECV) has been validated as a surrogate measure of interstitial fibrosis, that is increased in both hypertension-induced left ventricular hypertrophy (H-LVH) and hypertrophic cardiomyopathy (HCM). 30077834: BACKGROUND: Left ventricular hypertrophy (LVH) is an indicator of organ damage largely due to hypertension. 30341642: CONCLUSIONS: In hypertensive athletes LVH due to hypertension can be reduced and LV-function can be improved by long-term antihypertensive medication despite regular aerobic exercise. 30501597: Background The development and risk potential of hypertension-induced left ventricular (LV) hypertrophy has been well described in epidemiological studies. 30710427: Most importantly, we identify the efficacies of ATp300 inhibitors C646 and L002 in reversing hypertension-induced cardiac hypertrophy and fibrosis, and discover new anti-hypertrophic and anti-fibrotic candidates. Previously, we reported that acetyltransferase p300 (ATp300) inhibitor L002 prevents hypertension-induced cardiac hypertrophy and fibrosis in a murine model. Acetyltransferase p300 inhibitor reverses hypertension-induced cardiac fibrosis. In this short communication, we show that treatment of hypertensive mice with ATp300-specific small molecule inhibitor L002 or C646 reverses hypertension-induced left ventricular hypertrophy, cardiac fibrosis and diastolic dysfunction, without reducing elevated blood pressures. 30764689: Myocardial metabolic changes may thus serve as early diagnostic markers for hypertension-induced left ventricular hypertrophy. 31048225: Myocardial fibrosis is one of the components of left ventricular hypertrophy secondary to hypertension. 31051181: LV contraction-relaxation coupling was examined during LV hypertrophy induced by chronic hypertension. 31404095: BACKGROUND: Hypertension results in left ventricular hypertrophy and cardiac dysfunction. 3233803: Five groups were studied (total 152 patients): a control group of 30 healthy volunteers, 32 patients after surgical correction of infantile tetralogy of Fallot, 50 patients treated for childhood malignancies with doxorubicin, 17 patients with left ventricular hypertrophy due to systemic hypertension, and 23 patients with congestive cardiomyopathy. 3804402: Left ventricular hypertrophy resulting from hypertension is accompanied by significant morbidity and mortality and in advanced stages may be irreversible. 6213304: Inadequate coronary reserve is present in left ventricular hypertrophy secondary to hypertension. 6226196: Obesity and other high cardiac output states predominantly produce dilatation of the left ventricle, and their combination with arterial hypertension results in eccentric left ventricular hypertrophy. 6728806: These results indicate that high dietary calcium not only attenuates high blood pressure in turkeys but also reduces the development of left ventricular hypertrophy, which is a consequence of arterial hypertension. 7494927: Arterial hypertension can cause left ventricular hypertrophy and consequent hypertensive cardiopathy, a condition that is associated with the development of heart failure, arrhythmia and ischemia. 7498879: Chronic mechanical stress of the heart by arterial hypertension is a primary cause of left ventricular hypertrophy. 7585803: METHODS: LVH was induced by perinephritic hypertension in New Zealand White rabbits. 7586324: It was learned, for example, that the adverse consequences of hypertension do not derive chiefly from the diastolic pressure, left ventricular hypertrophy was not an incidental compensatory phenomenon, and small amounts of proteinuria were more than orthostatic trivia. 7628882: Our data suggest that marked afterload reduction has a negative impact on the myocardial ultrastructure in hypertension-induced left-ventricular hypertrophy. 7632023: In almost 200 case of left ventricular hypertrophy (LVH) secondary to hypertension (HT), including 75 cases with conduction disorders, 100 cases of normal adults and 20 cases of normal children, segmental (initial horizontal vector, maximal anterior and posterior vector of the QRS) and spatial vectorial parameters were correlated to segmental echocardiographic parameters (septum, anterior and posterior wall of the left ventricle) and mass parameters (left ventricular mass index). 7633909: Hypertension and lipid abnormalities which often lead to left ventricular hypertrophy and accelerated atherosclerosis as well as coronary artery disease are a common cause of death. 7788874: Twenty-one dogs were studied: 6 dogs with LV hypertrophy (LVH) induced by perinephritic hypertension, 5 sham-operated normotensive dogs, and 10 acute normotensive control dogs. 7807508: Left ventricular hypertrophy (LVH) is a common consequence of hypertension, and an independent risk factor for cardiovascular morbidity and mortality. 7898097: Furthermore, cilazapril decreased left ventricular mass index in essential hypertensive patients within 6 months of therapy at doses of 2.5-5.0 mg once daily, thus reversing left ventricular hypertrophy induced by hypertension. 8017304: Investigators have reported that patients with end-stage renal disease and left ventricular hypertrophy due to hypertension have diminished lateral/septal count ratios on stress and delayed imaging mimicking lateral myocardial infarction in approximately 35% of patients. In conclusion, myocardial thallium-201 distribution is normal in patients with left ventricular hypertrophy due to hypertension. The purpose of this study was to compare myocardial SPECT thallium-201 distribution in a broader group of patients with left ventricular hypertrophy resulting from hypertension with normal file subjects in order to determine the prevalence of abnormal studies and to compare the lateral/septal count ratio. 8103506: Among the clinical consequences of hypertension, left ventricular hypertrophy (LVH) is a prominent manifestation. 8103741: Hypertensives with or without LVH have reduced coronary vasodilator reserve due to hypertensive disease of small coronary arteries. 8159603: Left ventricular hypertrophy (LVH) is a consequence of long-standing hypertension and is considered to be an independent risk factor for cardiovascular morbidity and mortality. 8320834: It is well known that systemic hypertension induces cardiac hypertrophy, and it can be prevented by antihypertensive drugs. It is suggested that mechanism of left ventricular hypertrophy which is induced by systemic hypertension is related with cardiac angiotensinogen m-RNA expression. 8402746: Thus, nifedipine was an effective antihypertensive agent and reverted LV hypertrophy secondary to arterial hypertension without impairment of LV systolic function. 8485835: Arterial hypertension leads to left ventricular hypertrophy. 8547842: Hypertension induced significant left ventricular hypertrophy in DOCA-salt rats (26%) and in SHR (54%) and a 30% decrease in calpain activity in both groups (P < 0.01). 8608665: Left ventricular hypertrophy (concentric and eccentric), which can be due to hypertension and anemia, is commonly observed in ESRD patients and has been shown to be a predictor of cardiac morbidity and mortality in these patients. Renal failure itself obviously is a prerequisite in the pathogenesis of r-HuEPO-induced hypertension, since it was never observed in anemic patients without renal disease. Normalization, though, is generally not achieved and in patients with r-HuEPO induced hypertension the increase of blood pressure may oppose the beneficial effects of r-HuEPO treatment on cardiac hypertrophy. 8642802: The sympathetic system is also involved in the genesis of hypertension-induced LVH. 8762077: Our results show that hypertension causes not only left ventricular hypertrophy but also molecular transition of myocardium to a foetal phenotype and interstitial fibrosis-related molecular changes. 8776278: Furthermore, patients with left ventricular hypertrophy due to hypertension have a greater prevalence of late potentials (LP) compared with normal subjects. 8832558: In summary, the most common cause of death was infection (48%), followed by chronic rejection (19%), surgical complications (19%), post-transplantation lymphoproliferative disorder (7%), and unrelated causes (7%); rejection was not a major cause of death in the early and intermediate post-transplantation periods; in 30% of native lungs, significant pathologic findings were present in addition to the primary disease; and in the intermediate post-transplantation period, significant left ventricular hypertrophy occurred, which may be attributable to cyclosporine-induced hypertension but which needs to be further studied. 8863101: PURPOSE: Left ventricular hypertrophy (LVH) caused by systemic hypertension, myocardial infarction and congestive heart failure is associated with pathological changes in the structure of the heart, collectively described as remodelling (see part 1 of this review). 8922345: In conclusion, suprarenal aortic coarctation leads to progressive hypertension resulting in LVH, progressive increases in plasma ANP and BNP and, in most cases, death from heart failure. 8957600: BACKGROUND AND HYPOTHESIS: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. 8960451: Arterial hypertension frequently occurs in association with myocardial ischaemia and is an independent and significant risk factor for the development of coronary artery disease (CAD), as is left ventricular hypertrophy due to arterial hypertension. 8964117: Nine had HCM, and the remaining patients comprised three comparison groups: 11 with normal left ventricular (LV) function, 13 with LV hypertrophy secondary to chronic hypertension (LVH-HTN), and 9 with idiopathic dilated cardiomyopathy (DCM). 9040021: Alteration of coronary circulation observed in left ventricular hypertrophy secondary to hypertension could be associated with a decrease in NO production. 9045274: Left-ventricular hypertrophy is the main cardiac consequence of systemic hypertension. 9239425: The former causes concentric left ventricular [LV] hypertrophy, results from hypertension and aortic stenosis, and is also associated with diabetes mellitus and anemia. 9283537: Differences in myocardial velocity gradient measured throughout the cardiac cycle in patients with hypertrophic cardiomyopathy, athletes and patients with left ventricular hypertrophy due to hypertension. OBJECTIVES: We sought to compare the myocardial velocity gradient (MVG) measured across the left ventricular (LV) posterior wall during the cardiac cycle between patients with hypertrophic cardiomyopathy (HCM), athletes and patients with LV hypertrophy due to systemic hypertension and to determine whether it might be used to discriminate these groups. 9299358: Therefore, we studied the expression of TnT isoforms (SDS-PAGE, Western blots), myosin isoforms, myofibrillar ATPase activity, and left ventricular (LV) mechanoenergetics (rbc perfused, isovolumically contracting isolated heart) in a rabbit model of mild hypertrophy (LVH) due to gradual hypertension caused by 12 weeks of cellophane wrap of the kidneys (n=12). 9411588: The left ventricular hypertrophy is a deleterious consequence of the arterial hypertension, recognized as independent risk factor. 9469636: In hypertension-induced left ventricular hypertrophy, potentiation of endogenous kinins contributes to the improvement of cardiac function and energy metabolism and to capillary proliferation effected by ACE inhibitors. 9486935: The relationships between angiotensin-converting enzyme (ACE) gene insertion (I) / deletion (D) polymorphism and left ventricular hypertrophy induced by hypertension or idiopathic hypertrophic cardiomyopathy have been studied. 9493122: These findings suggest a direct interaction between Ang II and cardiac fibroblasts in mediating myocardial fibrosis in arterial hypertension, leading to pathologic left ventricular hypertrophy with initially impaired diastolic and ultimately reduced systolic function of the left ventricle. 9500863: In conclusion, LVH induced by perinephritis hypertension in the rabbit is associated with a prolongation in APD. 9535420: In Dahl-Iwai rats, salt-sensitive hypertension causes concentric left ventricular hypertrophy (LVH) at the age of 11 weeks, which is followed by LV dilatation with global hypokinesis and pulmonary congestion, ie, LV failure (LVF), at 16 to 18 weeks of age. 9601485: Chronic mechanical stress of the heart secondary to arterial hypertension is a primary cause of left ventricular hypertrophy (LVH). 9789465: The case report describes a 50-years-old patient with left ventricular hypertrophy, severe heart failure and ischemic chest pain due to untreated arterial hypertension. 9794745: Pathologic fibrosis and connective tissue matrix in left ventricular hypertrophy due to chronic arterial hypertension in humans. OBJECTIVE: To investigate pathologic fibrosis and connective tissue matrix in left ventricular hypertrophy due to chronic arterial hypertension in humans. 9808606: BACKGROUND: To investigate whether endogenous ET-1 participates in an adaptive process of left ventricular hypertrophy (LVH) or a maladaptive process from LVH to congestive heart failure (CHF), we used a Dahl salt-sensitive (DS) rat model, in which systemic hypertension caused compensated concentric LVH at the age of 11 weeks followed by marked LV dilatation and global hypokinesis at the age of 17 weeks. 9819015: BACKGROUND: Left ventricular hypertrophy (LVH) has been identified as a main target organ change resulting from hypertension, also being a long-term predictor of myocardial infarction, stroke and cardiovascular death. 9873225: Morphological changes in the myocardium after left ventricular hypertrophy, due to chronic experimental hypertension, require an understanding of the quantitative relationship between myocyte and nonmyocyte compartments forming the structural framework of the myocardium. 16719796: Studies in animal models of hypertension in pregnancy suggest that inadequate cytotrophoblast invasion of uterine spiral arteries causes reduction in uteroplacental perfusion pressure leading to placental ischemia/hypoxia. If untreated, PE leads to eclampsia with serious seizures and severe hypertension. 1730436: We hypothesize that hypertension causes artery wall hypoxia that contributes to the formation of atherosclerotic lesions. 1793456: Experimental hypertension, hyperlipemia and balloon injury produce medial hypoxia with steep PO2 gradients and redistribution of the pattern of arterial wall antioxidant enzymes. 19064797: White matter changes on MRI are thought to be due to hypoxic episodes related to hypoperfusion of the vulnerable deep white matter secondary to hypertension, diabetes, and other vessel diseases. 25651567: An additional simulation suggests that a sufficiently large reduction in tubular transport efficiency may be the key contributing factor, more so than oxidative stress alone, to hypertension-induced medullary hypoxia. 25772710: Physiological studies have identified that augmented carotid body chemosensory reflex and the resulting increase in sympathetic nerve activity are major contributors to CIH-induced hypertension. This article reviews the physiological and molecular basis of CIH-induced hypertension. Rodent models patterned after the O2 profiles seen with SDB patients showed that CIH is the major stimulus for causing systemic hypertension. 26418696: Sensitivity in detecting spinal cord blood flow and oxygenation changes during aortic occlusion, pharmacologically induced hypotension and hypertension, and physiologically induced hypoxia/hypercarbia was assessed. 26593642: An amplification of this respiratory modulation of sympathetic activity is observed in hypertension of both genetic, the spontaneously hypertensive rat, and induced, chronic intermittent hypoxia or maternal protein restriction during gestation, origin. 29357386: The intestines are very sensitive to IAH since the low splanchnic perfusion causes intestinal hypoxia, local acidosis and bacterial translocations. 36154596: Peripheral hypoxia, a consequence of hypertension, activates hypoxia-inducing factors 1-alpha and 1-beta (HIF-1alpha, HIF-1beta), which modulate innate immune cells and promotes inflammation. 37399715: Therefore, the current study aims to investigate the NOX4 inhibitor GLX351322 that targets NOX4 inhibition in acute ocular hypertension (AOH)-induced retinal ischemia/hypoxia injury in mice. 4039679: The data indicate that long-lasting high systemic arterial blood pressure leads to changes of the wall of the arterial vessels of the carotid and presumably also the aortic bodies thus inducing an ischemic hypoxia of the specific chemoreceptive tissue and a chronic stimulation of the arterial chemoreceptors. 11912866: It has been hypothesized that chronic hypertension may eventually result in small subcortical infarcts associated with some cognitive impairments. 12624287: BACKGROUND AND PURPOSE: Autopsy studies found that lacunar strokes differ in the size of the underlying brain infarct and that small lacunes are usually caused by hypertensive small-artery disease (SAD) and larger ones by atheromatous or embolic perforator occlusion. 15927823: Hypertension is a multifactorial disease with many causes and a profound impact on the cardiovascular system, whereas subarachnoid hemorrhage induced cerebral vasospasm is a pathological vasoconstriction often causing infarction that is thought to be 'caused' by a factor or factors in the CSF following the hemorrhage. 19021021: In terms of pathophysiology of hypertensive brain damage, several hypotheses were developed, such as that vascular alterations induced by hypertension can induce lacunar or cortical infarcts and leucoaraiosis, that hypertension is responsible for cerebrovascular disease and acts into the contest of a pre-existing subclinic Alzheimer's disease (AD), that hypertension determines neurobiologic alterations (such as beta-amyloid accumulation) resulting in neuropathologic damage, and that aging and cerebrovascular risk factors act together to cause cerebral capillary degeneration, mitochondrial disruption, reduced glucose oxidation, and reduced ATP synthesis. 25534370: CONCLUSIONS: The increased visibility of cerebral veins on SWI as a sign of venous hypertension and the thickened cerebral venous walls (venous collagenosis), which may play a role in cerebral ischemia and/or infarction, are both consequences of long-term hypertension in hypertensive rats. 29213787: VP is usually the result of conventional vascular risk factors, particularly hypertension, leading to strategic infarcts of subcortical gray matter nuclei, diffuse white matter ischaemic lesions and less commonly, large vessel infarcts. 36056308: The cause of hand knob hemorrhage was hypertension, while the causes of hand knob infarction were mainly small-vessel occlusion (SVO) (35.3%) and large-artery atherosclerosis (LAA) (35.3%), and the rare causes include carotid artery dissection and carotid body tumor. 395551: Arterial hypertension causes the formation of small lacunes, or ischemic brain infarcts, which may result in transient ischemic attacks, hemiparesis, sensory loss, ataxic hemiparesis, or dysarthria. 8443976: All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth. 86103: Thus it would seem that, in severe middle-aged hypertensives, attempts at \normalisation\ of high blood-pressure may precipitate as many infarctions as it prevents. 16481883: Renal and vascular hypertension-induced inflammation: role of angiotensin II. 17173244: Long-term treatment with an ACE inhibitor or an AT1 antagonist avoids hypertension-induced inflammation in the kidney. 19434050: Inflammation is an important part of the damage caused by hypertensive diseases. 19858409: Using smooth muscle-targeted receptor activity-modifying protein 2 transgenic mice with increased vascular density of functional AM1 receptors, we demonstrate that receptor activity-modifying protein 2 transgenic mice are not protected against angiotensin II-induced hypertension or cardiac hypertrophy. The finding that the vascular smooth muscle AM1 receptor acts at a local level to protect against hypertension-induced vascular hypertrophy and inflammation provides evidence that targeting this receptor may be a beneficial therapeutic approach. 20733571: HO-1 attenuates hypertension-induced inflammation/oxidative stress: support from Bartter's/Gitelman's patients. 23887740: Inhibition of platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis. Taken together, our results indicate Ang II infusion-induced hypertension stimulated platelet activation and platelet-leukocyte conjugation, which initiated inflammatory responses that contributed to cardiac fibrosis. Inflammation promotes the development of cardiac fibrosis and heart failure induced by hypertension. 23942950: Pro-inflammatory role of platelets in hypertension-mediated end-organ damage : Editorial to: \Inhibition of Platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis\ by L.-X. 24418158: Thus, improving autophagy may be a novel therapeutic strategy to ameliorate hypertension-induced inflammation and organ damage. OBJECTIVE: Hypertension induces end-organ damage through inflammation, and autophagy plays a crucial role in the regulation of cellular homeostasis. 25534368: The present findings suggest that a persistent hypertension caused a long-lasting inflammation after tMCAO in SHR-SR, which accelerated neurovascular disruption and emergent inflammasome, and that telmisartan greatly reduced such inflammation and protected the neurovascular unit via its pleiotropic effects in living hypertensive rat brain after ischemic stroke. 25915881: CONCLUSION: These findings highlight the link between purinergic signalling and inflammatory process and suggest a novel mechanism in which moderate aerobic exercise possesses the potential to attenuate inflammation caused by hypertension. 25921924: These results suggest that HDAC6 may be a valuable therapeutic target for the treatment of hypertension-induced kidney fibrosis and inflammation. Hypertension was induced by infusion of ANG in mice. 27121797: The results from the present study suggest that activated platelets secrete P-selectin to promote cardiac inflammation and fibrosis in Ang II-induced hypertension. Platelet activation is important in hypertension-induced cardiac inflammation and fibrosis. 27167462: CONCLUSIONS: Prediabetes and hypertension induce endothelial dysfunction and inflammation by elevating levels of soluble adhesion molecules and inflammatory cytokines. 29490666: The cause-and-effect relationship between hypertension and inflammation is two-way, but the role of blood pressure in the induction of cerebral inflammation is less clear. 29843153: Chronic high blood pressure induces inflammation. BACKGROUND/AIMS: Hypertension is the leading cause of death worldwide. 30606987: The chronic hypertension caused the inflammation and lipid peroxidation in kidneys, measured by of tissue level of cytokines such as interleukin-1beta (IL-1beta), IL-6, Tumor Necrosis Factor-alpha (TNF-alpha), IL-10 and malondialdehyde, and treatments for M. parviflora were able to modulate these parameters. 30664681: In this Review, we focus on evolving concepts regarding the roles of fibroblast growth factor 23 (FGF23), inflammation and systemic oxidant stress and their interactions with more established mechanisms such as pressure and volume overload resulting from hypertension and anaemia, respectively, activation of the renin-angiotensin and sympathetic nervous systems, activation of the transforming growth factor-beta (TGFbeta) pathway, abnormal mineral metabolism and increased levels of endogenous cardiotonic steroids. 30930414: Hypertension is one risk for atrial fibrillation (AF) and induces cardiac inflammation. 31896903: The pain in such patients is most likely due to ductal hypertension, parenchymal hypertension, and head mass causing perineural inflammation. 32029051: 12-HETE plays an important role in many diseases such as cancer, diabetes, hypertension, and participates in the pathogenesis of inflammation and oxidative stress and other pathological processes. 32971534: The Impact of Hypertension and Use of Calcium Channel Blockers on Tuberculosis Treatment Outcomes.BACKGROUND: Hypertension induces systemic inflammation, but its impact on the outcome of infectious diseases like tuberculosis (TB) is unknown. 33858279: BACKGROUND: Arterial hypertension causes cardiovascular adverse events mainly through endothelial dysfunction, atherosclerosis, and inflammation. 35069813: However, the possible effects of the statin pitavastatin on hypertension-induced endothelial inflammation and injury remain to be fully elucidated. 35305976: These in silico and in vivo results indicated that a change in lipid profile and hypertension led to diabetes-related inflammation by promoting ER stress and, as a result, accelerating the aorta by generating proinflammatory cytokines and lipid deposition. 35354938: Inflammation plays an important role in the pathophysiology and contributes to the deleterious consequences of arterial hypertension. 37098960: BACKGROUND: Hypertension causes subendothelial inflammation and dysfunction in resulting atherosclerosis. 37273847: Hypertension-induced inflammation and subsequent ventricular fibrosis are believed to underlie the development of HFpEF. 10854077: States of hyperinsulinaemia and insulin-resistance have been postulated as causes and/or consequences of hypertension. 11098553: Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). 15633625: Our results suggest that functional HNO is essential to achieve maximal insulin sensitivity and that HNO action is compromised in hypertension, resulting in HISS-dependent insulin resistance. 15775796: The relative change in MFVR and M/IG were inversely related, supporting the hypothesis that peripheral vascular changes in hypertension may induce insulin resistance. OBJECTIVE: Hypertension and insulin resistance might be associated through peripheral vascular hypertrophy/rarefaction which compromises skeletal muscle blood flow and decreases glucose uptake, inducing insulin resistance. 16767285: Experimental obesity and insulin resistance can be due to a deficient response to leptin, secondary to hypoleptinemia and/or mutations on leptin receptor, by modifications on insulin receptor, deletion or diminished insulin signal transduction, enhancement of the effects of orexigen peptides and/or diminution of anorexigen peptides actions on hypothalamus, as well as secondary to arterial hypertension, as in the spontaneously hypertension. 1889847: To test whether hypertension can cause hyperinsulinemia or insulin resistance, we performed intravenous glucose tolerance tests at 1 month and euglycemic clamps at 3 months after induction of two-kidney, one clip renovascular hypertension in rats. 21796124: We previously reported that chronic hyperinsulinemia and insulin resistance induced by fructose-drinking loading elicited hypertension associated with abnormal neuronal regulation of vascular tone in an in vivo study using pithed rats. Hyperinsulinemia induces hypertension associated with neurogenic vascular dysfunction resulting from abnormal perivascular innervations in rat mesenteric resistance arteries. 27320537: Its significance in the pathogenesis of CHD has been strengthened by observations showing that OW is responsible for the development of diabetes, hypertension and lipid disorders due to its induction of insulin resistance (IR). 28679946: BACKGROUND: Induction of insulin resistance is a key pathway through which obesity increases risk of type 2 diabetes, hypertension, dyslipidemia, and cardiovascular events. 32131408: Metabolic Fingerprint of Turner Syndrome.Girls with Turner syndrome (TS) are at increased risk of developing insulin resistance and coronary artery disease as a result of hypertension and obesity frequently seen in these patients. 33235693: The metabolic syndrome, a cluster of metabolic disorders, includes abdominal obesity, hypertension, dyslipidemia, and hyperglycemia leading to insulin resistance, development of diabetes mellitus, and cardiovascular diseases. 36912156: CONCLUSIONS: Our results suggest that elevated insulin concentration at birth plays a critical role in the early life origins of hypertension and support the hypothesis implicating insulin resistance in the etiology of hypertension. BACKGROUND: Although insulin resistance is closely related to hypertension, the debate continues as to whether insulin resistance is a cause or a consequence of hypertension. 7512468: Conversely, hypertension can cause insulin resistance by altering the delivery of insulin and glucose to skeletal muscle cells, resulting in impaired glucose uptake. 7642026: It is also possible, on the contrary, that hypertension may be the cause of insulin resistance, but in various forms of secondary hypertension, impaired insulin sensitivity has not been found. 7986471: Correlations between insulin resistance, hyperinsulinemia, and hypertension do not appear to be explainable by the concept that insulin resistance occurs secondary to hypertension. Although hyperinsulinemia and insulin resistance have been speculated to cause hypertension, most of the evidence supporting this hypothesis has come either from correlation studies or from short-term studies of the cardiovascular, renal, and sympathetic effects of insulin. 8677859: The mechanisms through which hypertension contributes to the occurrence of myocardial infarction should be discussed from two points of view: (1) common risk factors for the two diseases, such as genetic risk, insulin resistance, sympathetic hyperactivity, and vasoactive substances such as angiotensin K, and (2) linking factors that are induced by hypertension and contribute to the development of atherosclerosis and myocardial infarction, such as atherosclerosis and left ventricular hypertrophy. 8759412: According to some results hypertension causes hyperinsulinemia/insulin resistance through hemodynamic alterations and structural changes of blood vessels. 9244372: This study also shows that chronic sucrose treatment exacerbated the development of hypertension through these mechanisms, precipitating insulin resistance. 9284405: Moreover, hypertension was reported to be a possible cause of insulin resistance. 10923942: However, 14 years after surgery, the MTC and pheochromocytoma recurred and the patient died of intracranial hemorrhage due to hypertension. 122334: Hepatic encephalopathy and intracranial haemorrhage, the latter commonly due to hypertension, were found to be the commonest causes of admission in coma. 15959794: We report the autopsy case of a 40-year-old woman with severe intellectual and motor disabilities, who showed calcification in the cerebellum and pons but not in the basal ganglia on CT scan, and died of intracranial hemorrhage due to intractable hypertension. 19875473: Pathomechanisms include excitotoxicity, which may lead to an acute or subacute leukoencephalopathy, and vascular complications, including vasoconstriction, vasculitis, or hypertension, which may lead to intracranial hemorrhage or ischemia. 2068637: The combination of a local increase in intracerebral blood flow and simultaneously developing systemic hypertension in an occasional patient may lead to intracranial hemorrhage. 21034929: A 6-year-old girl presented with intracranial hemorrhage because of hypertension secondary to the bilateral UPJO. 25888199: The case of posterior reversible encephalopathy with intracranial hemorrhage was likely due to uncontrolled hypertension, and was unrelated and coincidental to long-term phentermine use. 26703004: Cranial imaging revealed right parietal intracranial hemorrhage likely secondary to cerebral amyloid angiopathy or hypertension. 26982061: OBJECTIVE: To present a case of intracranial haemorrhage due to decompensated hypertension in case of severe preeclampsia which resulted in acute caesarean section followed by hysterectomy. [Intracranial haemorrhage due to decompensationof hypertension in severe preeclampsia with the needof a hysterectomy - case report]. 30572539: LESSONS: Hypertension is still one of the causes of ICH after CAS. 8865836: Although chronic arterial hypertension is the leading cause of intracranial hemorrhage, an abrupt rise in systemic arterial pressure in normotensive people may sometimes induce a hemorrhagic stroke. 11342800: Intrarenal ischaemia, induced by hypertension, increased sympathetic nervous system activity, and hyperinsulinaemia have all been implicated in reduced renal clearance of urate. 11747366: In the in vivo study, enzyme-linked immunosorbent assay was used to investigate the expression of immunoreactive interleukin-1beta in the rat retina following a hypertension-induced ischemia/reperfusion, while the effect of a recombinant human interleukin-1 receptor antagonist or an anti-interleukin-1beta neutralizing antibody on the ischemia-induced damage was examined histologically. 19875473: Pathomechanisms include excitotoxicity, which may lead to an acute or subacute leukoencephalopathy, and vascular complications, including vasoconstriction, vasculitis, or hypertension, which may lead to intracranial hemorrhage or ischemia. 20230612: INTRODUCTION: The aims of our study were to evaluate the impact of increased intra-abdominal pressure (IAP) on central nervous system (CNS) cytokines (Interleukin 6 and tumor necrosis factor), lactate and perfusion pressures, testing the hypothesis that intra-abdominal hypertension (IAH) may possibly lead to CNS ischemia. 22679605: However, a contributing factor to this hypertensive disease of pregnancy is a reduction in uterine perfusion pressure resulting in placental ischemia. 23959444: METHODS AND RESULTS: Somal morphology of neurons from human (579.54+/-14.34 versus 327.45+/-9.17 MUm(2); P<0.01) and canine hearts (767.80+/-18.37 versus 650.23+/-9.84 MUm(2); P<0.01) failing secondary to ischemia and neurons from spontaneously hypertensive rat hearts (327.98+/-3.15 versus 271.29+/-2.79 MUm(2); P<0.01) failing secondary to hypertension reveal significant hypertrophy of neurons in cardiac ganglia compared with controls. 24103646: Preeclampsia (PCL) is a hypertensive disorder of pregnancy, of unknown origin, where a defective placentation resulting in placental ischemia plays an important role. 24365441: Two opposing hypotheses are commonly cited, but the issue is controversial: (1) the current more popular theory suggests that severe hypertension exceeds the limits of autoregulation, leading to breakthrough brain edema; (2) the earlier original theory suggests that hypertension leads to cerebral autoregulatory vasoconstriction, ischemia, and subsequent brain edema. 24683264: BACKGROUND: Abdominal compartment syndrome (ACS) refers to organ dysfunction and ischemia resulting from intra-abdominal hypertension (IAH). 24819953: Compartments bound by fascia are found in the extremities, buttocks, and abdomen; conditions that cause intracompartmental swelling and hypertension can lead to ischemia and limb loss. 2576672: Left ventricular hypertrophy may be a serious consequence of chronic untreated hypertension since it may accentuate the risk of congestive heart failure, arrhythmias, coronary ischaemias and sudden death. 2717992: Vasculitis and uncontrolled hypertension lead to arterial spasm, ischemia, and increased vascular permeability, all of which eventually cause cerebral edema. 32078923: The systemic role of MetS in OA pathophysiology is associated with obesity-related inflammation, the beneficial role of n-3 polyunsaturated fatty acids and deleterious role of cholesterol, physical inactivity, hypertension-induced subchondral ischemia, dyslipidemia-induced ectopic lipid deposition in chondrocytes, hyperglycemia-induced local effects of oxidative stress and advanced glycation end-products, low-grade systemic inflammation, and obesity-related adipokines by inducing the expression of proinflammtory factors. 33959027: Background: In preeclampsia, a hypertensive disorder of pregnancy, the poor remodeling of spiral arteries leads to placental hypoperfusion and ischemia, provoking generalized maternal endothelial dysfunction and, in severe cases, death. 35657785: Additionally, ischemia caused by hypertension and accumulated impairment of microvasculature due to prolonged T2DM would affect the DCP. 7216662: A case of ischemia of the hand resulting from Gaisbock's syndrome (polycythemia and hypertension without splenomegaly) is reported. 7303059: In chronic ischemia induced by long-lasting regional cerebral blood flow reduction due to severe hypertension, similar changes were observed only in SHRSP at the advanced stage. 8037592: An important role in the WM lesions belongs to its ischemia due to hypertension angiopathy and disturbances of hemodynamics and liquor circulation. 8263884: It is possible that some of these segmental sclerosing glomerular lesions were secondary to glomerular hyperfiltration caused by reduced renal mass from hypertension-induced glomerular ischaemia. 8281965: Left ventricular hypertrophy, as a consequence of arterial hypertension, influences the three factors involved in the prognosis and we express these as a triangle of risk: electrical instability, left ventricular dysfunction and ischaemia. 10582971: Compared with age-, race-, and sex- (proportionally) matched control subjects from the greater Cincinnati/northern Kentucky region, the attributable risk of hypertension for all causes of first-ever ischemic stroke is 27% (95% CI, 7 to 43); for diabetes, 21% (95% CI, 11 to 29); and for coronary artery disease, 9% (95% CI, 2 to 16). 17239801: Hypertension and atrial fibrillation were the most common risk factor and cause, respectively, of ischemic stroke in this population. 17345050: 58.5% of ischemic strokes and 26.2% of TIA cases were attributable to the 5 risk factors hypertension, diabetes mellitus, high alcohol consumption, hyperlipidemia, and smoking. 21063358: Most cases of ischemic stroke are attributable to hypertension and other risk factors, but in over 20% of cases, the cause is unknown. 23111888: The present study demonstrated that CYP1A1 genetic variants contribute to interindividual variability in smoking- and hypertension-induced ischemic stroke risk. 24126786: In these women, hemorrhagic stroke is more common than ischemic stroke, probably as a result of severe hypertension. 24365295: Hypertension causes pathologic changes in the walls of small (diameter<300 microns) arteries and arterioles usually at short branches of major arteries, which may result in either ischemic stroke or intracerebral hemorrhage. 24430051: We studied the characteristics of quality of life in patients in the acute and recovery phase of ischemic stroke in the vertebral-basilar basin due to hypertensive disease as the leading risk factor for the disease. 27683351: These data suggest a gene-dose effect of the examined gene variants and a synergistic effect of these polymorphisms and hypertension in the pathogenesis of early ischemic stroke. 32860372: Screening for phaeochromocytoma in patients with acute cerebrovascular disease: Is it necessary?INTRODUCTION: Phaeochromocytoma may present with uncontrolled hypertension leading to haemorrhagic stroke (HS), ischaemic stroke (IS) and transient ischaemic attack (TIA). 33348552: Thus, the present study examined the postmortem brain vasculature of human patients who died of ischemic stroke due to systemic hypertension. 37593071: The patient had a history of hypertension and ischemic stroke, and her episodes of PSR were often triggered by elevated blood pressure. 10099045: Because the renin angiotensin system (RAS) influences hypertension and renal disease, angiotensin-converting enzyme (ACE) inhibitors have been used successfully to treat and reduce renal consequences of hypertension. 10213836: Inference of the existence of high blood pressure as a cause of renal disease in the mid-19th century: observations on vascular structures in the kidney. 11015607: Neonatal antihypertensive therapy fails to ameliorate the renal abnormalities, arguing against the possibility that the nephropathy is a consequence of early hypertension. 11032351: Diabetes and/or hypertension cause renal disease in up to 40% of patients requiring dialysis. 11172555: Renal disease is often caused by hypertension or diabetes mellitus, both very strong risk factors for the development of CAD. 11369824: Hypertension leads to renal disease through a series of mechanisms that seem to be exaggerated in African-Americans, who have a higher prevalence of both hypertension and end-stage renal disease than whites. Renal disease itself leads to hypertension, which in turn can contribute to progression of renal disease. 11602906: The AA group was characterized by a higher incidence of renal disease due to hypertension (72% AA vs 37% C, P <.001), pretransplant dialysis (95% AA vs 82% C, P =.003), waiting time (1.9 years AA vs 1.1 years C, P =.02), cadaveric donation (88% AA vs 68% C, P =.01), HLA mismatching (mean 3.5 AA vs 2.4 C, P <.001), and delayed graft function (DGF; 50% AA vs 22% C, P =.001). 11684796: On the other hand, high blood pressure contributes substantially to a faster rate of progression of renal damage, regardless of underlying etiology of kidney disease. 14626575: Arterial hypertension is one of the most important factors leading to chronic graft nephropathy and causing cardiovascular complications following renal transplantation. 14727931: This paper reviews recent clinical trials evaluating hypertension-related kidney disease including the interim results of the African-American Study of Kidney Diseases and Hypertension (AASK) Study, to date the largest prospective study of African-American patients with kidney disease due to hypertension. 15331318: Diabetes and hypertension are common causes of nephropathy, which in turn is a common precursor to HF. 15465789: However, beneficial effects of L-arginine supplementation have been reported in several models of chronic kidney disease including renal ablation, ureteral obstruction, nephropathy secondary to diabetes, and salt-sensitive hypertension. 15735947: Atherosclerotic renal artery stenosis is a significant cause of poorly controlled hypertension and progressive renal dysfunction leading to ischemic nephropathy and other end-organ damage. 15928338: Patients in whom nephropathy develops as a result of hypertension or diabetes mellitus are more likely to die of cardiovascular disease (CVD) than of kidney disease. 16155654: Diabetes and hypertension were the most common cause of nephropathy, mean age was 51.2 years and mean time between operation and from the beginning of PD was 9 days (range 1-14 days). 16227775: The devastating long-term consequences of high blood pressure include stroke, heart disease, atherosclerosis, renal disease, and other end-organ damage. 16528251: To delineate the underlying mechanisms of hypertension-induced nephropathy, we generated transgenic mice that overexpress rat ANG (rANG) in the kidney to establish whether intrarenal RAS activation alone can evoke hypertension and kidney damage and whether RAS blockade can reverse these effects. 17059792: Kidney disease may be the cause or a consequence of hypertension. 18367025: Kidney disease may be the cause or a consequence of hypertension. 18472682: The African American Study of Kidney Disease and Hypertension (AASK) was conducted over a 7-year period at 21 clinical centers across the United States to investigate whether one of two levels of blood pressure control and/or one of three classes of antihypertensive medications was more effective at slowing the rate of renal disease in African Americans with renal insufficiency presumed secondary to hypertension. 19804180: The distribution of etiologies of these conditions varies among races; blacks tend to have heart and kidney disease predominantly due to hypertension, while whites tend to be affected by ischemic heart disease and Hispanics by diabetic kidney disease. 20051853: Mild to moderate hypertension may cause nephropathy in European Americans with intrarenal vascular disease improved by the treatment of hypertension, hyperlipidemia and smoking cessation. 2058070: Renal diseases have been recognized as both a cause and a consequence of hypertension. 2075280: This paper synthesizes the pathogenic steps of arterial hypertension in diabetes mellitus: hyperosmolarity due to the hyperglycemia and increased sodic tubular reabsorption accounting for the expansion of the extracellular volume with hypervolemia; abnormalities of the ionic membrane pumps leading to abnormal intracellular calcium distribution, thereby inducing an increased vascular tone; atypical vasomotor reactivity to cathecolamines; modifications of the renin-angiotension-aldosterone system. The pathophysiological derangements by which hypertension could induce nephropathy are examined: the vasodilatation which can be detected from the onset of diabetes, may be a determinant in the transmission of systemic hypertension to the glomerular microcirculation with resulting enhancement of the hydrostatic transglomerular pressure gradient (i.c. the major factor producing glomerular injury), glomerular plasmatic flow and filtration rate. 20853020: Unlike in other countries where long-standing diabetes and hypertension are the leading causes of renal diseases, the majority of CKD patients from this part of Sri Lanka do not show any identifiable cause. 2145301: Blood pressure remains normal until after development of microalbuminuria, indicating no primary role for hypertension in the pathogenesis of nephropathy. 21519246: RECENT FINDINGS: HIV-associated nephropathy (HIVAN), acute renal injury, HAART, and comorbid conditions such as hepatitis C, hypertension, and diabetes are among the multiple causes of renal disease. 2192500: The main objectives of medical and nutritional management of patients with chronic renal failure are to slow down the progression of renal disease and to prevent secondary complications due to hypertension, uremic metabolic disturbances, and bone disease. 22889490: Here, we further define the cellular composition of SRCs and apply this novel therapeutic approach to the ZSF1 rat, a model of severe progressive nephropathy secondary to diabetes, obesity, dyslipidemia, and hypertension. 25019021: Moreover, smoking, obesity, hypertension, and diabetes mellitus can also lead to kidney disease. 26526050: Negative predictors included age (OR: 0.95 per year), infectious cause of technique failure (OR: 0.48), underweight (OR: 0.50), kidney disease resulting from hypertension (OR: 0.38) or diabetes (OR: 0.32), race being Maori (OR: 0.65) or Aboriginal and Torres Strait Islander (OR: 0.30). 26553514: Unfortunately, nephrologists often indiscriminately apply a diagnosis of 'hypertensive nephrosclerosis' to patients in either scenario, which implies that the hypertension is causative of their renal disease. 27162301: Diabetes, hypertension and atherosclerosis have become most common causes of kidney diseases. 27270176: Regulation of renal microvascular tone is impaired in salt-sensitive (SS) hypertension-induced nephropathy, but the molecular mechanisms contributing to this impairment remain elusive. These results establish the adaptor protein p66Shc as a regulator of renal vascular tone and a driver of impaired renal vascular function in hypertension-induced nephropathy. p66Shc regulates renal vascular tone in hypertension-induced nephropathy. 27469147: The surge of hypertension and diabetes during the 1990s will probably have profound effects on prevalence and etiology of kidney disease in China. 27722964: Hypertension is a common but complex human disease, which can lead to a heart attack, stroke, kidney disease or other complications. 28405080: We present the case of an 84-year-old African American man with a history of renal disease secondary to hypertension and coronary artery disease without any prior history of malignancies who presented with airway obstruction. 28513510: BACKGROUND: Hypertension is a leading cause of kidney disease worldwide, and chronic kidney disease (CKD) is a known cause of secondary hypertension. 28746409: ZSF1 rats exhibit spontaneous nephropathy secondary to obesity, hypertension, and diabetes, and have gained interest as a model system with potentially high translational value to progressive human disease. 30395142: CONCLUSIONS: Hypertension affects millions of people in Africa and if left untreated is a major cause of heart disease, kidney disease and stroke. 3070895: Renal disease has been recognized as both a cause and a consequence of hypertension. 31288761: HIV associated nephropathy (27.6%), chronic glomerulonephritis (15.4%) diabetes (14.1%) and hypertension (13.5%) were the leading causes of kidney disease. 31822592: Our data revealed the metabolic aspects of hypertension-induced glomerular sclerosis, including lipid breakdown at early disease stages and activation of anaplerotic pathways to regenerate energy equivalents to counter stress. Overall, multilayered omics provides an overview of hypertensive kidney damage and suggests that metabolic or dietary interventions could prevent and treat glomerular disease and hypertension-induced nephropathy. 31993100: Early consumption of high-fat diet worsens renal damage in spontaneously hypertensive rats in adulthood.The association between hypertension and obesity has been shown to be an important cause of kidney disease. 32328308: We conclude that hypertension, chronic glomerulonephritis, diabetic nephropathy, and sepsis are the most common causes of renal diseases. 32405420: Results: Approximately 85% of patients properly identified high blood pressure, but more than two-thirds were unaware that hypertension lasts a lifetime once diagnosed; one-third were unaware that hypertension could lead to renal disease. 32917166: AA is involved in many pathologic conditions, such as inflammation, asthma, cancer, diabetes, hypertension, and the pathogenesis of kidney disease. 33191808: Hypertension makes up the leading cause of stroke, kidney disease, arterial disease, eye disease, and cardiovascular disease (CVD) growth. 33369304: Does indeed non-malignant hypertension also cause kidney disease that can lead to end-stage kidney failure? 33899372: The literature regarding the relationship between the renal resistance index and primary kidney disease (as a cause of hypertension) or kidney disease as a result of hypertension is low and limited. 35035931: Hypertension either as a cause of kidney disease or as a complication of chronic kidney disease is the most frequently encountered comorbidity of KT patients. 35409698: Most importantly, uncontrolled HPT can lead to severe complications (stroke, heart attack, kidney disease, and heart failure), mainly ignoring the signs in nascent stages. 36507052: Hypertension and diabetes were etiologies of kidney disease in 31% and 25% of patients, respectively. 36959153: BACKGROUND/AIMS: Hypertensive nephropathy (HN) is one kind of kidney disorder caused by long-term uncontrolled hypertension, usually resulting in severe kidney damage, including inflammation and oxidative stress, no matter in cells or tissues, from patients with nephropathy. 7672704: Renal disease was secondary in most cases to diabetes mellitus or hypertension. 7758051: Hypertension is a potentially life-threatening condition that can lead to heart failure, stroke, and kidney disease. 7842274: Untreated essential hypertension leads to cardiovascular and renal disease and stroke, but antihypertensive drug therapy effectively reduces these consequences of hypertension. 7928500: PURPOSE: This study was undertaken to investigate whether the hypertension observed in a subgroup of patients with progressive radiation-induced nephropathy has a renovascular component. 8046316: Renal disease may be due to hypertension, to AIP or to SLE. 8078835: OBJECTIVES: The increased risk of renal disease due to high blood pressure observed in Black Americans would suggest ethnic factors are involved. 8783600: Is nephroangiosclerosis a hypertension-induced nephropathy? 8889350: Compared to the ESRD patient population whose renal disease is caused by hypertension, women were underrepresented in the AASK Pilot Study. 9145973: CONCLUSIONS: Medical renal disease secondary to diabetes or hypertension appears to be the most likely cause of elevated serum creatinine measurements in men with BPH and renal insufficiency. 9233121: The consequences of untreated hypertension include myocardial infarction, stroke, congestive heart failure, peripheral vascular disease and renal disease. 9745278: [Etiology and therapy of kidney disease due to hypertension]. 10833241: The program was initiated as a effort to understand hypertension as a cause of renal failure. 11011224: BACKGROUND: Both diabetes and hypertension, two conditions that can lead to renal failure, have a high prevalence in Guadeloupe. 11190296: Hypertension is also an increasingly common cause of renal failure, which may become terminal by its consequences associating vascular and ischaemic lesions of the renal parenchyma. 11281346: Hypertension-induced renal failure. 11350495: These data show that in this sodium deficient renovascular model of hypertension, blockade of angiotensin II receptors normalizes blood pressure but causes renal failure, whereas the vasodepressor action of the clonidine analogue AL-12 occurs without detriment to renal function. 11818026: The mechanism by which hypertension produces renal failure is incompletely understood. 11863128: Her clinical records included a long past of hypertension, which was the cause of her renal failure. 12022207: Hypertension is a major public health problem both in the developing and developed countries of the world and if untreated, can lead to various fatal complications like cerebral stroke, encephalopathy, ischaemic heart disease (IHD), renal failure and sudden cardiac death, etc. 12694071: In Cox Regression analysis, recipients who were older age, experienced graft loss, rejection, had higher body mass index, renal failure due to hypertension, and cyclosporine use (vs. tacrolimus use) were associated with increased risk of hospitalized AF. 12714866: Of the 18 R563Q patients, 11 had severe hypertension, leading to renal failure in two cases, while only two had hypokalaemia. 1349931: A 75-year-old woman with longstanding hypertension, resulting in congestive heart failure and renal failure. 14736007: Atherosclerosis and hypertension can also damage the kidney parenchyma causing renal failure. 15700394: If left unchecked and untreated, uncontrolled high blood pressure can lead to heart failure, kidney failure, heart attack and stroke. 1575175: Hypertension is a major cause of renal failure, particularly in black males, but control of the hypertension does not necessarily prevent deterioration of renal function. 16053995: African Americans were more knowledgeable about the definition of hypertension and were more aware that hypertension can cause kidney failure than Hispanics and whites (64.2% v 54.8% and 46.3%, P<.0001). 16389855: [Health practitioner with renal failure. Is it due to hypertension, osteomyelitis--or something entirely different?]. 16429165: Hypertension is a leading cause of stroke, heart disease, and kidney failure. 16983943: Her renal failure was probably attributable to hypertension. 17000273: Although asymptomatic early on, untreated hypertension leads to cardiovascular disease, strokes, renal failure, and blindness. 17329578: Diabetes and hypertension are the leading causes of renal failure. 17363892: Many of these persons had a diagnosis of diabetes (40%) or hypertension (30%) as the primary cause of kidney failure. 17469709: INTRODUCTION: Increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) is a cause of organ dysfunction in critically ill patients and is independently associated with mortality. The kidneys seem to be especially vulnerable to IAH induced dysfunction and renal failure is one of the most consistently described organ dysfunctions associated with IAH. CONCLUSION: IAH can cause renal dysfunction. 17591527: BACKGROUND: African Americans are at increased risk of kidney failure caused by hypertension. 1777585: Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. 17969496: We herein report a case of spontaneous bacterial peritonitis (SBP) caused by Staphylococcus epidermidis in an adult patient on regular hemodialysis (due to terminal renal failure caused by hypertension) and not on immunosuppressive therapy. 18382839: The percentage of parents responding correctly to a question of whether high BP could lead to kidney failure increased after the intervention from 45.5% to 64.3%. Parents had high baseline knowledge about certain aspects of hypertension, but baseline knowledge that high BP could lead to kidney failure was relatively low. 18603454: Secondary patency was worse in loop grafts (P=.02) and intermediate graft thrombosis (occurred between 31-182 days after graft placement, P<.001) and better when renal failure was due to hypertension or diabetes (compared to other or cryptogenic causes, P=.048) or isolated angioplasty for graft dysfunction during follow-up had been performed (P<.001). 1889853: Can renal failure due to hypertension be prevented? 19245692: BACKGROUND: Hypertension affects 29% of the adult U.S. population and is a leading cause of heart disease, stroke, and kidney failure. 19763921: Hypertension is a leading cause of heart attack, stroke, and kidney failure and represents a serious medical issue worldwide. 20433426: Incidence and prevalence on RRT are continuously increasing, and hypertension and diabetes are becoming the leading cause of ESRD. Hypertension and diabetes are increasing and have become the leading cause of renal failure in incident patients at day 91, unadjusted, in 2007 (26.8 and 21.4% respectively). 22334794: RESULTS: There was no difference between groups in terms of baseline age, gender, hypertension, cause of renal failure, hemoglobin, cholesterol, albumin, CRP levels, cardiac biomarkers, adiponectin, body mass index, or Malnutrition-Inflammatory Score. 23785797: Recent advances in research into salt-sensitive hypertension revealed that mineralocorticoid receptor activities independent of aldosterone induce both salt-sensitive hypertension and organ damage, which is closely related to oxidative stress. Although novel therapeutic agents have become available and blood pressure tends to be lowered, the morbidity and mortality rates of hypertension-induced renal failure or stroke in Japan have not decreased in recent decades. 24034664: It is frequently associated with hypertension and impaired renal function, and is perceived by many physicians to be the cause of hypertension and renal failure. 24179353: Forty years abuse of baking soda, rhabdomyolysis, glomerulonephritis, hypertension leading to renal failure: a case report. 24881708: INTRODUCTION: Increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH) is a cause of organ dysfunction in critically ill patients and is independently associated with mortality. The kidneys seem to be especially vulnerable to IAH induced dysfunction and renal failure is one of the most consistently described organ dysfunctions associated with IAH. CONCLUSION: IAH can cause renal dysfunction. 25184913: Males--71.9%; low skin phototypes (up to Fitzpatrick III)--89%; mean age--57.0 years--and mean age at transplant--47.3 years; sun exposure--67.2% occupational--and 64.1% recreational; photoprotection--78.2% (although only 34.4% in a regular manner); squamous cell carcinoma--67.2%; squamous cell carcinoma/basal cell carcinoma ratio--2:1; personal history of nonmelanoma skin cancer--25%--and family history--10.9%; location at photoexposed area--98.4%; average latency time between transplantation and first nonmelanoma skin cancer appearance--78.3 months; viral warts (HPV) after transplant--53.1%; average timing of transplantation--115.5 months; living donor--64.1%; triple regimen (antirejection)--73.2%; comorbidities--92.2%; pre-transplant dialysis--98.4%; hemodialysis--71.7%; average duration of dialysis--39.1 months; previous transplants--3.1%; hypertension as cause of renal failure--46.9%. 2560358: It is important to maintain adequate blood pressure control among hypertensive patients as uncontrolled hypertension can lead to accelerated renal failure. 25767287: Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke. 26454916: Uncontrolled hypertension in turn can lead to kidney failure and other complications. 27194834: We initiated a program for early detection of diabetes and hypertension, the main causes of kidney failure in Guyana, South America. 2812171: Among the 18 patients, hypertension was the most common underlying cause of renal failure. 28621634: Those with dialysis vintage (length of time on dialysis) up to 3 years (odds ratio = 2.10; 95% confidence interval, 1.09-4.06; P = .027) and hypertension as the cause of renal failure (odds ratio = 1.79; 95% confidence interval, 1.05-2.87; P = .002) had more abnormal findings. 28750875: BACKGROUND: Hypertension (HT) is the second leading cause of kidney failure. 29649151: Systemic hypertension, which eventually results in heart failure, renal failure or stroke, is a common chronic human disorder that particularly affects elders. 30309463: Certainly combined and persistent heart and kidney failure can arise from a common pathologic insult, for example, as a consequence of poorly controlled hypertension or of severe diffuse arterial disease. 30618265: Hypertension was the most common cause of renal failure in both study groups. 30723314: Hypertension is the most prevalent cause of cardiovascular disease and kidney failure, but only about 50% of patients achieve adequate blood pressure control, in part, due to inter-individual genetic variations in the response to antihypertensive medication. 30958891: BACKGROUND AND PURPOSE: Hypertension adversely affects the kidney and is the second leading cause of kidney failure. 3120215: Hypertension, when severe, damages small blood vessels, causing kidney failure, hemorrhage, strokes, and heart failure; when the condition is mild to moderate, it produces atherosclerosis. 3153277: Therapy was discontinued in two patients at week 4, one because of worsening renal failure and one because of hypertension. 31836042: Autosomal-dominant polycystic kidney disease (ADPKD) is the most prevalent inherited kidney disease, characterized by growth of bilateral renal cysts, hypertension, and multiple extrarenal complications that eventually can lead to renal failure. 32317757: Among them, hypertension is a leading cause for stroke, heart disease and kidney failure. 3306205: Hypertension can directly damage blood vessels, and leads to renal failure, intracranial bleeds, and lacunar infarctions. 33102379: Hypertension (34.36%) was the most common cause of kidney failure, while diabetes mellitus (21.80%) took the second place. 33275317: On the other hand, patients with blood group AB + and those with hypertension etiology of kidney failure demonstrated a lower incidence of COVID-19. 3364467: Hypertension can precipitate renal failure in blacks. 33785443: Assessment of Lens Autofluorescence in Patients with Well-Controlled Essential Hypertension and those with Renal Failure secondary to Hypertension and have Undergoing Hemodialysis. 34178223: Arterial hypertension resulted in renal failure (95,9%), left ventricular hypertrophy (92.81%), stroke (16,67%), and cardiac and renal involvement (85%). 35425650: The patient's renal insufficiency was the result of chronic immunosuppression and hypertension. 3687804: Systemic hypertension can lead to renal failure in blacks. 38158371: In fact, hypertension is the second leading cause of kidney failure in the United States; it is a complex disease characterized by, leading to, and caused by renal dysfunction. 38596899: BACKGROUND: Hypertension is a leading cause of kidney failure, affects most dialysis patients and associates with adverse outcomes. 6991710: Hypertension is the leading cause of renal failure in this dialysis and transplant center. 8026061: In diabetes mellitus and hypertension, the two most common causes of kidney failure, sustained hypertension within the glomerulus damages the glomerular membrane and eventually results in loss of kidney function. 8205461: Hypertension itself commonly causes severe renal failure when the malignant phase develops, but the question of whether benign hypertension causes renal impairment remains controversial. 8834167: The various end-stage renal disease registries have documented a progressive and substantial increase of hypertension as a cause of renal failure. 8931412: Hypertension and diabetes mellitus were the most common causes of renal failure. 9395558: In this review, we propose that the greater propensity of black hypertensives to develop renal failure as a consequence of hypertension may be due to abnormal hemodynamic adaptation of the renal circulation to a rise in blood pressure caused by high dietary sodium intake. 9839286: This lower survival of patients with renal vascular disease seems to be related to higher cardiac mortality, which is in alignment with the diagnosis of hypertension as cause of renal failure. The incidence of hypertension as cause of ESRD has doubled in the ERA-EDTA Registry in the past two decades, going from 7 to 13%. It is very possible that this is not a real increase in the incidence of hypertension as cause of ESRD, but rather a consequence of greater acceptance of older patients, a phenomenon that has simultaneously occurred. There are geographic differences in the incidence of hypertension as cause of ESRD, from 6% in Japan to 28.5% in the U.S., and 13% in Europe. Hypertension as cause of end-stage renal disease: lessons from international registries. 10155747: Elderly patients are susceptible to acute renal failure largely because of functional impairment of the kidneys secondary to diseases such as arteriosclerosis, hypertension, and heart failure. 12828593: Acute renal failure due to hypertension: malignant hypertension in an adolescent. 14733067: In both groups the chronic risk factors for ANV such as hypertension, diabetes mellitus, chronic cardiac failure, chronic hepatic failure and pre-existing renal impairment and the causes of a traumatic ARF were compared. 16935902: Intra-abdominal hypertension is an under-appreciated cause of acute renal failure. 19847731: Due to hypertension-induced acute renal failure, a hemodialytic treatment was initiated. 24557670: Intra-abdominal hypertension is an independent cause of acute renal failure after orthotopic liver transplantation. 28174355: This case report describes acute kidney failure probably due to intra-abdominal hypertension following an unknown bite. 34107912: Hypertensive disorders of pregnancy(HDP) was the leading cause of Pr-AKI(35.3 %). 37011566: Hypertensive disorders are now the leading cause of PRAKI in many regions, followed by hemorrhage and sepsis. 962294: Although acute renal failure, nephrotic syndrome and renal tubular disorders result from acute nephrotoxicity, chronic renal failure with renal failure and hypertension result from chronic nephrotoxicity. 11338095: Atheromatous renovascular disease (ARVD) is a common cause of hypertension and chronic renal failure (CRF). 11725171: Hypertension and diabetes mellitus, two leading causes of chronic renal failure in the elderly, may accelerate this decline. 11863082: Hypertension is a major underlying cause of chronic progressive renal disease and continues to be a leading reason for the heavy burden of ESRD observed in African Americans. 12616031: ARVD is a common cause of hypertension and chronic renal failure (CRF), and it is one of the most common renal diagnoses in elderly patients accepted on to dialysis programmes with end-stage renal failure (ESRF). 12864889: Chronic glomerulonephritis and hypertension are principal causes of CRF in tropical Africa and East Africa, together with diabetes mellitus and obstructive uropathy. In a six-year study of 3632 patients with ESRD, based on SADTR statistics, hypertension was reported to be the cause of ESRD in 4.3% of whites, 34.6% of blacks, 20.9% mixed race group and 13.8% of Indians. 15599329: Disturbances in renal autoregulation and the susceptibility to hypertension-induced chronic kidney disease. 15884664: The prevalence of HTN varies with the cause of CRF. 16202696: Both hypertension and diabetes are the causative factors for the occurrence of CKD and its consequences. 16395270: In the southeastern United States, the estimated prevalence of chronic kidney disease due to hypertension is five times greater for African Americans than white subjects. 16672914: Patients with diabetes mellitus, uncontrolled hypertension, known causes of chronic kidney disease, and serum creatinine above 250 mumol/l were excluded. 16752661: The consequence of hypertension of the kidney is chronic renal failure; Prevalence rates of CRF range from 25 -100 per 100,000 populations and the incidence continues to grow increasingly at a rate of about 8-10% per year thereby posing a major public health problem especially in the developing countries. 17212202: Arterial hypertension is one of the most frequent causes of chronic kidney failure but also one of most frequent complications in patients on long-term haemodialysis. 17534087: Diabetes and hypertension, the two leading causes of CKD, are themselves reaching near epidemic proportions. 18072419: Hypertension, chronic glomerulonephritis and diabetes mellitus were the leading causes of chronic renal failure. 18177590: Diabetic nephropathy and hypertension are the major causes of chronic kidney disease. 18255009: In addition, several observational, cross-sectional, and longitudinal studies document obesity as an independent risk factor for the onset, aggravated course, and poor outcomes of chronic kidney disease, even after adjustment for confounding comorbidities, including diabetes and hypertension, the two major causes of chronic kidney disease. 18607140: Chronic kidney disease is both a cause and a consequence of hypertension. 18679391: Although the ESRD epidemic is attributed in greater part to the increasing rate of diabetes, hypertension remains the second most common reported cause of ESRD and is present in approximately 90% of cases of diabetes-related ESRD. Although the role of hypertension as a primary cause of CKD is debated, hypertension is commonly recognized as the most important CKD progression factor. 19041334: These results suggest that obesity and hypertension have differing oxidant handling and signalling pathways that act in the pathogenesis of age-related CKD. 19299892: The link between obesity and kidney disease begins with obesity's well-known associations with diabetes and hypertension, the two leading etiologies of CKD. 19420116: Improvement of renal hemodynamics during hypertension-induced chronic renal disease: role of EGF receptor antagonism. 19667681: Hypertension, a condition that also results from or is exacerbated by excess body weight, remains an important cause of CKD as well. 19772598: The benefits of this approach will extend to patients with related conditions, e.g. those with chronic kidney disease caused by hypertension or diabetes. 20352009: A 36 year-old female with chronic kidney failure due to hypertension and who was being treated with hemodialysis for eight months, was admitted to the hospital on the suspicion of being pregnant. 20359530: Diabetes and arterial hypertension continue to be the main causes of chronic renal failure in 2010, with a rising prevalence in part due to the worldwide obesity epidemic. 20380486: Inappropriate activation of the RAAS is important in hypertension-induced cardiovascular disease (CVD) and chronic kidney disease (CKD). 20583691: The registry identified hypertension, diabetes mellitus and Chronic Glomerulonephritis (CGN) as the commonest causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) in these countries. 20655398: Arterial hypertension is a leading cause of both vascular diseases and chronic renal failure. 20729727: Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. 20846379: He had a past medical history of chronic renal failure secondary to hypertension. 21079654: Identifying the precise prevalence of CKD attributable to hypertension is difficult owing to the absence of uniform criteria to establish a diagnosis of hypertensive nephropathy. The prevalence of hypertension, chronic kidney disease (CKD) and end-stage renal disease (ESRD) attributable to hypertension continues to rise worldwide. 21144326: Obesity represents an important risk factor for the development of chronic kidney disease (CKD), due to its known strong association with diabetes mellitus and hypertension, the two major causes of CKD, but also as an independent renal risk factor. 21309411: Arterial hypertension is a leading cause of both vascular diseases and chronic renal failure. 21359472: Most patients are young adult males with arterial hypertension as the main cause of chronic renal failure. 21623393: In addition, several observational, cross sectional and longitudinal studies document that obesity is as an independent risk factor for the onset, aggravated course, and poor outcomes of chronic kidney disease, even after adjustment for confounding co-morbidities including metabolic syndrome, diabetes and hypertension, the major causes of chronic kidney disease. 21660521: Hypertension, an important cause of chronic renal failure, leads to afferent arteriolopathy, segmental glomerulosclerosis and tubular atrophy in the juxtamedullary cortex. 21694926: Type 2 diabetes and hypertension are the two main causes of CKD. 2192500: The main objectives of medical and nutritional management of patients with chronic renal failure are to slow down the progression of renal disease and to prevent secondary complications due to hypertension, uremic metabolic disturbances, and bone disease. 22089804: Diabetes mellitus (33%) and hypertension (22.6%) were the most common causes of chronic renal failure, followed in order by obstructive uropathy in 17.3%, undetermined causes in 14%, pyelonephritis in 4.7%, glomerulonephritis in 4.3%, and polycystic kidney disease in 3.9%. 22093280: The analysis identified five statistically significant factors associated with longer time until first fistula: higher age (Hazard-risk - HR 0.99, 95% CI 0.99-1.00); having hypertension and cardiovascular diseases (HR 0.94, 95% CI 0.9-0.98) as the cause of chronic renal disease; residing in capitals cities (HR 0.92, 95% CI 0.9-0.95) and certain regions in Brazil - South (HR 0.83, 95% CI 0.8-0.87), Midwest (HR 0.88, 95% CI 0.83-0.94), Northeast (HR 0.91, 95% CI 0.88-0.94), or North (HR 0.88, 95% CI 0.83-0.94) and the type of renal unit (public or private). 22441176: Hypertension was the cause of CKD in 56.5%. 22648290: Diabetes and hypertension have become leading causes of CKD in Chinese elderly patients: a comparison between 1990-1991 and 2009-2010. Diabetes and hypertension have become the most common causes of CKD in elderly patients in 2009-2010 period, representing 39.5 % and 24.2 % of all CKD causes, respectively. CONCLUSIONS: Diabetes and hypertension have increased and become the leading causes of CKD in elderly Chinese patients. 22695895: The most prevalent underlying diseases leading to CKD are diabetes and hypertension. 22954611: The prevalence of CKD is rising in the HIV-infected population and CKD is increasingly likely to be caused by comorbid conditions, such as diabetes and hypertension, that frequently cause CKD in the general population. 23167047: CKD is often caused by diabetes mellitus (DM) and hypertension (HTN). 23198935: Chronic kidney disease is a public health problem with increasing prevalence caused by diabetes, hypertension and glomerulonephritis. 23291030: CKD aggravates pre-existent traditional risk factors such as hypertension and dyslipidemia due to secondary renal parenchymal hypertension and secondary dyslipidemia. 23431980: MATERIALS AND METHODS: The recipient was a 48-year-old man with chronic renal failure owing to hypertension who had been on hemodialysis for 2 years. 23998047: METHODS: Thirty patients with chronic renal disease which was caused by chronic glomerulonephritis and hypertension, who were on Maintenance Haemodialysis (MHD) with serum creatinine levels of > 2.5 mg/dl, were included in this study. 24066938: Diabetes and hypertension are the leading causes of chronic kidney disease and their incidence is increasing at an alarming rate. 24447093: In this study, we evaluated biplane LA volume as well as LA function (LA global systolic strain (GS) and strain rate [SR]) in stage 3 CKD patients (eGFR 30-59 mL/min per 1.73 m(2) ) to determine if LA function parameters are more significantly altered by the presence of CKD in addition to changes due to hypertension alone. 24616621: Hypertension and diabetes, the most common causes of chronic kidney disease, are particularly common in southeast Asian Countries. Chronic noncommunicable diseases (NCDs) such as hypertension, atherosclerosis, acute myocardial infarction, stroke, diabetes, obesity, and chronic kidney disease are the major cause of death not only in high income, but also in medium and low income countries. 24658007: Chronic kidney disease (CKD) can be a consequence of diabetes, hypertension, immunologic disorders, and other exposures, as well as genetic factors that are still largely unknown. 24850151: To investigate the role of Cx43 in the progression of CKD, we interbred RenTg mice, a genetic model of hypertension-induced CKD, with Cx43+/- mice. 25098066: CONCLUSION: Lead exposure with HTN can be a cause of CRF. 2525334: We measured the levels of protein C, total protein S, and free protein S antigens in 42 patients (21 nephrotic and 21 non-nephrotic) with one of four types of glomerular pathology: diabetic nephropathy (DM), focal glomerular sclerosis (FGS), membranous glomerulonephritis (MGN), and chronic renal failure due to hypertension (CRF). 25415613: PURPOSE OF REVIEW: Hypertension and hyperglycaemia are major risk factors that result in chronic kidney disease (CKD). 25607123: In 14 women described, hypertension was the most frequent cause of chronic renal failure (half of cases). 25672966: The high prevalence of noncommunicable diseases (NCD) such as hypertension, diabetes, and obesity, which are the main causes of CKD, is a big concern in the world health scenario. 25715141: This article aims to assess whether there is family clustering of chronic kidney disease in relatives of individuals in renal replacement therapy caused by hypertension and/or diabetes mellitus. 25787679: Chronic kidney disease of uncertain etiology was diagnosed in 70.2% of patients, while 15.7% and 9.6% were due to hypertension and diabetic mellitus, respectively. 26320040: Diabetes and hypertension are the most common causes of CKD. 26496378: A man who had chronic kidney disease secondary to hypertension had a preemptive living-donor kidney transplant from his wife. 26760124: CONCLUSION: Our results suggest that DN and HPT are the major attributable causes of CKD among patients at a Malaysian tertiary-care hospital. 26788727: Preemptive kidney transplant was performed on a 51-year-old woman who had a chronic kidney disease because of hypertension. 26997406: Hypertension and diabetes remain the main causes of chronic renal failure in Fars Province, Iran 2013. 27247097: Chronic kidney disease (CKD) carries a large cardiovascular burden in part due to hypertension and neurohumoral dysfunction - manifesting as sympathetic overactivity, baroreflex dysfunction and chronically elevated circulating vasopressin. 27418091: This is an innovative contribution to the ongoing debate on whether mild to moderate hypertension causes chronic kidney disease. 27509586: Hypertension and chronic glomerulonephritis (CGN) remain the two leading causes of CKD in Nigeria. 27692815: High blood pressure is a common cause of chronic kidney disease. 27757226: Such alterations have been found to correlate directly with the increased incidence of diabetes and hypertension, the main causes of chronic kidney diseases (CKDs), which, in turn, have a high estimated prevalence. 27887750: Diabetes and hypertension are the main causes of CKD in all high-income and middle-income countries, and also in many low-income countries. 28045952: Hypertension was the main cause of primary CKD (31.8%). 28064215: Diabetes and hypertension are the two principal causes of CKD. 28201666: A substantial component of the observed increase in mortality attributable to CKD relates to that caused by diabetes mellitus and hypertension. 28451853: Chronic kidney disease (CKD) is both a common cause and sequel of uncontrolled hypertension. 28513510: BACKGROUND: Hypertension is a leading cause of kidney disease worldwide, and chronic kidney disease (CKD) is a known cause of secondary hypertension. 28572913: BACKGROUND: Sexual difference has been shown in the pathogenesis of chronic kidney disease induced by hypertension. 28637384: Chronic kidney disease (CKD) has a prevalence of approximately 13% and is most frequently caused by diabetes and hypertension. 28701959: Despite significant research into various pathways involved in the pathophysiology of CKD, the therapeutic options are limited in diabetes and hypertension induced CKD to blood pressure control, hyperglycemia management (in diabetic nephropathy) and reduction of proteinuria, mainly with renin-angiotensin blockade therapy. 28794651: In contrast to adults where hypertension is a leading cause of chronic kidney disease, in pediatrics, hypertension is predominantly a sequela, however, an important one that, like in adults, is likely associated with a more rapid decline in kidney function or progression of chronic kidney disease to end stage. 28847045: In 2013, among the Chinese people aged 25 years old and above, deaths caused by cardiovascular disease and chronic kidney disease attributable to high blood pressure were 19.912 million and 0.966 million, accounting for 52.31% of the total deaths due to cardiovascular diseases and 62.11% to the total chronic kidney diseases. 28875847: Hypertension is the second leading cause of CKD after diabetes and is strongly related to morbidity and mortality. OBJECTIVE: Since there is a strong relation between hypertension and CKD, and hypertension seems to lead to cardiovascular diseases, which have epidemic proportions in CKD, this review article discusses the etiology of hypertension and the existing optimal therapies that contribute to the hypertension and heart rate management. Since this relation exists and hypertension leads to cardiovascular diseases, the management of hypertension and increased heart rate should be a main therapeutic target in these patients. 29456222: On bivariate analysis, hypertension was the cause of CKD in 48.8% of patients under 35 years, 66.4% in patients between 35 and 64 years, and 85.4% in patients >=65 years (P = 0.001). 29903699: RPS causes high blood pressure that may lead to severe chronic kidney disease and end-stage renal disease (ESRD). 29942501: It is well known that one of the main determinants of mortality and morbidity in chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients is fluid overload acting on the cardiovascular system causing hypertension, increased arterial stiffness, left ventricular hypertrophy and eventually heart failure. 29982610: The prevalence of hypertension, type 2 diabetes and metabolic syndrome, which are the main causes of CKD in Western countries, is lower in vegetarian populations. 30043957: High blood pressure and diabetes mellitus, major causes of chronic kidney disease, were reported by 34.7% and 10.5% of the individuals, respectively. 30078514: Globally and in most Global Burden of Disease study regions, age-standardized DALY rates decreased, except in High-income North America, Central Latin America, Oceania, Southern Sub-Saharan Africa, and Central Asia, where the increased burden of CKD due to diabetes and to a lesser extent CKD due to hypertension and other causes outpaced burden expected by demographic expansion. 30148296: Besides hypertension, variations in blood pressure caused by baroreflex control dysfunction can lead to chronic kidney disease progression. 30298651: While diabetes and hypertension remain the major causes of CKD in developing countries, environmental pollution, pesticides, water, analgesic abuse and herbal medications are common causes in these regions. 30327190: BACKGROUND: Albuminuria is an early marker of kidney disease in patients with diabetes and/or hypertension undetected or untreated albuminuria is a leading cause of chronic kidney disease and cardiovascular events, The purpose of the present survey was to assess the prevalence of albuminuria in patients with diabetes and hypertension, treated with a combinations of renin angiotensin aldosterone system inhibitors and dihydropyridine calcium channel blockers. 30354805: Hypertension, an important cause of chronic kidney disease, is characterized by peritubular capillary (PTC) loss. 30366170: The indication for a combined liver-kidney transplant was non-alcoholic steatohepatitis (NASH) cirrhosis with chronic kidney disease secondary to hypertension and diabetes compounded by hepato-renal syndrome. 31010804: High blood pressure was the main cause of chronic kidney failure (55%). 31123838: PURPOSE OF REVIEW: Despite enhanced screening and therapeutic management, hypertension remains the most prevalent chronic disease in the United States and the leading cause of heart disease, chronic kidney disease, and stroke in both men and women. 31508666: Hypertension and Diabetes mellitus are the two main causes of chronic kidney disease that culminate in the final stage of kidney disease. 31591338: The subgroup of 56 patients with primary HT comprised 26 subjects without renal complications and 30 with CKD (stage 2-3) secondary to HT. 32106202: This was consistent among subgroups of recipients at higher risk for adverse outcomes due to hyperfiltration: African American recipients (aHR 1.10, 95% CI 0.70-1.73, P = 0.68) and those with ESRD caused by hypertension (aHR 1.10, 95% CI 0.65-1.85, P = 0.73) or diabetes (aHR 0.80, 95% CI 0.56-1.13, P = 0.20). 32784355: Background/Aims: This study aimed to investigate long-term temporal trends and outcomes of biopsy-proven kidney diseases in a multicenter kidney biopsy cohort, focusing on hypertension and diabetes, the leading causes of end-stage kidney disease (ESKD). 33238361: Diabetic nephropathy (DN) and hypertension are prime causes for end-stage renal disease (ESRD) that often coexist in patients, but are seldom studied in combination. 33363216: A 68-year-old woman with end-stage kidney disease due to hypertension was initiated on PD 2 years prior to the present event. 33377622: Hypertension is the second leading cause of end-stage renal disease (ESRD) after diabetes mellitus. 33537809: Hypertensive nephropathy is the most common complication of hypertension, and is one of the main causes of end-stage renal disease (ESRD) in numerous countries. 34012688: A 52-year-old African-American male patient with end-stage renal disease due to hypertension underwent deceased donor kidney transplant procedure with no immediate complications. 34105618: In the multivariate analysis, the variables associated with fear of failure or loss of graft were female sex (OR = 1.763; 95%CI: 1.224-2.540) and end-stage renal disease (ESRD) due to hypertension (OR = 1.732; 95%CI: 1.178-2.547), while monthly income (number of minimum wages) showed a protective association (OR = 0.882; 95%CI: 0.785-0.991). Female sex, low income, and ESRD due to hypertension were risk factors for lack of enrollment on the kidney transplant waitlist due to fear of loss of graft, resulting from lack of information on this treatment modality. 34305630: Diseases, such as diabetes and hypertension, often lead to chronic kidney failure. 34317424: A 54-year-old male with history of end-stage renal disease secondary to hypertension on hemodialysis with moderate aortic valve insufficiency presented with progressive exertional dyspnea and lower extremity edema over several weeks. 34371188: CASE DESCRIPTION: A 72-year-old Hispanic woman presented for renal transplantation due to end-stage renal disease secondary to hypertension. 34408965: We report the case of a 53-year-old man with a history of end-stage renal disease due to uncontrolled hypertension who underwent renal transplantation in 2013. 34775322: CASE PRESENTATION: A 37 years old male, who had chronic renal failure secondary to hypertension, and presented to the emergency room following a seizure episode, in which he developed a generalized tonic-clonic convulsion secondary to electrolyte imbalances with metabolic acidosis. 35285447: Diabetic nephropathy, arterial hypertension and smoking were the underlying causes of the patient's end-stage renal disease. 35360013: Importance: Hypertension is a leading cause of end-stage renal disease (ESRD), but currently, those at risk are poorly identified. 36577802: Nephroangiosclerosis (NAS) associated with hypertension continues to be one of the most causes of end stage renal diseases in Europe, but it is still poorly studied. 36875008: Background: Diabetes mellitus and hypertension are the most prominent conditions causing chronic kidney disease and eventually end-stage renal disease. 37203887: Hypertension and Diabetes mellitus was found to be the leading cause of end-stage kidney disease with 61 (61%) and 27 (27%) respectively. 37497635: BACKGROUND: Hypertension is a major cause of end-stage renal disease. 3752152: A 69-year-old white woman with chronic renal failure due to hypertension was admitted for back pain, and while she was under observation, paraplegia developed. 3784442: Renal function and hypertension were unpredictable despite normalization of the hyperactive parathyroid metabolism and were of decisive prognostic significance; 6% died of acute or chronic renal failure, or of the consequences of hypertension. 37899243: A 42-year-old Japanese woman with end-stage renal failure due to hypertension presented with a systolic blood pressure of 160-200 mmHg despite treatment with 4 different antihypertensive agents. 7716558: Chronic renal failure caused by hypertension or by parenchymal kidney disease is a very common global health problem. 8525152: Experimental evidence suggests that glomerular hypertension/hyperfiltration constitutes a potential mechanism by which hypertension leads to chronic renal failure. 8715259: It is interesting to note that arterial hypertension is found to be among the leading causes of chronic renal failure. 8935467: Future planning must take these factors into account and should include strategies for preventing chronic renal failure, especially that due to non-insulin dependent diabetes and hypertension. 9715116: Hypertension induced chronic renal failure: clinical features, management and prognosis. 9735977: A 49-year-old black man with hypertension-induced chronic renal failure requiring hemodialysis and a history of arteriovenous access graft infection was admitted with Staphylococcus aureus sepsis, dyspnea, and peri-incisional erythema over his arteriovenous graft fistula. 11451538: A multiple logistic regression analysis demonstrated that suspected IUGR, severe PIH (but not mild PIH), chronic hypertension and placental abruption were independent risk factors for induction of labor among preterm SGA neonates. 11518901: RESULTS: The following outcomes increased significantly with increasing glucose values during the oral glucose tolerance test: shoulder dystocia, macrosomia, emergency cesarean section, assisted delivery, hypertension, and induction of labor. 11929650: Using a multivariable analysis, the following obstetric risk factors were found to be significantly associated with arrest of descent: nulliparity (OR=7.8, 95% CI=6.9-8.7; P<0.001), birth weight >4 kg (OR=2.3, 95% CI=1.9-2.8; P<0.001), epidural analgesia (OR=1.8, 95% CI=1.6-2.0; P<0.001), hydramnios (OR=1.6, 95% CI=1.3-2.0; P<0.001), hypertensive disorders (OR=1.5, 95% CI=1.3-1.8; P<0.001), gestational diabetes A1 and A2 (OR=1.5, 95% CI=1.2-1.8; P<0.001), male gender (OR=1.4, 95% CI=1.2-1.5; P<0.001), premature rupture of membranes (PROM, OR=1.3, 95% CI=1.04-1.6; P=0.021), and induction of labor (OR=1.2, 95% CI=1.02-1.4; P=0.030). 14981376: RESULTS: Comparison showed increased rates of nonproteinuric hypertension (P<.05), induction of labor (P<.001), and fetal cardiovascular malformations (P<.001) among women with epilepsy. 15387860: RESULTS: While all three hypertensive groups had high incidences of induction of labour and emergency Caesarean, only pre-existing hypertension and superimposed pre-eclampsia were significantly associated with elective Caesarean section. 16123476: In multivariate analyses, increasing weight gain was associated with significantly higher rates of hypertension (OR 4.8 [95% CI for group 4 vs. group 1: 1.7-13.1]), cesarean section (3.5 [1.6-7.8]), induction of labor (3.7 [1.7-8.0]), and large-for-gestational-age infants (4.7 [2.0-11.0]). 16272036: Significant risk factors for PPH, identified using a multivariable analysis, were: retained placenta (OR 3.5, 95%CI 2.1-5.8), failure to progress during the second stage of labor (OR 3.4, 95%CI 2.4-4.7), placenta accreta (OR 3.3, 95%CI 1.7-6.4), lacerations (OR 2.4, 95%CI 2.0-2.8), instrumental delivery (OR 2.3, 95%CI 1.6-3.4), large for gestational age (LGA) newborn (OR 1.9, 95%CI 1.6-2.4), hypertensive disorders (OR 1.7, 95%CI 1.2-2.1), induction of labor (OR 1.4, 95%CI 1.1-1.7) and augmentation of labor with oxytocin (OR 1.4, 95%CI 1.2-1.7). 16753771: Using a multivariable analysis, the following conditions were significantly associated with PUPPP: multiple pregnancies (odds ratio (OR) = 4.9, 95% confidence interval (CI) 1.7-14.1), hypertensive disorders (OR = 2.2, 95% CI 1.1-4.7), and induction of labor (OR = 7.6, 95% CI 4.0-14.5). CONCLUSION: Pruritic urticarial papules and plaques of pregnancy is a condition significantly associated with multiple pregnancies, hypertensive disorders, and induction of labor. 17446955: There were three major indications for induction of labour, namely hypertension (45%), postdates (22.1%) and prelabour rupture of membranes (20.6%). 18072452: RESULTS: Main indications for induction of labour were prolonged pregnancy and hypertensive diseases of pregnancy. 18399337: Hypertension in pregnancy was the commonest indication for induction of labour followed by prolonged pregnancy. 1972487: The only perinatal death in the aspirin group followed a cord accident during labour, whereas the 3 perinatal deaths in the placebo group were all due to severe hypertensive disease. 21054760: METHODS: The week-specific risks of stillbirth between 36 and 41 completed weeks of gestation were contrasted with the week-specific risks of neonatal mortality or serious neonatal morbidity among births following induction of labour in women with pre-existing hypertension. 23157030: STAN was used significantly more in case of hypertension, diabetes and induction of labour and was associated both in univariate and multivariate analysis with significantly more secondary caesarean section for suspected foetal distress, instrumental vaginal delivery, low Apgar score and need for neonatal intensive care. 23571133: Use of oxytocin or misoprostol, an epidural, hypertension, and induction of labor were associated with an increased risk of TS. 24011382: CONCLUSION: In women with hypertensive disorders in pregnancy at term, induction of labour does not affect the clinical and biochemical cardiovascular profile at 2.5 years postpartum. 24533534: The CTD model replaces prepregnancy BMI with third-trimester BMI and adds estimated gestational age at delivery, hypertensive disease of pregnancy, cervical examination and induction of labour. 25830646: The main indications for the induction of labor were hypertensive disorders (75%). 26115020: We adjusted for induction of labor, maternal age, ethnicity, cephalic position, preexisting hypertension, and gestational age at delivery. 26868065: Labor induction for hypertensive disorders of pregnancy was the most expensive obstetric indication for induction of labor (?4347.32, 95% CI 3890.45-4804.18). 28120427: Metformin versus glibenclamideThere was no evidence of a difference between metformin- and glibenclamide-treated groups for the risk of hypertensive disorders of pregnancy (RR 0.70, 95% CI 0.38 to 1.30; three studies, 508 women, moderate-quality evidence), birth by caesarean section (average RR 1.20, 95% CI 1.20; 95% CI 0.83 to 1.72, four studies, 554 women, I2 = 61%, Tau2 = 0.07 low-quality evidence), induction of labour (0.81, 95% CI 0.61 to 1.07; one study, 159 women; low-quality evidence) or perineal trauma (RR 1.67, 95% CI 0.22 to 12.52; two studies, 158 women; low-quality evidence). 28639706: The overall risk of bias was judged to be unclear due to lack of methodological detail in the included studies.For the mother, there was no clear evidence of a difference between women in the exercise group and those in the control group for the risk of pre-eclampsia as the measure of hypertensive disorders of pregnancy (risk ratio (RR) 0.31, 95% confidence interval (CI) 0.01 to 7.09; two RCTs, 48 women; low-quality evidence), birth by caesarean section (RR 0.86, 95% CI 0.63 to 1.16; five RCTs, 316 women; I2 = 0%; moderate-quality evidence), the risk of induction of labour (RR 1.38, 95% CI 0.71 to 2.68; one RCT, 40 women; low-quality evidence) or maternal body mass index at follow-up (postnatal weight retention or return to pre-pregnancy weight) (mean difference (MD) 0.11 kg/m2, 95% CI -1.04 to 1.26; three RCTs, 254 women; I2 = 0%; high-quality evidence). 28668289: INTERPRETATION: Oral misoprostol was more effective than transcervical Foley catheterisation for induction of labour in women with pre-eclampsia or hypertension. Women (aged >=18 years) who were at 20 weeks' gestation or later with a live fetus and required delivery as a result of pre-eclampsia or hypertension were randomly assigned (1:1), via computer-generated block randomisation (block sizes of four, six, and eight) with concealment by use of opaque, sequentially numbered, sealed envelopes, to receive labour induction with either oral misoprostol 25 MUg every 2 h (maximum of 12 doses) or a transcervical Foley catheter (silicone, size 18 F with 30 mL balloon). 29094431: 25?kg/m2 , 2.22 (1.24-3.98) for hypertensive disorder during pregnancy, 3.43 (1.31-8.95) for large-for-date fetus and 4.64 (3.23-6.69) for induction of labor. 31167579: In multivariable logistic regression, adjusted for confounding variables, including maternal race, insurance status, prepregnancy BMI, maternal age, number of fetuses, number of vaginal exams, intrauterine pressure catheter and fetal scalp electrode placement, mode of delivery, group B streptococcus positivity, maternal education level, induction of labor, prelabor rupture of membranes, tobacco use, presence of diabetes (pregestational and gestational), gestational age at delivery, and chronic hypertension, the association between preeclampsia and composite maternal peripartum infection did not persist. 31823535: In contrast, non-elective induction of labor can be performed because of medical or obstetrical indications such as hypertension, intrauterine growth restriction, oligohydramnios or post-term pregnancy. 3189904: A case of inadvertent intravascular injection of PGF2alpha during induction of labor by intraamniotic injection for fetal demise, involving alternating extreme hypotension and hypertension, is described. 32649502: Prediction Model for Vaginal Birth After Induction of Labor in Women With Hypertensive Disorders of Pregnancy.OBJECTIVE: To identify characteristics associated with vaginal delivery compared with cesarean delivery after labor induction among women with hypertensive disorders of pregnancy and to develop and validate a prediction model to assist in clinical care. Prediction Model for Vaginal Birth After Induction of Labor in Women With Hypertensive Disorders of Pregnancy. 33243171: BACKGROUND: Mothers with hypertensive disorder of pregnancy can be managed with either immediate or delayed induction of labour with expectant monitoring of both mother and baby. Hence, this review was conducted to compare outcomes of immediate and delayed induction of labour among women with hypertensive disorder of pregnancy based on disease severity and gestational age. 34507611: A dataset of 602 women with hypertensive disease in pregnancy, in India, randomised to either Foley catheter or oral misoprostol for induction of labour. 34740851: A multivariable logistic regression analysis was calculated after adjusting for smoking, induction of labour, epidural use, hypertensive disorders, gestational diabetes, and birth weight. 34743219: Adverse pregnancy outcomes associated with eGDM were macrosomia, caesarean delivery, induction of labour, hypertension, preterm delivery, and shoulder dystocia. 36134591: Higher BMI was significantly associated with a higher abdominal circumference and estimated fetal weight at the third trimester, a higher risk of hypertension disorder, induction of labor and a higher birthweight. 36302236: Objective: The study intended to retrospectively analyze the factors influencing the outcomes of cervical dilatation using a cervical double balloon in the induction of labor for pregnant women with hypertensive disorders and to establish a predictive model based on the random forest (RF) method that is able to manage multifeatured data, provide fast training speeds, offer high predictive accuracy, and analyze the impact of various features. Conclusions: Medical practitioners can use the cervical double balloon effectively for the induction of labor for women with hypertensive disorders during the third trimester of pregnancy, and the prediction model for induction of labor based on RF had a good working efficiency. 36316725: There are many causes of low birth weight, including early induction of labor or cesarean birth, multiple pregnancies, infections, diabetes, and high blood pressure. 36539028: Outcomes were corrected for: maternal age, parity, ethnicity, year of registered birth, induction of labor, hypertensive disorders in previous pregnancies, multiple gestation and low socioeconomic status. 37550089: Multivariate logistic regression models adjusted on maternal age, body mass index, smoking, parity, induction of labour, hypertensive disorders, diabetes, placenta praevia and/or accreta, history of caesarean section, mode of delivery, birthweight, birth place and year of delivery, were used. 37595821: In singletons with GDM, compared to controls, there was increased risk of hypertensive disorders of pregnancy (RR 1.85; 95%CI 1.69, 2.01), induction of labour (RR 1.36; 95%CI 1.05,1.77), caesarean delivery (RR 1.31; 95%CI 1.24,1.38), large for gestational age neonate (RR 1.61; 95%CI 1.46,1.77), preterm birth (RR 1.36; 95%CI 1.27,1.46), admission to neonatal unit (RR 1.43; 95%CI 1.38,1.49). 38531390: Among NHBP, factors associated in multivariable regression analysis with SMM in order of strength of association included cesarean delivery, earlier gestational age at delivery, preeclampsia, induction of labor, chronic HTN, prior preterm birth, multifetal gestation, advanced maternal age, and pregestational diabetes. 719463: We did not study mothers with pre-eclampsia and hypertension, but we conclude that there is a strong case for preloading all other mothers in whom lumbar epidural analgesia is induced in labour. 8213098: Maternal indication for induction of labor because of uncontrollable hypertension was present in 77% of the cases in the parous group as compared to 31% in the primiparous group (p < 0.05). 8819999: MAIN OUTCOMES MEASURED: The development of proteinuria (1+ or greater on urine Albustix); the need for oral antihypertensive medication, the need for the 'pre-eclampsia regime' intra- or post-partum; the need for induction of labour because of hypertension. 12875853: Excellent preoperative control of hypertension was achieved with alpha adrenergic blockade but induction of anaesthesia, rather than tumour handling was noted to be associated with most hypertensive surges of blood pressure. 16104539: BACKGROUND: Marked hypertension may occur during induction of isoflurane anesthesia. 16715914: CONCLUSIONS: Reduction of the isoflurane concentration from 4% to 2.5% during induction of anesthesia made the circulation stable, and decreased the incidence of excessive tachycardia and hypertension after tracheal intubation. BACKGROUND: High concentration of isoflurane often induces not only tachycardia but also hypertension during induction of anesthesia and causes further hyperdynamic changes after tracheal intubation. 18803627: Data from 71 orthotopic liver transplantation recipients were used to develop a risk stratification model by binary logistic regression analysis containing the following variables: pretransplant hepatitis B and/or C infection; arterial hypertension; intra-operative mean arterial blood pressure before induction of anaesthesia; units of packed red blood cells required; hypotension (mean arterial blood pressure <or=50 mmHg); and maximum lactate concentration. 21878869: CONCLUSION: One-day cataract surgery performed under topical anesthesia with monitored anesthesia care required anesthesiologist intervention in 21.6% of cases, mainly because of agitation or hypertension. 21937996: SDPTG indices are useful for predicting hypertension during induction of sevoflurane anesthesia, regardless of a history of hypertension or hypertensive factors. 22287376: Three patients withdrew from the study, and 1 was withdrawn by the investigator due to severe hypertension after induction of anesthesia. 22471829: CONCLUSIONS AND CLINICAL RELEVANCE: In isoflurane-anesthetized horses, premedication with medetomidine followed by administration of medetomidine as a constant rate infusion resulted in decreased heart rate, higher arterial blood pressure from 20 through 40 minutes after induction of anesthesia, and better preserved body temperature, compared with conventional treatment with xylazine. 2686488: UNLABELLED: Recommendations for prevention of hypertension and tachycardia during the induction of anesthesia include the use of fentanyl and antihypertensive drugs and superficial anesthesia of the throat. 2895596: The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk. 5453244: Acute hypertension during induction of anaesthesia and endotracheal intubation in normotensive man. 8055603: Patients with difficult tracheal intubation had an increased rate of desaturation (< 90%), hypertension (> 200 mm Hg) and dental damage on induction of anaesthesia. 9163278: Three patients in the racemate group showed severe arterial hypertension after induction of anaesthesia and were withdrawn from the study. One patient in the S-(+)-ketamine group showed severe arterial hypertension and tachycardia after induction of anaesthesia and was withdrawn from the study. 10234500: During pregnancy no signs of hypertension or cardiovascular disease were reported, but at the end of the surgical procedure, the patient developed acute hypertension, leading to myocardial infarction, severe heart failure and death. 10522259: Morbidity and mortality in hypertension are mainly determined by arterial lesions which may occur in different regional circulations: kidney, cerebral, coronary ..., causing respectively nephroangiosclerosis, stroke or myocardial infarction... 10731625: Its abuse can, however, be associated with massive hypertension resulting in strokes, ruptured aneurysms, or myocardial infarction. 10960209: Plaque rupture was triggered by hypertension and led to MI as the first symptom of disease. 11355426: Plaque rupture is often triggered by hypertension and may lead to myocardial infarction, instable angina pectoris, or sudden ischemic death. 11920902: Myocardial infarction and hydrops are considered to be consequences of hypertension in the recipient. 12735271: Seventy-one percent and 62% of patients were aware that stroke and heart attack respectively are possible consequences of high blood pressure. Forty-five percent attributed a variety of symptoms to their high blood pressure while 55% believed that stress was a cause of their high blood pressure. 12782643: The rationale for their study in hypertension follows the observation that the major consequences of hypertension are stroke and myocardial infarction. 14627591: Blood pressure response to renal artery stenting or enhanced medical therapy varied according to blood pressure, as did the incidence of myocardial infarction and stroke resulting from hypertension. 15700394: If left unchecked and untreated, uncontrolled high blood pressure can lead to heart failure, kidney failure, heart attack and stroke. 19763921: Hypertension is a leading cause of heart attack, stroke, and kidney failure and represents a serious medical issue worldwide. 20729727: Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. 20730072: Global health care resources and economies in general will be stressed to breaking point if this condition is not dealt with in an aggressive and timely manner because the consequences of untreated hypertension such as stroke, myocardial infarction, and dementia are exceedingly costly in the long term. 21167778: First data using C21 revealed tissue protective effects and functional improvement after myocardial infarction and in hypertension-induced end organ damage, notably in a blood-pressure independent way. 21331710: As a consequence of the sustained high BP, there is an increased risk of mortality and morbidity that is characterized by myocardial infarction, congestive heart failure, stroke, end-stage renal failure, and peripheral vascular disease (1-3). 22380695: Cardiac remodelling is defined as changes in the size, shape, and function of the heart, which are most commonly caused by hypertension-induced left ventricular hypertrophy and myocardial infarction. 23064369: In this issue of the JCI, Young et al. show that endoplasmic reticulum (ER) stress is an essential signaling event for angiotensin II-induced hypertension in cells of the central nervous system. Hypertension occurs in approximately 30% of individuals in Western populations and is known to be a major cause of stroke, heart failure, and myocardial infarction. 24352797: Hypertension is the most common condition seen in primary care and leads to myocardial infarction, stroke, renal failure, and death if not detected early and treated appropriately. 25065067: Compared to White respondents, Chinese respondents were less likely than White respondents to know high blood pressure can cause heart attacks (adjusted odds ratio [aOR]: .43, 95% confidence interval [CI]: .19-.96] and Indian respondents were less likely to know losing weight usually decreases blood pressure (aOR: .38, 95% CI: .21-.68). 2570426: Chronic beta-blockade inhibits atheroma formation (in animals) and beneficially modifies the incidence of stroke and myocardial infarction, which in man are the long-term consequences of hypertension. 25767287: Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke. 27049661: Of the cases fulfilling the previously established criteria for homicide by heart attack, more than 80% displayed significant changes because of hypertension. 27722964: Hypertension is a common but complex human disease, which can lead to a heart attack, stroke, kidney disease or other complications. 28159195: In Cox regression analysis, low SVi was associated with higher risk of incident HF (hazard ratio 1.38; 95% confidence interval 1.06 to 1.80), independently of age, gender, body mass index, heart rate, hypertension, prevalent cardiovascular disease, left atrial dimension index, LV mass index, LV concentric geometry, EF or MFS, and abnormal wall motion, also accounting for myocardial infarction as a competing risk event. 2928822: Concurrently, SMR for myocardial infarctions and cerebrovascular diseases due to hypertension has declined. 29702856: OBJECTIVE: Uncontrolled hypertension (HTN) results in strokes, myocardial infarction (MI), and other complications, which are the leading cause of disability, death, and severe economic consequence. 30281618: Hypertension, which leads to heart attacks and strokes, already affects one billion people worldwide, making it a global public health issue. Log-binomial regression was used to estimate predictors of hypertension at ART initiation, while competing risks regression was used to evaluate the relationship between predictors of incident hypertension, accounting for death as a competing risk. 32073427: Results from some studies identified nine risk factors, including low consumption of fruits and vegetables, smoking, alcohol, diabetes, psychosocial factors, sedentary lifestyle, abdominal obesity, hypertension and dyslipidemia as the cause of myocardial infarction in 90% of the patients in this population. 32269522: Pathological remodeling of the heart muscle is caused by several etiologies such as prolonged hypertension or injuries that can lead to myocardial infarction and in serious cases also the death of the patient. 32848742: Hypertension is a major cause of heart attack and stroke. 3489158: Twenty-four per cent of the first AMIs that occurred in the study population were attributable to hypertension (after adjustment for smoking) and twenty-seven per cent were attributable to smoking (after adjustment for hypertension). 35409698: Most importantly, uncontrolled HPT can lead to severe complications (stroke, heart attack, kidney disease, and heart failure), mainly ignoring the signs in nascent stages. 38128897: Hypertension remains a leading preventable cause of myocardial infarction, stroke, kidney disease, and cardiovascular death worldwide. 38131147: The consequences of uncontrolled hypertension such as stroke, myocardial infarction, retinal damage and others are significantly affecting individual and the community in large. 8131780: Recent studies have illustrated that in addition to the well known risk factors, such as lipoproteins, smoking, hypertension, there are others that cause atherosclerosis and myocardial infarction. 8517427: Effects of nadolol on hemodynamic and hemostatic responses to potential mental and physical triggers of myocardial infarction in subjects with mild systemic hypertension. 9233121: The consequences of untreated hypertension include myocardial infarction, stroke, congestive heart failure, peripheral vascular disease and renal disease. 9293963: In this article, we summarize recent studies performed in our laboratory to investigate (1) the contribution of the renin-angiotensin system to the cardiac remodeling process, which is triggered by myocardial infarction (MI) or hypertension-induced cardiac hypertrophy; (2) the effects of angiotensin-converting enzyme (ACE) inhibition and angiotensin AT1 receptor antagonism on cardiac parameters, such as myocardial infarct size, cardiac hypertrophy, heart function, and myocardial metabolism; (3) the mechanism of an ACE inhibitor-induced increase in cardiac capillary density in spontaneously hypertensive rats (SHR) and stroke prone SHR (SHR-SP). 12022207: Hypertension is a major public health problem both in the developing and developed countries of the world and if untreated, can lead to various fatal complications like cerebral stroke, encephalopathy, ischaemic heart disease (IHD), renal failure and sudden cardiac death, etc. 12641877: Increased vascular volume causes hypertension, which in turn causes LVH, cardiac failure, and ischemic heart disease (IHD). 15257371: RESULTS: In regard to total deaths in the elderly, the proportional mortality due to cerebrovascular disease and ischemic heart disease decreased 42.5% and 34.4%, respectively, while that due to hypertension increased 119%, increasing from 2.1% to 4.6%. 15902797: The resultant tachycardia and hypertension limited diastolic filling of the coronary arteries, resulting in myocardial ischemia. 17143176: Overall, the fraction of IHD attributable to hypertension ranged from 4-28% in men and from 8-39% in women. 17910144: CONCLUSION: Hypertension was the major aetiology of heart failure followed by IHD. 17952226: OBJECTIVES: To estimate the burden of disease attributable to high blood pressure (BP) in adults aged 30 years and older in South Africa in 2000. Estimating the burden of disease attributable to high blood pressure in South Africa in 2000. Overall, 50% of stroke, 42% of IHD, 72% of hypertensive disease and 22% of other CVD burden in adult males and females (30+ years) were attributable to high BP (systolic BP >or= 115 mmHg). 18456100: METHODS: Worldwide burden of disease attributable to high blood pressure (> or =115 mm Hg systolic) was estimated for groups according to age (> or =30 years), sex, and World Bank region in the year 2001. About 54% of stroke and 47% of ischaemic heart disease worldwide were attributable to high blood pressure. 20119930: Traditional and nontraditional risk factors, hypertension, fluid overloading and anemia can lead to myocardial ischemia, chamber hypertrophy and dilatation, and low left ventricular ejection fraction (LVEF) in CKD patients. 2048707: On the other hand, the risks attendant on indiscriminate cerebral support (embolism after shunt placement, cardiac ischemia due to induced hypertension) can be avoided in the presence of cortical potentials. 20924360: Mitral stenosis was reported as the most frequent cause of PH several decades ago, but PH with left-sided heart disease is now usually caused by systemic hypertension and ischemic heart disease. 21785704: Hypertension can cause myocardial ischemia in the absence of CHD. 22093163: The myocardial ischemia was due to severe resistant hypertension complicated with concentric left ventricular hypertrophy and increased arterial stiffness. 22404687: Worldwide, 7.6 million premature deaths (about 13.5% of the global total), 54% of strokes, and 47% of cases of ischemic heart disease were caused by high BP in 2001. 28581677: Extracellular fluid volume overload and its inevitable consequence, hypertension, increases cardiovascular mortality in the long term by leading to left ventricular hypertrophy, heart failure, and ischemic heart disease in dialysis patients. 3137065: Hypertension with the ensuing increase in myocardial oxygen demand is a major factor in the aetiology of perioperative myocardial ischaemia. 38308346: INTRODUCTION: In rural and remote South Africa, most strokes and ischaemic heart diseases are as a consequence of hypertension, which is a modifiable risk factor. 7237726: The role of systemic arterial hypertension as a possible trigger of myocardial ischemia during angina at rest was studied in 13 consecutive patients who also had a history of exertional angina. 7404085: The high prevalence of diastolic blood pressures of 105 mmHg or more, together with the high prevalence of hypertension in White male subjects aged under 40 years, could be an important factor in the aetiology of ischaemic heart disease in White males in the 25-34-year age greup. More effective screening and therapeutic programmes should therefore be initiated in the White population because of the high prevalence of hypertension which may lead to complications. 7585223: Obesity is accompanied by complications such as hypertension, non-insulin-dependent diabetes mellitus and atherosclerosis, which in turn cause ischaemic heart disease, stroke and premature death. 7887106: Tachycardia and hypertension may cause myocardial ischaemia in patients with coronary heart disease going through major surgery. 8042763: Hypertension, coronary artery disease, renal insufficiency and autonomic neuropathy are common and can result in myocardial ischaemia, cardiovascular instability and gastroparesis, with an increased risk of aspiration. 9747909: Cardiac ischaemia and ventricular arrhythmias that can result from hypertension are likely to benefit from such effects. 11549350: Diabetes and hypertension both produce myocardial dysfunction that accelerates cardiovascular morbidity and mortality. 11726985: Diastolic heart failure is most often due to coronary artery disease and/or hypertension; therefore, other noninvasive or invasive tests are needed to define the etiology of myocardial dysfunction. 14718362: On the other hand, antioxidant intervention had little effect on the hypertension-induced myocardial vascular dysfunction observed in response to dobutamine. 15631334: Hypertension and coronary heart disease are important causes of myocardial dysfunction in end-stage renal disease. 16342344: CONCLUSION: Regional diastolic dysfunction measured by Color Doppler myocardial imaging was the first sign of myocardial dysfunction due to arterial hypertension, while the parameters of global diastolic dysfunction measured by conventional Doppler and Color Doppler myocardial imaging were still normal. 16762434: This study aims at finding out whether inflammation is involved in the early stage of heart dysfunction due to hypertension. 19918393: Sarcoidosis, a disease of unknown etiology, is also a cause of pulonary hypertension and right heart dysfunction. 20979745: CONCLUSION: The arterial stiffness and heart dysfunction may result from hypertension. 24419904: Antagonist of C5aR prevents cardiac remodeling in angiotensin II-induced hypertension. METHODS: Hypertension was induced by angiotensin II (Ang II) subcutaneously infused at a dose of 1500 ng/kg/min for 7 days. CONCLUSIONS: Our data suggest that inhibition of C5aR could be a potential therapeutic strategy in preventing organ damage in Ang II-induced hypertension. BACKGROUND: Inflammatory responses mediate the development of perivascular fibrosis and heart dysfunction induced by hypertension. 2944394: The data provide further evidence that the combination of hypertension and diabetes mellitus produces greater myocardial dysfunction than with either disease alone and is associated with a significant mortality. 31226341: Sodium nitrite improves hypertension-induced myocardial dysfunction by mechanisms involving cardiac S-nitrosylation. 31668736: These include pulmonary and systemic hypertension which can lead to myocardial dysfunction as a result of the increase in the right and left ventricular afterload, respectively. 32054378: Here we discuss new reports pointing to participation of Sigma1 receptor in muscle specific processes like contraction, EC-coupling, calcium currents and in diseases like left ventricular hypertrophy, transverse aortic stenosis and hypertension-induced heart dysfunction. 11447089: CONCLUSIONS: Systemic HTN induces LV hypertrophy, myocardial fibrosis, and isolated diastolic dysfunction in the absence of local or systemic activation of Ang II or ET. 14504689: In addition, in separate preclinical studies, the NHE-1 inhibitor cariporide also prevented and/or caused regression of age-related and hypertension-induced myocardial fibrosis and hypertrophy. 18174773: Consequently, the authors speculate that myocardial fibrosis, as a result of long-standing hypertension, could be the main pathogenetic mechanism leading to the development of such phenomena, resulting from a potential expanding of the fibrotic process to the atrioventricular conduction system. 21769867: The aim of this study was to evaluate whether miR-133a and miR-29b play a role in myocardial fibrosis caused by Angiotensin II (Ang II)-dependent hypertension. 26345970: This study evaluated the inhibitory effects of spironolac-tone, a non-selective aldosterone receptor antagonist, on hypertension-induced myocardial fibrosis. 27220372: The present study investigated the importance of periostin in hypertension-induced myocardial fibrosis. Periostin expression induced by oxidative stress contributes to myocardial fibrosis in a rat model of high salt-induced hypertension. 27482263: BACKGROUND AND OBJECTIVES: Left ventricular diastolic dysfunction is known to be a marker of myocardial damage, in particular myocardial fibrosis resulting from hypertension (HT). 28287886: CTGF may be a therapy target for hypertension-induced myocardial fibrosis, but the detailed mechanism still needs in-depth studies. 31320543: Ventricular remodeling (VR) is a complex pathological process of cardiomyocyte apoptosis, cardiac hypertrophy, and myocardial fibrosis, which is often caused by various cardiovascular diseases (CVDs) such as hypertension, acute myocardial infarction, heart failure (HF), etc. 32865120: MicroRNA-26a Protects the Heart Against Hypertension-Induced Myocardial Fibrosis. 32982761: The aim of the present work is to investigate the effect of electroacupuncture (EA) at PC6 on hypertension-induced myocardial fibrosis in spontaneously hypertensive rats (SHRs). 33867340: Hypertension can cause myocardial fibrosis, during which tumor growth factor-beta 1 (TGF-beta1) can facilitate myocardial cell proliferation and transition towards myofibroblast (MFB). 34588407: Myocardial fibrosis is an important pathological phenomenon of cardiac remodeling that is induced by hypertension, myocardial ischemia, valvular heart disease, hypertrophic cardiomyopathy, and other heart diseases and can progress to heart failure. 35142478: Electroacupuncture combined with irbesartan treatment improves myocardial fibrosis caused by hypertension. 37089092: The present study was aimed to investigate the role and mechanism of glutaminolysis of cardiac fibroblasts (CFs) in hypertension-induced myocardial fibrosis. 37116729: CONCLUSION: Compound Qidan Formula, composed of traditional Chinese herbs, can significantly improve cardiac function, improve atrial and ventricular remodeling, and prevent myocardial fibrosis and hypertrophy in rats with HFpEF induced by hypertension and diabetes mellitus. 7607712: Myocardial fibrosis resulting from arterial hypertension alters myocardial structure and function. 8129511: UNLABELLED: Myocardial fibrosis as a consequence of systemic hypertension is a determinant factor in alteration of cardiac function. 10383002: RESULTS: The study revealed decreased IgG2/ IgG4-ratio in membranous glomerulonephritis (0.57) compared to healthy controls (2.09) and to all other diagnosis groups; crescentic necrotizing glomerulonephritis (1.28), diffuse proliferative glomerulonephritis (1.10), IgA nephropathy (1.11), mesangial proliferative glomerulonephritis (1.55), minimal change nephropathy (1.00), and nephrosclerosis secondary to hypertension (1.06). 10624386: The prevalent causes of end-stage renal disease (ESRD) in the elderly are diabetes mellitus and nephrosclerosis due to long-term arterial hypertension. 10920669: Hypertension alone can lead to chronic nephrosclerosis and in addition promote the progressive worsening of renal function in various forms of renal disease, such as diabetic nephropathy, glomerular nephritis or interstitial nephritis. 11786102: Comparisons with one control group of 13 (12 males and one female) patients with nephrosclerosis due to systemic hypertension and a second control group of 16 (14 males and 2 females) healthy controls were made. 1291661: BACKGROUND: Nephrosclerosis is a term used to define the renal damage induced by arterial hypertension. 17918136: The morphological findings of so-called hypertensive nephrosclerosis, rather than implying a linear direct relationship to damage induced by hypertension, may indicate complex environmental and genetic factors, which together foster the coexistence of renal lesion and hypertension in this clinical setting. 18212435: Recent data regarding the link between low birthweight and hypertension of early onset might have bearing on future developments in understanding the pathogenesis of nephrosclerosis. 18633755: OBJECTIVE: Molecular mechanisms of nephrosclerosis caused by hypertension are not well known. 19057047: Reno-vascular disease is a broad term, which includes renal artery stenosis, ischemic nephropathy, such as atherosclerotic obstruction, thrombo-embolic phenomenon, nephrosclerosis secondary to hypertension and acute occlusion of renal arteries (either bilateral or unilateral in singlekidney patients). 2301030: A history of nephrosclerosis secondary to hypertension was more common in blacks, with 51% (67/130) vs. 2399711: Causes of failures: nephrosclerosis due to prolonged hypertension, concomitant diseases of the upper urinary tract, technical complications of the operation. 7541781: To elucidate the mechanism of hypertension-induced nephrosclerosis, we examined gene expression and localization of transforming growth factor-beta 1 and cellular phenotype in the kidney of 25-week-old SHRSP with moderate renal damage. 7649584: Transgenic kidneys showed severe hypertension-induced nephrosclerosis. 7847347: Nephrologists credit hypertension as the etiology of nephrosclerosis in 25% of patients initiating Medicare-supported renal replacement therapy, even though other processes may cause similar renal pathologic findings. 9596080: Cultured mesangial cells (MC) exposed to cyclic mechanical strain or high glucose levels increase their secretion of transforming growth factor-beta1 (TGF-beta1) and collagen, suggesting possible mechanisms for the development of diabetic renal sclerosis resulting from intraglomerular hypertension and/or hyperglycemia. 10691995: It appears unlikely, however, that hypertension is a direct consequence of hyperinsulinaemia. CONCLUSION: The data are consistent with the concept that hypertension and insulin resistance are a characteristic consequence of the genetic constellation leading to obesity in the NZO strain, and that these traits reflect related mechanisms. 12643137: Rare inactivating mutations of the gene encoding PPAR gamma are associated with insulin resistance type 2 diabetes, and hypertension, whereas a rare gain of function mutation causes extreme obesity. 15051670: Obesity and hypertension-induced restrictive cardiomyopathy: a harbinger of things to come. 15505128: BACKGROUND: In the United States, obesity is a major clinical and public health problem causing diabetes, dyslipidemia, and hypertension, as well as increasing cardiovascular and total mortality. 15726478: The prolonged duration of the surgery, obesity and microvascular affectation due to hypertension, could be factors implicated in the development of the syndrome. 16350321: Serum gamma-glutamyl transpeptidase levels and hypertension in non-drinkers: a possible role of fatty liver in the pathogenesis of obesity related hypertension. 16767285: Experimental obesity and insulin resistance can be due to a deficient response to leptin, secondary to hypoleptinemia and/or mutations on leptin receptor, by modifications on insulin receptor, deletion or diminished insulin signal transduction, enhancement of the effects of orexigen peptides and/or diminution of anorexigen peptides actions on hypothalamus, as well as secondary to arterial hypertension, as in the spontaneously hypertension. 18154717: Various diseases such as arterial hypertension, diabetes and obesity result in renal diseases which are often irreversible and resistant to currently available therapies. 19521241: Review of this case, as well as a handful of other cases of infantile Cushing disease in the literature, suggests that features such as hypertension and slowed linear growth, which are rare in nutritional causes of obesity in infants, can help identify this rare, but life-threatening, illness among an increasing number of overweight infants. 28978986: The growing obesity epidemic is a major source of unsustainable health costs and morbidity and mortality because of hypertension, type 2 diabetes mellitus, dyslipidemia, certain cancers and major cardiovascular diseases. 29236710: Obesity was recorded in 10.5% of maternal deaths, with higher proportions of deaths due to hypertension in pregnancy (27.5%), circulatory/ cardiovascular disorders (13.0%), and diabetes (4.3%) compared to 21.9%, 6.9% and 2.6% respectively in non-obese women. 29540174: BACKGROUND: Hypertension may result from high-fat (HF) diet induced-obesity and overexposure to glucocorticoids in utero. 29572376: In men and women, respectively, 5.7 (4.4 to 8.1) and 5.4 (4.3 to 7.3) years of functioning were lost by age 60 due to insufficient physical activity, 5.1 (3.9 to 7.0) and 7.5 (6.1 to 9.5) due to obesity, 2.3 (1.6 to 3.4) and 3.0 (2.3 to 4.0) due to hypertension, 5.6 (4.2 to 8.0) and 6.3 (4.9 to 8.4) due to diabetes, and 3.0 (2.2 to 4.3) and 0.7 (0.1 to 1.5) due to tobacco use. 32002075: The Relationship of Physical Activity and Obesity with the Incidence of Hypertension in Adults Aged 26-45 Years in Medan.BACKGROUND: The incidence rate of hypertension is increasing in Indonesia concerning unhealthy behaviours such as unhealthy physical activity and eating pattern which trigger obesity. 35686157: Obesity may also be a factor that promotes kidney damage caused by hypertension. 6681853: Obesity and duration of hypertension appeared to contribute to the later development of hypertension because of a higher blood pressure. 10550659: CONCLUSION: After excluding more common causes of spontaneous subarachnoid hematoma in this patient, we suggest that chronic spinal cord compression (spondylotic myelopathy) and arterial hypertension in this patient may have caused the pathogenesis of this rare clinical entity. 11026377: [Pathogenesis of renal damage due to hypertension]. 16674982: Long-term swimming training relieved the pathogenesis of hypertension and reversed the downregulation of the cardiovascular apelin/APJ system induced by hypertension, which suggests that the improving effect of exercise training on hypertension could be mediated by upregulating the cardiovascular apelin/APJ system. 21245762: SUMMARY: This article reviews the role of AT2R expression signaling and function in the pathogenesis of the functional and structural alterations induced by hypertension on the cardiovascular system. 21248758: These results demonstrate that the PPAR-gamma agonist rosiglitazone had beneficial effects on myocardial remodeling in SHRs by way of decreasing AP-1 activation and NF-kappaB expression, which may help in further inhibiting transcription of the downstream genes involved in the pathogenesis of myocardial remodeling induced by hypertension. 21266535: IRF3 regulates cardiac fibrosis but not hypertrophy in mice during angiotensin II-induced hypertension. Thus, our present study reveals a hitherto unrecognized function of IRF3 in cardiac remodeling, providing new insight into the progression of hypertension-induced cardiac pathogenesis. 23393608: These observations suggest that the pathogenesis of postmenopausal hypertension and its target organ complications is more complex than projected, and that loss of endogenous estrogens induces epigenetic changes that alter genetic susceptibility to end-organ complications per se resulting in pathogenetic mechanisms beyond correction by hormone replacement. 27334059: The DOCA-salt treatment induced hypertension in both genotypes, as observed by increases in systolic blood pressure. In conclusion, the results of this study suggest that the presence of KLF5 in postn-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension. 5671356: The pathogenesis of the intimal thickenings produced by hypertension in large arteries in the rat. 8652147: However, whether altered immunological function is a primary factor in the pathogenesis of hypertension or secondary to tissue damage of vascular beds induced by hypertension is still poorly defined. 9989765: Moreover, angiotensin II is known to be actively involved in the pathogenesis of progressive kidney injury induced by hypertension. 10567184: We hypothesized that during hypertension, the impairment of mediation of shear stress-induced dilation by nitric oxide (NO) is due to the prevailing hemodynamic forces, and that mediation of this response by NO should still be present in young spontaneously hypertensive rats (SHR). 10854007: Angiotensin-converting enzyme: induction by hypertension-induced vessel distension. We hypothesized that vascular ACE activity might be increased by hypertension-induced vessel distension. These results demonstrate an induction of ACE in large arteries that had been exposed to elevated blood pressure, and they imply that the induction of vascular ACE is due to hypertension-induced vessel distension. 1277403: In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. 15152541: It documented the presence of systemic venous and portal pulsatility associated with severe ectasia and varicosity of infracardiac systemic venous system due to systemic venous hypertension. 15344302: A common pathophysiological mechanism for arrhythmia development is atrial distention and fibrosis induced by hypertension, coronary artery disease or ventricular dysfunction. 16117487: The dilation of venous angioma due to high blood pressure was thought to cause the paresis of face and arm in this patient. 22641984: Although segmental dilatation is frequently seen in association with hypertension, one should think of microfistulae as an underlying cause of diffuse coronary ectasia. 23076772: BACKGROUND: Telangiectasia is the dilation of dermal capillaries mainly due to hypertension and vein insufficiency. 23321401: Although it is well known that endothelial function is compromised in the presence of either hypertension (HTN) or hypercholesterolemia (HCh), less is known about whether and how the combination of these risk factors (HTN+HCh) results in impaired endothelium-dependent dilation (EDD). 2939831: The data show the presence of increased circulating atrial natriuretic factor immunoreactivity in hypertensive salt-sensitive Dahl rats which may be due either to the hypertension-induced left atrial distention, to volume expansion or indirectly renal hyposensitivity to the atrial natriuretic factor in these rats. 34713986: RESULTS: As expected, the exercise significantly elevated blood pressure and led to decreased FMD (p < 0.05). 32001911: Inadequate pain control in the post-operative period may cause hypertension that may lead to subsequent PRES. 32632712: Posterior reversible encephalopathy syndrome (PRES) due to acute hypertension in children: 12 years single-center experience. Posterior reversible encephalopathy syndrome (PRES) due to acute hypertension in children: 12 years single-center experience.The objective of the study is to evaluate the clinical and neuroradiological findings, the risk factors for recurrence and the prognosis in patients with posterior reversible encephalopathy syndrome developed secondary to acute hypertension in children. 32871646: Brain computerized tomography (CT) suggested posterior reversible encephalopathy syndrome due to hypertension. 33269231: Hypertension is the most common cause of posterior reversible encephalopathy syndrome (PRES) and acute cerebral infarction. 33298478: Herein, we report a case of SS who had posterior reversible encephalopathy syndrome (PRES) because of high blood pressure.A young male with a 5-month history of chronic tension-type headache and depression had been receiving amitriptyline and paroxetine. 33992168: In patients with severe COVID-19, PRES can be triggered by uncontrolled hypertension, or occur independently in the setting of systemic illness and certain medications. 34645762: The first PRES episode with confusion and the second PRES episode with vertigo and nausea were caused by MPA, hypertension and renal failure. 34812747: SUMMARY: Hypertensive disorders of pregnancy are a continuum of failure of autoregulation mechanisms that may lead to eclampsia, posterior reversible encephalopathy syndrome, reversible cerebral vasoconstriction syndrome and stroke. 35261852: Posterior reversible encephalopathy syndrome due to arterial hypertension may mark the onset of the symptomatic phase in Huntington's disease. 35584601: RESULTS: HTN was the most common PRES etiology (65%). 36919059: Posterior reversible encephalopathy syndrome (PRES) and cerebral infarction are both caused by hypertension, but they rarely occur together. 37123791: PRES is predominantly caused by uncontrolled hypertension though it has been associated with illicit drug use, specifically cocaine use. 37200718: This is one of the first documented cases of CVS-induced hypertension causing PRES. A Case of Cyclic Vomiting Syndrome-Induced Hypertension Causing Posterior Reversible Encephalopathy Syndrome. 37229077: Hypertension along with other key components of sickle cell pathology is one of the reversible causes of posterior reversible encephalopathy syndrome (PRES). Although its triggering factors and pathophysiology is not well documented, hypertension is one of the easily reversible causes of PRES. 38126184: Although the pathophysiology of PRES remains elusive, 2 main pathogenic hypotheses have been suggested: cerebral hyperperfusion due to acute hypertension and cerebral hypoperfusion related to endothelial dysfunction. 10464002: Hypertension appears to be a consequence, rather than a primary cause of preeclampsia. 10549228: While the prognosis of an isolated hypotension is good, the combination of hypertension and proteinuria leading to preeclampsia is the primary cause of maternal death in many countries and is responsible for 20-25% of perinatal mortality. 11455993: We also found that the point estimate of population attributable risk percent of preeclampsia attributable to chronic hypertension was significantly higher for African-American women (10.3, 95% CI = 8.6-12.5) compared to White women (5.3, 95% CI = 4.7-6.4). Furthermore, the two-fold higher population attributable risk percent of preeclampsia among African-American compared to White women quantifies the burden of preeclampsia attributable to chronic hypertension, and indicates a greater opportunity for prevention. 17403433: CONCLUSION: SFlt-1 induces hypertension and fetal growth restriction in pregnant mice, which supports its hypothesized role in the pathogenesis of preeclampsia. 18259014: BPH/5 exhibit impaired placentation before the onset of hypertension and proteinuria, supporting a causal role for the placenta in the pathogenesis of preeclampsia. 20513456: The non-treated pathology is associated with higher risk of maternal morbidity, including arterial hypertension, which could lead to preeclampsia or eclampsia, ideation and suicide attempts, and postpartum depression. 21159041: We managed a case of CS in pregnancy that was considered to be severe pre-eclampsia due to uncontrolled hypertension. 22389120: This article reviews the physiologic changes in blood pressure during pregnancy, current definitions of hypertensive diseases of pregnancy and preeclampsia, and postulated pathophysiologic mechanisms leading to preeclampsia that might contribute to later CV risk. 25189485: This hypothesis proposes pre-eclampsia is caused by intra-abdominal hypertension in pregnancy. 26116450: Preeclampsia (PE) is a severe pregnancy-induced disorder characterized by hypertension and proteinuria and a leading cause of perinatal maternal-fetal mortality and morbidity in developing countries. 26564287: CONCLUSIONS: Being over-weight, having gestational diabetes and chronic hypertension were main risk factors leading to recurrent preeclampsia. 26693822: During the last year (2014-2015), several articles published in Hypertension have provided important insights into the pathogenesis of preeclampsia and its related complications.1-38 In addition, Hypertension also published some key research communications that translated important basic science observations into the clinic. 27181106: Certainly further investigations are required in preeclampsia, since counteracting the damages to the mother and fetal sides resulting from hypertension and elevated sFlt-1 levels may provide a great benefit in this gestational hypertensive disease. 29273682: Preeclampsia (PE) is a pregnancy-induced disorder characterized by hypertension and proteinuria after 20 weeks of gestation, affecting 5-7% of pregnancies worldwide. 31230552: These findings further suggest air pollution may affect the development of hypertension in pregnancy, although differing causes of preeclampsia and gestational hypertension may alter these relationships. 32114578: Ten subjects delivered by Caesarean section (in 3 cases due to early-onset preeclampsia and 2 subjects due to significantly increased blood pressure), and 9 cases spontaneously (1 subject complicated twice due to late-onset preeclampsia). 33193759: The increased BMI and blood pressure level observed indicate overweight and possible hypertension which could subsequently lead to preeclampsia and other adverse pregnancy outcomes. 36683540: SUMMARY: We will summarize the different types of hypertensive disorders in pregnancy, updates on the pathogenesis of preeclampsia, and appropriate HTN management based on the latest evidence in order to better care for mother and child. 8568184: The risk of Takayasu's arteritis associated with pregnancy, as reported in the literature, is mainly due to the consequences of arterial hypertension with pre-eclampsia (60%), heart failure and cerebral vascular events (5%). 10568452: Mortality during pregnancy in women with undiagnosed pheochromocytoma is high (approximately 50%), typically because of hypertension and/or hemorrhage associated with catecholamine release from the tumor. 10883996: Laparoscopic adrenalectomy was performed early in the second trimester of pregnancy in a woman with an aldosteronoma causing hypertension (254/154 mm Hg). 12808338: We experienced a case of Cushing s syndrome in pregnancy, which had been considered as the severe preeclampsia and gestational diabetes due to uncontrolled hypertension and hyperglycemia. 1453404: Two groups of 32 patients each underwent oxytocin induction for postdatism, diabetes or hypertensive disorders of pregnancy. 14578949: A 40-year-old woman, gravida 2, para 0, was admitted to our hospital at 25 weeks' gestation because of high blood pressure. 14647564: Despite aggressive medical treatment, cesarean section had to be carried out at 34 weeks of pregnancy because of uncontrolled hypertension. 15055149: The low quality of screening and management of hypertension in pregnancy makes it less realistic to expect any impact of antenatal care programme in reducing morbidity or mortality due to hypertension in pregnancy. 16585887: The second patient was hospitalized at 26 weeks' gestation because of cranial hypertension, right hemiparesis and aphasia. The third patient was admitted to the hospital at 12 weeks' gestation because of cranial hypertension. 19483448: The predominant indication for induction was post term pregnancy (51.28%) followed by PROM (17.3%), isolated oligohydramnios (8.97%), hypertensive disorders of pregnancy (8.33%), maternal perception of decreased foetal movements (7.69%) and others. 19736477: Two patients had abortions one stillbirth and 2 required termination of the pregnancy; one due to severe hypertension, and other due to renal impairment. 24827646: A neonate with antenatally diagnosed intrathoracic mass by ultrasound scan was delivered uneventfully at 35 weeks gestation by caesarean section due to pre-eclampsia and fluctuating hypertension in the mother. 25193157: METHODS/DESIGN: A total of 602 women with an ongoing pregnancy with a live fetus requiring delivery because of pre-eclampsia or uncontrolled hypertension will be randomly assigned to labor induction with a transcervical Foley catheter or oral misoprostol 25 micrograms. 26909159: She was switched to intensive hemodialysis at 8 weeks of gestation and had a C-section because of hypertension at 35 weeks, with delivery of a healthy girl weighing 2012 g. 27579135: Hypertensive disorders in pregnancy are common and can occur as a result of pre-existing hypertension or as new onset hypertension usually in the second half of pregnancy. 27957708: We have discussed various terminologies used to describe hypertension during pregnancy, risk factors, etiopathogenesis, pathophysiology, management guidelines, complications and long term consequences of hypertensive disorders of pregnancy in this chapter. 28484292: Correlation of Oxidative Stress Markers with Ultrasound and Cardiotocography Parameters with Hypertension Induced Pregnancy. 28668289: INTERPRETATION: Oral misoprostol was more effective than transcervical Foley catheterisation for induction of labour in women with pre-eclampsia or hypertension. Women (aged >=18 years) who were at 20 weeks' gestation or later with a live fetus and required delivery as a result of pre-eclampsia or hypertension were randomly assigned (1:1), via computer-generated block randomisation (block sizes of four, six, and eight) with concealment by use of opaque, sequentially numbered, sealed envelopes, to receive labour induction with either oral misoprostol 25 MUg every 2 h (maximum of 12 doses) or a transcervical Foley catheter (silicone, size 18 F with 30 mL balloon). 28913102: CASE 1: A nulliparous woman aged 37 years was referred at 26 weeks of gestation because of arterial hypertension, edema, and growth restriction in one twin. CASE 2: A nulliparous woman aged 33 years with a 27-week twin pregnancy was referred because of arterial hypertension and discordant growth. 29405968: INTRODUCTION: Preeclampsia is a hypertensive, gestational disease, which is still the leading cause of pregnancy related morbidity and mortality. 30996172: The patient was diagnosed with hypertension at 17 years of age and underwent emergency Caesarean section at 26 weeks of gestation during 2 pregnancies due to severe high blood pressure. 32212388: CONCLUSION: Among children born before 32 weeks of gestation because of suspected fetal growth restriction or hypertensive disorder who survived until age 2, prenatal ARED in the umbilical artery was associated with more frequent moderate or severe neuromotor or sensory disabilities. 32268819: On the 38th week of gestation, we conducted labor induction because of elevated blood pressure. 32314609: We present a case of a 38-year-old, multiparous woman admitted at 36 weeks of gestation due to hypertension. 3408228: The indications for induction were prolonged pregnancy greater than 42 weeks (N = 12), hypertensive disorders of pregnancy (N = 26), suspected intra-uterine growth retardation (N = 30) and a combination of two or more of the above (N = 7). 35607726: METHODS: The study included pregnant women (n=107) hospitalized in the period from July 1, 2020 to October 10, 2021 at the Department of Pathology of Pregnancy of the University Clinic of Obstetrics and Gynecology, University Clinical Center Sarajevo (UCCS) (Bosnia and Herzegovina), due to hypertensive disorder in pregnancy without symptoms of impaired thyroid function. 36164558: Study Design: This is a quality improvement, retrospective cohort study of postpartum patients with antenatal hypertensive disorders in pregnancy who delivered and were readmitted due to hypertensive disorders in pregnancy at NYU Langone Health on 3/1/2019-2/29/2020 (control cohort) to 4/1/2020-3/31/2021 (COVID cohort). 36825099: She had a natural pregnancy and elective cesarean section at 38 weeks of gestation due to hypertensive disorders of pregnancy. 37411030: Outcomes of interest were elective induction, unplanned cesarean births, hypertensive disorders of pregnancy, a composite of perinatal adverse outcomes, and neonatal intensive care unit admissions. 6329893: Frequent prenatal care and treatment of the hypertension resulted in a pregnancy of 34 weeks gestation. 7951836: A 34 year-old woman was given enalapril from the onset of her pregnancy because of hypertension from the age of 18 years. 8575678: 30 of them were the women with a normal course of pregnancy, and 34 were the ones with hypertension induced pregnancy (PIH). 9916846: A triplet pregnancy in a 23-year-old woman was terminated at 15 weeks of gestation because of her severe hypertension, lung edema, and secondary hyperthyroidism. 12715438: OBJECTIVES: Arterial hypertension is an important cause of preterm delivery. 15777440: Conversely, no association was found between induced abortion and very preterm delivery due to hypertension. 15901269: There was no association between smoking and risk of very preterm birth caused by hypertensive diseases. 20175043: Recurrence rates of premature deliveries due to hypertensive disorders were calculated for each study separately. 23700849: Psoriasis may cause recurrent miscarriages, chronic hypertension, diabetes or obesity leading to perinatal complications and premature birth. 23705099: When mimics of HELLP syndrome, such as disseminated HSV infection, are the cause of critical illness, the presence of AIN-induced proteinuria may falsely implicate a hypertensive disorder of pregnancy, resulting in iatrogenic premature delivery of the fetus and failure to initiate definitive potential lifesaving treatment. 26105032: Pre-eclampsia or hypertension resulting in preterm birth associated with a threefold (95% CI 1.3 to 7.0, p=0.01) greater risk of being hypertensive by age 20 years, with no differences in body mass index. 26411137: CONCLUSION: In was concluded that the hypertensive disorders of the pregnancy adversely influence the morphology of placenta, which leads to the premature delivery. 26444006: INTRODUCTION: Preeclampsia is a maternal hypertensive disorder with uncertain etiology and a leading cause of maternal and fetal mortality worldwide, causing nearly 40% of premature births delivered before 35 weeks of gestation. 28620518: SLE pregnancies are also more likely to be complicated by pre-eclampsia and hypertension and to result in preterm birth and small-for-gestational aged infants. 28791264: RESULTS: There were 23 cases with one more pregnancy complication (FGR, 9; gestational hypertensive disorders, 8; PTB caused from PTB or PPROM, 12). 31520257: The concurrency of a demonstrated higher risk of hypertensive gestational disorders and placenta previa suggests that placental development plays an important role in the pathogenesis of PTB. 32176323: Addressing hypertension should help reduce preterm inductions. 33627204: Iatrogenic preterm birth is the main cause of preterm birth in Henan Province, and hypertensive disorders of pregnancy and fetal intrauterine distress are the main causes of iatrogenic preterm birth. 33627822: Compared with those born after preterm labor, infants born very preterm because of hypertensive disorders of pregnancy and/or fetal growth restriction display an increased risk for late-onset sepsis. 34536318: Additionally, 87% (95% CI 84%, 90%) of perinatal deaths could be eliminated if preterm deliveries, as a result of chronic hypertension, were preventable. 9101251: Preeclampsia is a hypertensive disorder of human pregnancy that is a leading cause of premature delivery and fetal growth retardation. 9859861: Pre-eclampsia is a hypertensive disorder of human pregnancy that is a leading cause of premature delivery and fetal growth retardation. 11475153: The female patient was known to have proteinuria from the age of 14 and was hospitalized in 1980, at the age of 25 years, because of hypertension and proteinuria (1.5 g/day). 12344838: Hypertension in its most severe form produces convulsions, proteinuria, and edema and may lead to fetal and maternal death. 12966648: Renal injury is mediated by protein glycation, proteinuria and hemodynamics alterations induced by arterial hypertension and impaired renal autoregulation. 1360561: It is possible that hypertension causes glomerular enlargement, proteinuria, and segmental glomerular lesions because of loss of functioning glomeruli due to ischaemia. 17076139: It will also review the significance of the development of proteinuria in the elderly population and discuss other common causes of proteinuria apart from those secondary to diabetes and hypertension. 18821091: AIMS: Hypertension causes proteinuria and is an important factor in the progress of renal dysfunction. 26135138: CONCLUSIONS: Proteinuria in both patients was caused by glomerular hypertension with hyperfiltration. Proteinuria caused by glomerular hypertension during adolescence associated with extremely premature birth: a report of two cases. 27307141: Conclusions and relevance Hypertension can be excluded as a common cause of renal damage leading to proteinuria in FIV-infected cats. Objectives Hypertension is a common cause of proteinuria in HIV-infected people. 28994226: Acute rejection and uncontrolled hypertension were the most frequent causes of proteinuria. 29465714: BACKGROUND: Preeclampsia is a major hypertensive disease caused by pregnancy, inducing proteinuria and increased blood pressure starting from the second half of pregnancy (early preeclampsia) or near the end of pregnancy (late preeclampsia). 30669309: Proteinuria and hypertension did not remit after delivery, which was made via caesarean section, due to uncontrolled hypertension, at an estimated gestational age of 29 weeks. 3281046: Moreover, a direct correlation was found between the diastolic blood pressure (BP) values and the urinary excretion of albumin in the entire group of psoriatics, thus suggesting systemic hypertension as one of the factors responsible for proteinuria in these patients. 7006541: Exacerbation of hypertension and a marked excretion of protein in the urine were observed in three patients in the absence of underlying renal parenchymal disease or other causes of proteinuria. 7594441: CONCLUSION: Dietary omega-3 fatty acids retard the development of hypertension-induced proteinuria. 7756590: Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. 8766645: Development of hypertension causes increased proteinuria, decline in glomerular filtration rate and reduced life span in experimental models of glomerulonephritis. 15952297: Multiple factors including hypertension caused by sudden catecholamine release may result in pulmonary edema. 20640214: In most of the instances, coronary artery disease, valvular heart diseases, hypertension may precipitate pulmonary oedema due to increased hydrostatic pressure while acid aspiration, airway obstruction may cause it due to increased vascular permeability. 21229687: [Case of pulmonary edema due to excessive hypertension following extubation]. 3019261: Finally, alpha 1-agonists cause maximum arterial hypertension at all doses used, irrespective of induction of LE and of protective pretreatment against LE. 34584816: Additionally, pulmonary edema secondary to hypertension should be considered as a differential in either postpartum or peripartum women who present with respiratory symptoms and elevated blood pressure. 6806959: The cause of death in our animals exposed to hyperbaric oxygen was pulmonary edema secondary to a systemic hypertension. 7460203: The hypertension rapidly led to pulmonary edema and death. 7922220: LV diastolic dysfunction, resulting from an increase in LV mass due to the effects of hypertension or to uremic interstitial fibrosis, can both lead to pulmonary edema and hypotensive periods during hemodialysis and is a severe risk factor for mortality in hemodialysis patients. 8285450: Half of the patients presented extrarenal manifestations of disease, including: seizures (30%), colonic ischemia requiring intestinal resection, and heart failure with lung edema due to severe hypertension. 8404085: Thus, impaired left ventricular diastolic filling in the non-MI segments due to higher incidence of hypertension and left ventricular hypertrophy was considered to be the possible cause of pulmonary edema. 15493050: Differentiating thrombotic microangiopathies induced by severe hypertension from anemia and thrombocytopenia seen in thrombotic thrombocytopenia purpura. 17176910: Although other possible causes of thrombotic microangiopathy, such as anti-phospholipid antibody syndrome, were excluded in only two patients, the thrombotic microangiopathy injury process may be a cause or a consequence of the severe hypertension encountered in most of the patients which, in turn, may be a consequence of the disease progression of IgA nephropathy. 18497467: Renal thrombotic microangiopathies induced by severe hypertension. 25130726: The complete resolution of thrombocytopenia occurred once blood pressure was controlled favoring a diagnosis of hypertension-induced thrombotic microangiopathy. Absolute immature platelet count helps differentiate thrombotic thrombocytopenic purpura from hypertension-induced thrombotic microangiopathy. 29858281: Background Severe hypertension can induce thrombotic microangiopathy (TMA) in the renal vasculature, the occurrence of which has been linked to mechanical stress to the endothelium. 30014486: METHODS AND RESULTS: Renal biopsies of 15 patients who had received anti-VEGF (aVEGF) therapy evaluated between 2013 and 2017 at a single centre were morphologically characterised with light microscopy, electron microscopy, and immunohistochemistry (IgA, IgG, IgM, C1q, and C3), and compared with cases with acute TMA caused by atypical haemolytic-uraemic syndrome or hypertension. 30963011: Owing to the preexisting proteinuria prior to severe hypertension and the complex renal histopathology, we postulated that chronic TMA, which was initially triggered by tacrolimus, was aggravated by severe hypertension, resulting in overt renal TMA. 31401947: We postulate that endothelial damage due to hyperhomocysteinemia and hypertension could have triggered the TMA episode in this patient with two possible predisposing pathogenic mutations in the alternative complement pathway. 31420192: Malignant hypertension is listed among the causes of secondary thrombotic microangiopathy, but pathogenic mutations in complement genes have been reported in patients with hypertension-induced thrombotic microangiopathy. 31755918: The association with hypertension (HTN) was so strong that it led to the hypothesis that MA/TMA in IgAN was a mere consequence of severe HTN. 32426663: Typically, these occur in patients secondary to dialysis, cerebral amyloid angiopathy, or thrombotic thrombocytopenic purpura.1,2,3 However, this is the unique case of a 62-year-old Asian female who presented with a hemorrhagic stroke suspected to be secondary to refractory hypertension from intracranial large vessel atherosclerotic flow limiting stenosis, with rapid subsequent large vessel occlusion and ischemic stroke. 32746791: Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and secondary TMA other than that caused by hypertension were excluded. 34544963: Thrombotic Microangiopathy Due to Severe Hypertension in a Patient With Primary Aldosteronism. 10454788: Although end-organ injury due to chronic hypertension occurs frequently in adults, no previous reports of renal insufficiency due to hypertension exist in children or adolescents. 10618564: BACKGROUND: Renal artery stenosis is a common disorder and is an established cause of hypertension and renal insufficiency. 1111483: The patient had a history of rheumatoid arthritis, mild hypertension, and mild renal insufficiency presumed due to his hypertension. 15592570: Subtle renal insufficiency that interferes with sodium excretion is a common consequence of uncontrolled hypertension. 16336577: High blood pressure levels are a well-recognized feature in chronic renal disease, but the ability of mild-to-moderate hypertension to produce renal insufficiency has been questioned. 21566296: Hypertension was the most common cause of renal insufficiency (34.4%), while in 41.4% of the patients, the causative pathology was unknown. 25903027: She had moderate renal insufficiency and secondary hyperparathyroidism due to hypertension. 29399101: Kidney damage in response to hypertension eventually leads to renal insufficiency. 32301620: We also address the mechanisms underlying renal microvascular injury and impaired renal autoregulation, focusing on purinoceptor signaling and hypertension-induced renal microvascular dysfunction. 33224436: Our aim was to examine the possible preventive role of curcumin on renal dysfunction secondary to hypertension. 33258308: However, only limited progress has been made in differentiating this haemodynamic phenotype of renal dysfunction, because of a significant overlap with pre-existing renal impairment due to long-term hypertension, diabetes, and renovascular disease. 34731131: ABSTRACT: Using animal models and molecular biology researches, hyperuricemia has been shown to instruct renal arteriolopathy, arterial hypertension, and microvascular injury involving the renin-angiotensin system and resulting in renal function impairment. 35398499: The 28-day treatment normalized the hemodynamic, electrocardiographic, morphological, and renal impairments, as well as reversed the changes in ventricular function induced by hypertension. 7967780: RESULTS: Renovascular disease is an important cause of resistant hypertension and progressive renal insufficiency, particularly in the elderly population. 8889351: Several approaches for recruitment of African American adults with renal insufficiency due to hypertension (glomerular filtration rate between 25 and 70 ml/min/1.73 m2) were explored in the Pilot Study for the African American Study of Kidney Disease and Hypertension (AASK). 9211180: PARTICIPANTS: Patients with ESRD due to hypertension (n = 214), diabetes (n = 239), other specified causes (n = 181), unknown causes (n = 82) and control subjects drawn from the general population (n = 361). This result supports the hypothesis that nonmalignant hypertension of long duration may cause renal insufficiency. 9648058: This is especially true for blacks of African descent, in whom hypertension and nephrovasculopathies are a major cause of renal insufficiency. 12480731: The consequences of hypertension include cerebrovascular disease, coronary heart disease, and general atherosclerosis. Hypertension and related factors in the etiology of Alzheimer's disease. 17362841: In recent years the renin-angiotensin system, already of recognised importance in the pathogenesis of hypertension, has become a source of interest in the pathogenesis of Alzheimer's disease. 19555872: Cumulative evidence implicates hypertension in the pathogenesis of Alzheimer disease. 22615109: Overall we demonstrate that RAGE activation in brain vessels is a crucial pathogenetic event in hypertension-induced Alzheimer disease, suggesting that inhibiting this target can limit the onset of vascular-related Alzheimer disease. Interestingly, RAGE inhibition protected from hypertension-induced Alzheimer pathology, as showed by rescue from cognitive impairment and parenchymal Abeta deposition. 25976367: Several preclinical and epidemiological studies have linked metabolic risk factors such as hypertension, obesity, dyslipidemia, and diabetes to the pathogenesis of AD. 29568075: Hypertension-induced endothelial dysfunction is associated with beta-amyloid (Abeta) deposition, a typical pathology of Alzheimer's disease (AD). In conclusion, eNOS downregulation contributed to hypertension-induced Alzheimer pathology and cognitive impairment. 30854970: Chronic, low-level environmental lead (Pb) exposure is associated with cognitive impairment, hypertension and mortality, and has been proposed as a potential cause of AD. 31889399: The study result showed that HTN-induced AD regulated long-term memory (LTM) loss and neuronal degeneration in the SHR animals. Dipeptide IF prevents the effects of hypertension-induced Alzheimer's disease on long-term memory in the cortex of spontaneously hypertensive rats. 34897090: Hypertension is a major risk factor for the pathogenesis of vascular dementia and Alzheimer's disease. 38062190: The results suggest that the increased risk of AD owing to hypertension is mediated through stroke. This implies that approximately 55% of the risk of AD owing to hypertension can be attributed to stroke. 9894287: A possible consequence of these findings would be to prevent, or to postpone, AD by an early treatment of arterial hypertension. 10078562: Mechanical stretch due to glomerular hypertension has been proposed as one of the factors leading to an increase in the production of ECM proteins in mesangial cells, but the precise mechanism of stretch-induced overproduction of ECM proteins has not been elucidated. 10415519: Mechanical stretch induced by high blood pressure is an initial factor leading to cardiac hypertrophy. 10750588: Mechanical stretch induced by hypertension is an initial factor leading to cardiac hypertrophy. 12817064: Glomerular hypertension results in glomerular capillary wall stretch, endothelial damage and a rise in protein glomerular filtration. AH is also a well known consequence of chronic renal disease, and at the same time one of the main factors which causes diabetic and/or non-diabetic chronic renal failure progression. 15855808: The magnitude of GLUT1 overexpression caused by hypertension is higher than that induced by diabetes alone. BACKGROUND/AIM: Diabetes and mesangial stretch caused by hypertension increase mesangial matrix deposition which is induced by local production of transforming growth factor beta 1 (TGF-beta1). 23120821: Glomerular hypertension results in glomerular capillary wall stretch, endothelial damage and a rise in protein glomerular filtration. 2531253: Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. 29170451: Taken together, these results indicate that CMS of VSMCs induces inflammation-related gene expression, including that of CXCL1 and CX3CL1, which may play important roles in the stress response against CMS caused by hypertension. The expression of Cxcl1 was also induced in VSMCs by hypertension produced by abdominal aortic constriction (AAC). 31690818: Moreover, exposure on long-term stretch due to hypertension causes arterial stiffness with subsequent systolic and diastolic function loss resulting in further heart muscle remodeling. 8995718: In diabetes, the largely unaltered glomerular stiffness renders hypertension-induced MC stretch unopposed. 10472076: The structural and functional changes in arterial wall material associated with hypertension-induced hypertrophy may explain why medium-sized arteries maintain their distensibility characteristics despite a distending pressure increase; these changes may not be associated with an intrinsic (isobaric) decrease in the distensibility of large arteries. The purpose of this article is to review the relations between hypertension-induced hypertrophy and stiffness of the arterial wall. 10981136: In hypertension, the increase in matrix deposition results in vascular stiffness and cardiac dysfunction. 12887125: Thus high night time blood pressure is associated with a greater morbidity and high salt intake causes cardiac hypertrophy and vascular stiffness independent of blood pressure levels. 15254965: Excessive fibrosis, which has been associated with certain forms of hemodynamic overload such as hypertension, is thought to result in increased ventricular chamber stiffness, and eventual heart failure. 19836611: Hypertension is a risk factor for a long-lasting arterial wall-remodelling leading to stiffness. 22808030: Hypertension resulted in enhanced aortic stiffness accompanied by increased circulating and aortic NO levels and an upregulation of aortic inducible NO-synthase, NFkappaB, superoxide anions and nitrotyrosine. 26063669: Prolonged hypertension led to increased cardiac stiffness, cardiac fibrosis, and thrombi formation. 26837677: Thus, aortic root stiffness may be a consequence of hypertension and other risk factors. 30174171: The first stage is driven mainly by mechanical changes such as increased stiffness of the heart due to hypertension and cellular contractility. 30442693: Because hypertension results in vascular stiffness and impaired cerebral perfusion, we hypothesized that it would be the most relevant risk factor for microstructural white matter disruption in apparently healthy middle-aged individuals with a family history of early-onset coronary artery disease. 37422907: The increased stiffness of ventricular myocytes caused by hypertension leads to hypersensitivity of cellular calcium flow to mechanical stimuli is one of the mechanisms that cause arrhythmias. 12707297: Our results suggest that symptoms of aortic stenosis develop with larger valve area and lower stroke work loss in hypertensive patients, probably because of the additional overload due to hypertension itself. 15284592: The authors report one case, which is not only of interest in its own right, but also emphasizes the importance of including blood pressure measurement in the clinical examination of children, especially when hypertension could be the cause of the symptoms. 15847946: BACKGROUND: Comorbidities in hypertension complicate the course causing more symptoms and deterioration in a patient's daily life. 16882435: The initial symptoms of the patient are mostly nonspecific caused by hypertension. 19622599: Two experimental rat models of cardiovascular remodeling were used in this project: the deoxycorticosterone acetate (DOCA)-salt-induced model of chronic hypertension (study I) and a high-carbohydrate/high-fat diet-induced model producing chronic symptoms of the metabolic syndrome and its associated cardiovascular complications (study II). Our results in these rat models of hypertension and diet-induced obesity show that treatment with Avemar improved cardiac function, decreased macrophage infiltration resulting in decreased collagen deposition in the ventricular myocardium, reversed an increased stiffness of the left ventricle in the diseased hearts and attenuated increased plasma malondialdehyde concentrations. 21443071: Coarctation of aorta (COA) in adults usually manifests as uncontrolled severe hypertension, which may cause symptoms of heart failure, headaches, epistaxis, or aortic dissection. 23291504: In this study, 78 patients were asked to describe their symptoms due to EDS-HT. 23533459: Hypertension can cause few symptoms until it reaches the advanced stage and poses serious health problems with lifelong consequences. 23794677: Both diagnosed treated hypertension and untreated hypertension and measured high BP resulted in increased cardiorespiratory symptoms during the cold season. 24988610: Diseases that traditionally are linked to inappropriate life style of adults, such as type 2 diabetes, obesity, and arterial hypertension, can be \programmed\ in the early stage of life and the disturbed growth of the fetus leads to the symptoms of the metabolic syndrome. 25091828: Participants attributed HTN as a cause of their symptom(s) to a greater degree than HTN treatment. 27180561: The symptoms are related to the consequences of hypertension or condition in question. 27357953: They were also awareness that severely high blood pressure could result in death. It was widely believed that stress and weakness caused high blood pressure in pregnancy and it caused symptoms of headache. 31173541: It is important for radiologists to accurately diagnose the secondary causes of hypertension, as many of them are treatable, and treatment may result in improved symptoms or resolution of hypertension. 35597538: Surgical Obliteration of a Posterior Fossa Dural Arteriovenous Fistula Presenting with Exclusive Spinal Signs and Symptoms Caused by Spinal Cord Venous Hypertension. 37710330: All participants remained well, and acute symptoms secondary to hypertension were not reported. 3815903: All patients but one were male and had no knowledge of their renal disease and sought medical advice for symptoms due to hypertension. 38217486: However, snapping symptoms in the metacarpophalangeal (MP) joint caused by hypertension and hyperplasia of the lateral band are rare. 38615191: The stone formation can be attributed to a diversity of factors, all of them leading to obstruction in the duct, hypertension of its distal part, increased intraductal and parenchymal pressure, and inflammation, causing the standard symptom, epigastric pain. 3902676: Fenquizone showed also a significant decrease of symptoms (headache, dizziness) due to hypertension. 7469469: In 2 the hypertension was so severe that at first it had to be considered as a possible cause of the presenting symptoms. 11273900: Hypertension and high-dose methylprednisolone administration to the patient in the nephrotic state may be causes of this uncommon syndrome in this case. 11605499: The method for quantification of retinal blood vessels in cases of arteriovenous crossing pressure syndrome caused by hypertension was studied. [A research on the quantification of retinal blood vessels in cases of arteriovenous crossing pressure syndrome caused by hypertension]. 12001577: The most important diseases leading to CHF syndrome were chronic ischemic disease, arterial hypertension, COPD with chronic cor pulmonale and valve diseases. 13026490: [Intracranial pseudo-tumoral syndrome caused by arterial hypertension]. 15553373: The study aimed at (1) identification of the main vestibulometric characteristics of peripheral cochleovestibular syndrome caused by arterial hypertension, atherosclerosis and vegetative vascular dysfunction, (2) elucidation of the pathogenic peculiarities of its formation and (3) evaluation of therapeutic efficacy of betaserc in peripheral vertigo. 16150287: Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy. 16329634: It is shown that peripheral cochleovestibular syndromes caused by arterial hypertension, atherosclerosis and autonomic vascular dystonia are rarely characterized by focal cerebral changes (11 patients by CT data and 17 by MRI). 16482004: All the patients have undergone comprehensive otoneurological examination, RCT and MRI which showed that peripheral cochleovestibular syndromes (PCVS) caused by arterial hypertension (AH), atherosclerosis (AS), vascular dystonia (VD) are rarely characterized by focal alterations in the brain. 16555725: The role that ENaC and Na+ transport deregulation play on human placental tissues still remains unknown although in aldosterone-responsive epithelial cells (kidney, colon), abnormalities upregulating its activity lead to increased Na+ uptake and hypertension (i.e. Liddle's syndrome) whereas a diminished channel activity can result in the pseudohypoaldosteronisn syndrome with salt loss and hypotension. 16887004: The syndrome results from sustained intra-abdominal hypertension, which is indirectly identified by measuring intra-bladder pressures (IBPs) using various priming volumes. 18436158: Posterior reversible encephalopathy syndrome caused by hypertension is well recognized with magnetic resonance imaging. 18854436: MR imaging findings of medulla oblongata involvement in posterior reversible encephalopathy syndrome secondary to hypertension. 19893725: Hypertension and age might be the most important causative factors to evoke combined HDS. 20677621: Initially, this syndrome was believed to be secondary to hypertension, renal disease, or immunosuppressive therapy. 20887113: Posterior reversible encephalopathy syndrome can occur as a result of severe hypertension during surgery, even among young children. 21458199: Posterior nutcracker syndrome (PNS) is a rare condition due to left renal vein (LRV) hypertension, caused by compression of the LRV between the vertebral column and the abdominal aorta. 22453037: While a number of factors such as hypertension, medication and others have been reported as causes of posterior reversible encephalopathy syndrome (PRES), comparatively rapid anemia correction could also possibly precipitate PRES as like as this case. 22736265: Arterial hypertension, drugs inducing hypertension or drug side effects may cause PRES but sometimes the reason remains unknown. 23110418: CONCLUSION: The triad of central obesity, high blood pressure and low HDL were most responsible for the syndrome in this rural population. 23117272: Hypertension is a common cause of PRES. 23210935: WHAT IS KNOWN AND OBJECTIVE: Posterior reversible encephalopathy syndrome (PRES) can be the result of acute hypertension, eclampsia, renal failure and the use of immunosuppressive or cytotoxic agents. 23757909: This article describes a unique case of this syndrome in a 24-year old female admitted to hospital because of arterial hypertension and obesity. 23921191: CASES: We report 4 cases of adult patients on PD who presented with PRES, all of which were due to hypertension and inadequate management of fluid balance. 25006290: Hypertension is a well-known adverse effect of high-dose corticosteroid therapy primarily mediated by its effects on the mineralocorticoid receptor especially in pediatric population and we hypothesize that this may be the etiology of PRES in two of these patients. 25017835: We report the case of an elderly man who presented with convulsions and was diagnosed to have PRES due to hypertension. 25062302: Posterior reversible encephalopathy syndrome is a well-characterized but uncommon syndrome in children that is generally triggered by severe hypertension. 25802777: We aim to report a case of PRES induced by arterial hypertension and very early systemic sclerosis (SSc) not previously known. 26034631: CONCLUSIONS: Hypertension seems to be the most important coexisting risk factor for development of PRES; however, the potential effects of chemotherapeutic agents in the pathogenesis of PRES should also be examined. 26412031: Arterial hypertension was suspected to be the cause of PRES in five patients. 27103268: A higher blood pressure seems to be 1 of the factors responsible for developing widespread PRES, with involvement of carotid vascular territory. 27365964: Preexisting extremely high blood pressure may trigger atypical PRES, and failure to lower blood pressure may lead to a concomitant aneurysm rupture. 274940: Hypertension due to a renin-secreting tumour localised by segmental renal vein sampling. Although the immediate post-operative blood pressure fell to normal, hypertension recurred temporarily and was associated with elevated plasma aldosteron, producing a syndrome similar to primary aldosteronism. 27773902: Posterior reversible encephalopathy syndrome in Parkinson disease probably caused by prominent supine hypertension and blood pressure fluctuation. PRES may result from marked supine/nocturnal hypertension and fluctuation in blood pressure. 28018468: Inflammatory condition and severe hypertension in TA can cause PRES. 28407303: Six days after rifampicin initiation, she presented with Posterior Reversible Encephalopathy Syndrome due to uncontrolled hypertension. 28560105: The aim of this study was to characterize metabolic profiles of a rat model of chronic kidney disease (CKD) with cardiorenal syndrome (CRS) induced by prolonged hypertension. 28571231: We hereby report a rare case of central variant of PRES secondary to severe hypertension diagnosed with 3T MRI. 2858712: A disturbance in the oestrogen/progesterone ratio as a consequence of localised hypertension at the ovary, when the utero-ovarian arterial loop is occluded at tubal ligation, is proposed as a possible cause of oestrogen deficiency syndrome, dysfunctional uterine bleeding, and menorrhagia after tubal ligation. A possible cause of the estrogen deficiency syndrome might be a disturbance in the estrogen/progesterone ratio resulting from localized hypertension at the ovary when the utero-ovarian arterial loop is occluded at tubal ligation. 28646716: A variety of syndromic diseases such as Marfan syndrome, Loeys-Dietz syndrome, and bicuspid aortic valve with aneurysm along with risk factors of smoking and hypertension result in ascending aortic aneurysms and dissections. 29629684: Hypertension as the trigger for posterior reversible encephalopathy syndrome in paediatric renal patients: An important diagnosis that should not be missed. 29877278: We herein report a patient with MSA who showed posterior reversible encephalopathy syndrome (PRES) caused by hypertension during sleep. Nocturnal Hypertension in Multiple System Atrophy May Cause Posterior Reversible Encephalopathy Syndrome. 30322196: Metabolic syndrome (MetS) is defined as a constellation of many metabolic disorders such as hypertension, impaired glucose tolerance, dyslipidemia and obesity, being this last disorder a key factor in the etiology of the syndrome. 30532887: Hypertension-induced posterior reversible encephalopathy syndrome as the presentation of progressive bilateral renal artery stenosis. 31110866: Posterior reversible encephalopathy syndrome is a clinical condition presenting secondary to acute hypertension that results in neurologic symptoms including headache, seizures, altered sensorium, and loss of vision. 31383036: CONCLUSION: Our results reveal that extracellular 5-HT is the cause of a syndrome and activity of postsynaptic receptors critical for the course of syndrome intensification. 31607895: She was diagnosed with the demyelinating form of GBS and PRES caused by intermittent hypertension. 35223819: A concurrence of metabolic disorders such as obesity, insulin resistance, atherogenic dyslipidemia, and systematic hypertension leads to metabolic syndrome. 36686705: Background: Hypertensive cerebral small vessel disease (HT-CSVD) is a cerebrovascular clinical, imaging and pathological syndrome caused by hypertension (HT). 37757131: Diagnostic Value of the Ocular Syndrome Due to Hypertension in Wounds of the Skull. 7055180: Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy. 7259266: Hypertension and segmental renal hypoplasia causing a syndrome of haemolysis and uraemia. 913227: The presence of hypertension and focal neurological findings in a patient with otherwise classic clinical and radiologic features of NPH syndrome should alert one to the possibility of hypertensive cerebrovascular disease as the cause of the syndrome. 10499558: In hypertension, elevated blood pressure causes vascular disease by inducing endothelial dysfunction. 12067905: Insulin resistance is commonly associated with hypertension, a condition that causes vascular disease in people with obesity and type 2 diabetes. 1288451: The 2 oldest patients (n0 3 and 4) developed progressive kidney failure, possibly due to reno-vascular disease secondary to hypertension. 14704595: Clinical and experimental evidence suggests that the pathways by which hypertension and dyslipidemia lead to vascular disease may overlap and that angiotensin II (Ang II) is involved in restructuring of the arterial wall in both atherosclerosis and hypertension. 16894244: This review traces the history of hypertension management from the 1940s, when President Franklin Delano Roosevelt died of a cerebrovascular accident-a result of uncontrolled hypertension-to today, when a large number of patients, even those with less severe hypertension, are being treated successfully, with a resulting dramatic decrease in hypertension-related vascular disease. 17550504: CONCLUSION: The results of this preliminary study suggest that patients with systemic arterial hypertension may have cochlear dysfunction associated with the vascular disease because of hypertension, which could be silent and without clear evidence of vestibular dysfunction. 19234499: Understanding the mechanism by which chronic high blood pressure induces vascular disease is of fundamental importance for prevention of the adverse consequences of hypertension. The role of interleukin 18 in the pathogenesis of hypertension-induced vascular disease. 20655398: Arterial hypertension is a leading cause of both vascular diseases and chronic renal failure. 21309411: Arterial hypertension is a leading cause of both vascular diseases and chronic renal failure. 21839001: Hypertension is a disease with numerous etiologies which consequences led to systemic vascular damage leading to other cardio-vascular diseases increasing morbi-morbility. 22726353: These findings suggest that arterial hypertension is a main cause of vascular brain disorder (VBD). 33505509: Background: Hypertensive vascular remodeling (HVR) is the pathophysiological basis of hypertension, which is also an important cause of vascular disease and target organ damage. 36026961: Hypertension is the most established risk factor for SVD, but the pathophysiological mechanisms following hypertension that cause SVD remain poorly understood. 36082259: Discussion: The Hyperintense study will improve the understanding of the pathophysiological mechanisms following hypertension that may cause SVD. 7648669: BACKGROUND: Many factors cause acute systemic hypertension, which in turn can result in damage to the vessel wall and lead to vascular disease. 7878405: Hypertension-induced vascular disease is preceded by numerous alterations in the expression, secretion and action of mediators and receptors of endothelial cells, vascular smooth muscle, platelets and monocytes. 10944991: CONCLUSIONS: The evolution of severe systolic left ventricular dysfunction due to arterial hypertension is favourable at long-term, with null mortality and clinical ejection fraction and functional improvement. 11305972: Over 60% of black patients with heart failure have an antecedent history of hypertension as a putative cause of left ventricular (LV) dysfunction, whereas only 30% have coronary artery disease as the suspected cause of LV dysfunction. 11817974: Diabetes with and without hypertension is an important cause of LV dysfunction and CHF. 11960591: The overwhelming burden of hypertension as a putative cause of left ventricular dysfunction identifies this illness. 12232949: These findings are consistent with possible diastolic LV dysfunction due to hypertension as the primary cause of cardiac failure in the population. 12269522: BACKGROUND: In the absence of a prior history of myocardial infarction (MI), left ventricular (LV) dysfunction is commonly due to hypertension, valvular heart disease, or hibernating myocardium. 15580162: Pheochromocytomas are neuroendocrine tumors that typically present with paroxysms of hypertension, but occasionally can lead to marked hemodynamic instability, left ventricular dysfunction, and cardiovascular collapse. 15702614: Hypertension represents the most common associated cause of heart failure, and it is frequently involved in the pathogenesis of left ventricular dysfunction and its progression towards congestive heart failure. 20605820: Tachycardia, hypertension, and severe metabolic abnormalities can independently cause global LV dysfunction, which typically improves with addressing the precipitating factor. 25983883: Left ventricular dysfunction (LVDys), often as a result of hypertension, ischaemic cardiac disease or dilated cardiomyopathy, has not been uniformly defined in the literature making diagnosis and therapy problematic. 27298800: Patients with venoarterial extracorporeal membrane oxygenation (ECMO) frequently suffer from pulmonary edema due to left ventricular dysfunction that accompanies left heart dilatation, which is caused by left atrial hypertension. 38242833: Cardiovascular toxicities caused by cancer therapies include different severities of cardiomyopathy, arrhythmia, myocardial ischaemia, hypertension, and thrombosis, which may lead to left ventricular dysfunction and heart failure. 6458260: These findings are similar to the abnormalities described for non-African hypertensive patients; and show that hypertension causes LV dysfunction before the onset of overt heart failure. 8281965: Left ventricular hypertrophy, as a consequence of arterial hypertension, influences the three factors involved in the prognosis and we express these as a triangle of risk: electrical instability, left ventricular dysfunction and ischaemia. 10779123: Hypertension leads to ventricular hypertrophy and, eventually, to heart failure. These results show that cardiac responses are only minimally affected during the development of DOCA-salt hypertension-induced hypertrophy, despite the reported decreases in adenylate cyclase activity, in these rats. 12509479: Although non-conditional eNOS gene deletion may engender phenotypic adaptations (e.g. ventricular hypertrophy resulting from chronic hypertension, or upregulation of the other NOS isoforms) potentially confounding the interpretation of comparative studies, the use of eNOS-/- mice has undoubtedly advanced (and will probably continue to improve) our understanding of the complex role of eNOS (in conjunction with the other NOSs) in the regulation of cardiac function. 21432982: It is generally assumed that ventricular hypertrophy is a result of hypertension. 23293462: It is therefore advisable not to prescribe pioglitazone in diabetic patients having congestive heart failure as well as in patients having chronic hypertension, since chronic hypertension leads to ventricular hypertrophy which might get worsened. 25308856: To investigate whether inhibition of miR-29a functioning prevents the hypertension-induced ventricular hypertrophy and fibrosis. 2689025: Reduction of blood pressure with these agents appears to lead to the concomitant reduction of hypertension-induced ventricular hypertrophy and improvement of ventricular function. 27915452: It has been well established that chronic pressure overload resulting from hypertension leads to ventricular hypertrophy and electrophysiological remodeling. 29582957: Arterial hypertension would be responsible for ventricular hypertrophy. 7006655: Patients selected from a diabetic clinic frequently have impaired left ventricular function, and ventricular hypertrophy, when present, in primarily caused by hypertension. 8034891: Analysis of transmural trend of myocardial integrated ultrasound backscatter for differentiation of hypertrophic cardiomyopathy and ventricular hypertrophy due to hypertension. CONCLUSIONS: Hypertrophic cardiomyopathy and ventricular hypertrophy due to hypertension can be differentiated on the basis of quantitative analysis of the transmural gradient in integrated backscatter. 9019211: Drugs to treat hypertension must not only reduce blood pressure, but also modify the facts which lead to ventricular hypertrophy. 1691394: To clarify mechanisms underlying an enhanced susceptibility to cardiac rhythm disturbances in hypertension and myocardial hypertrophy, we evaluated the vulnerability to histamine-induced arrhythmias of isolated left ventricles from spontaneously hypertensive rats (SHR) and age-matched controls (Wistar-Kyoto rats, WKY). 2576672: Left ventricular hypertrophy may be a serious consequence of chronic untreated hypertension since it may accentuate the risk of congestive heart failure, arrhythmias, coronary ischaemias and sudden death. 26619661: Abstract Hypertension is the major cause of cardiovascular disease. Persistent hypertension leads to cardiovascular remodeling and resulted in heart diseases such as coronary artery disease, heart failure, and arrhythmia. 26995439: Hyperactive sympathetic nervous system aggravates hypertension and it can cause complications like left ventricular hypertrophy, heart failure, arrhythmias and atherogenesis. 28290817: They did not use prognostication of development of cardiac arrhythmias caused by hypertension. 2970857: Prevention of hypertension is associated with reduced susceptibility to histamine-induced arrhythmias in SHR. 3216239: We conclude that hypertension induces arrhythmias, and that age increases their severity. 3273435: [Arrhythmia caused by left ventricular hypertension. Development of an experimental model]. 574353: Chronic experiments were also carried out on wakeful dogs with induced hypertension, on animals fed on an atherogenic diet, and on animals with induced arrhythmia and coronary spasm. 7808691: Heart failure, arrhythmia, or chest pain can be a consequence of diabetes independent of coronary disease or hypertension. 32700580: Increasing ACE2 could potentially increase the risk of infection, severity or mortality in COVID-19 or it might be protective as it forms angiotensin-(1-7) which exhibits anti-inflammatory/anti-oxidative effects and prevents diabetes- and/or hypertension-induced end-organ damage. 33234808: OBJECTIVE: Hypertension-induced end-organ damage is one of the important determinants of morbidity and mortality in patients with hypertension. All types of hypertension-induced end-organ damages start with vascular damage. 34111864: We therefore investigated cardiorenal protection of respective mono- and combination therapy in a preclinical model of hypertension-induced end-organ damage. Effects of Finerenone Combined with Empagliflozin in a Model of Hypertension-Induced End-Organ Damage. 34218268: Hypertension (HTN) causes end-organ damage and is a major cause of morbidity and mortality globally. 34305645: Finally, we evaluate the use of proANP 3 1 - 6 7 as a new therapeutic strategy to repair end-organ damage secondary to hypertension, diabetes mellitus, renal diseases, obesity, heart failure, and other morbidities that can lead to impaired cardiac function and structure. 35667713: INTRODUCTION: Hypertension is a global healthcare burden that affects the structure and function of the macrocirculation and microcirculation and induces disease-specific end-organ damage. METHODS AND ANALYSIS: The 'Hypertension and retinal microvascular dysfunction' trial will investigate macrovascular and microvascular impairments in hypertensive patients compared with healthy controls to investigate hypertension-induced end-organ damage by using gold-standard methods as well as newly developed unique retinal microvascular biomarkers. 35870482: In these animals, hypertension-induced end-organ damage is also decreased. Therefore, Ang-(1-9) is a promising antihypertensive drug that reduces hypertension-induced end-organ damage. 36529872: CONCLUSION: When normative data are available, OCTA might be used as a potential tool in the prevention and follow-up of end-organ damage secondary to HTN. 38166023: Hypertension leads to water-electrolyte disturbances and end-organ damage. 38289749: Hypertension has also been found to cause end-organ damage in children with 11beta hydroxylase deficiency. 10100688: There is substantial evidence from both observational epidemiology studies and randomized controlled trials that dietary intake of sodium and potassium is important in the etiology of hypertension. 12111752: This review focuses its attention on sodium, potassium, calcium, and magnesium ions in order to investigate whether these electrolytes play a role in the pathogenesis of arterial hypertension and its treatment. 14643581: METHODS: Male Sprague-Dawley rats weighing 240 to 250 g were fed a fructose-enriched diet consisting of 21% protein, 5% fat, 60% carbohydrate, 0.49% sodium and 0.49% potassium for 5 weeks, which produced hyperinsulinemia, hypertension, and hypertriglyceridemia. 17494929: Sodium and potassium in the pathogenesis of hypertension. 2677140: Mean arterial pressure (MAP), plasma renin activity (PRA), plasma aldosterone concentration (ALDO), para-aminohippurate (PAH) clearance, glomerular filtration rate (GFR), urine volume, and sodium and potassium excretion were measured before and weekly after induction of the hypertension. 2693847: The roles of sodium, potassium and magnesium in the etiology of high blood pressure are reviewed. 27906749: Sodium and potassium in the pathogenesis of hypertension: focus on the brain. RECENT FINDINGS: Animal studies point to a small increase in plasma and cerebrospinal fluid (CSF) [Na], a small decrease in CSF [K], and increased levels of circulating angiotensin II, aldosterone, and endogenous ouabain as the central signals evoking hypertension. 30446179: Alterations in metabolic pathways associated with the sensitivity of sodium, potassium, magnesium and calcium may lead to obesity, hypertension, and insulin resistance. 4790000: [Significance of sodium and potassium metabolism for genesis of hypertension in kidney failure]. 6984027: An independent role of potassium in the aetiology of high blood pressure would have important public health implications. 11002548: The role of immunological system in pathogenesis of PE is well known but the hypothesis that immunological events are engaged in pathogenesis of chronic hypertension has not been proved so far. 11327631: BACKGROUND: One hypothesis of the pathophysiology of pre-eclampsia is that placentally derived, yet unidentified, vasoactive factors are released into the maternal circulation, causing hypertension. 12859402: Pre-eclampsia is a potentially life-threatening disease of women during pregnancy leading to hypertension and proteinuria. 13280100: Does toxemia produce hypertension? 1457532: One case had severe arterial hypertension, proteinuria and pedal edema, which was thought to be due to pre-eclampsia. 14933778: Epidural analgesia in the treatment of hypertension due to toxaemia of pregnancy. 15186215: Pre-eclampsia results in oedema, hypertension and proteinuria, and is associated with increased vascular permeability. 16719796: Studies in animal models of hypertension in pregnancy suggest that inadequate cytotrophoblast invasion of uterine spiral arteries causes reduction in uteroplacental perfusion pressure leading to placental ischemia/hypoxia. If untreated, PE leads to eclampsia with serious seizures and severe hypertension. 17127257: Preeclampsia induced hypertension is the result of increased vascular reactivity and endothelial dysfunction, however, the mechanisms underlying this state remain elusive. 18884787: Does eclamptogenic toxemia cause chronic hypertension? 19452431: We performed a retrospective review of the outcomes of 318 singleton pregnancies with chronic hypertension or prior preterm delivery due to preeclampsia whose antihypertensive therapy was guided by impedance cardiography. 21134030: Increasingly, the accuracy of inducing 'pure' systemic endothelial dysfunction is regarded as critical in differentiating mechanisms of pre-eclampsia from other conditions which induce hypertension (e.g. glomerulonephritis, renal denervation or manipulation of the renin-angiotensin system). 21182804: CONCLUSION: Combined VitCE supplementation does not decrease the risk of preeclampsia and should not be offered to gravidas for the prevention of preeclampsia or other pregnancy induced hypertensive disorders. 21916260: UNLABELLED: Preeclampsia is a disease regarding with altered vascular reactivity leading to hypertension of the mother and metabolic alterations in the fetus. 23087548: Preeclampsia was the most common (91.7%) cause of hypertension during pregnancy, and chronic hypertension was present in 8.3% of patients. 24553299: Preeclampsia is thought to arise from inadequate cytotrophoblast migration and invasion of the maternal spiral arteries, resulting in placental ischemia and hypertension. 26000015: In this review, we analyze the molecular mechanisms of preeclampsia with a particular focus on the pathogenesis of the hypertension in preeclampsia and its association with the renin-angiotensin system. 27784685: The objective of this study was to determine a role for TH17s, from the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia, in the etiology of hypertension and chronic inflammation during pregnancy. 28228456: BACKGROUND: Preeclampsia is a pregnancy-specific disorder resulting in hypertension and multiorgan dysfunction. 30090069: Actually, peripheral vasoconstriction secondary to maternal systemic inflammation and endothelial cell activation is sufficient for the development of preeclampsia-induced hypertension. 30414975: Preeclampsia (PE) reverts these normal changes inducing hypertension. 30451990: Preeclampsia is a placentally induced hypertensive disorder of pregnancy that is associated with substantial morbidity and mortality to mothers and fetuses. 31632289: Preeclampsia is considered to be caused by the systemic vasoconstriction of small arteries and disruption of the endothelial integrity, resulting in hypertension, proteinuria, and multiple organ dysfunction. 31746004: Original investigative findings suggest that abnormal placentation triggers preeclampsia and leads to hypertension, proteinuria, endothelial dysfunction, and inflammation, which are characteristics of the disease. 32075602: We classified the patients based on the severity of the preeclampsia into three groups: pregnant induced hypertension (PIH), mild preeclampsia (MPE) and severe preeclampsia (SPE). 35555312: Th17 cells stimulated by a rat model of PE have been shown to cause HTN, FGR, and mt dysfunction. 35560619: Current studies have only investigated B cells in animal models of PE; yet, no studies have examined the effects of B cells from PE patients to cause hypertension during pregnancy. 35571013: Preeclampsia is a pregnancy-induced hypertensive disorder, the pathophysiology of which includes underlying maternal cardiovascular disease, deficient spiral artery remodeling during placenta development, and inflammatory immune responses at the maternal-fetal interface. 36027376: This work provides basic information needed to understand blood pressure regulation and volume expansion in normal pregnancy, and why it fails to occur in women with preeclampsia, resulting in hypertension and fetal growth restriction. 36193555: Pre-eclampsia (PE) is a major cause of hypertension in maternal and fetal. 37645383: These results show that placental CD4 + T cells play an important role in the pathophysiology of PE, by activating B cells secreting AT1-AA to cause hypertension during pregnancy. 3778278: Ocular fluorophotometry was performed in 24 patients with hypertension due to toxemia of pregnancy and in ten normal subjects. 37976060: Preeclampsia is a pregnancy-induced hypertensive disorder with generalized endothelial dysfunction. 38008458: A 37-year-old woman with chronic kidney disease stage (CKD) G4 with membranoproliferative glomerulonephritis was hospitalized for nephrotic syndrome and hypertension due to superimposed preeclampsia at 27 weeks into her third pregnancy. 38419047: BACKGROUND AND AIMS: Preeclampsia (PE) is a serious medical condition that usually causes high blood pressure and affects multiple organs. 38572182: Pheochromocytoma and paraganglioma (PPGL) are chromaffin cell tumors that produce, store, and secrete catecholamines, leading to HT and other adrenergic manifestations. Even though primary HT, obesity, and preeclampsia are the main causes of HT in this period, other less familiar conditions must be considered during the investigation. 38629095: Conclusion: These findings suggest that PE can induce hypertension in offspring, and (P)RR seems to play an important role through the canonical WNT pathway and that gender seems to influence this response. 6994768: Guanfacine in the treatment of hypertension due to pre-eclamptic toxaemia in thirty women. 9259891: Substantial variability was observed in the association between preeclampsia and preterm birth in relation to the subtypes defined by gestational age and pathway, with strong associations between hypertension and medically induced preterm births. 9855592: OBJECTIVE: Preeclampsia is a complication of pregnancy that causes maternal vasoconstriction and hypertension. 1192558: The impaired renal perfusion and abnormal elevation of plasma renin activity during salt restriction is analogous to clinical and experimental observations in hypertensive states associated with total renal underperfusion and supports a major role for the renal pressor system in the pathogenesis of coarctation hypertension. 2024278: Oxygen radicals are known to be produced by the cerebral vasculature during acute, pressor-induced hypertension and are also known to inactivate endothelium-derived relaxing factor. Superoxide dismutase decreases mortality, blood pressure, and cerebral blood flow responses induced by acute hypertension in rats. 2455198: Increased cerebral pressor activity can cause hypertension in some patients with the Guillain-Barre syndrome, where disinhibition of cerebral centres may result from an afferent baroreflex lesion. The use of drugs (including alcohol), or at times their withdrawal, results in hypertension through neurogenic mechanisms. 32582357: The present study aimed to compare the effects of angiotensin converting enzyme inhibitors (captopril) and angiotensin type 1 receptor blocker (losartan) on the hypertension induced by NPP injection in normal (sham-2NX) and bilaterally nephrectomized rats (2NX). The effects of two types of renin-angiotensin system inhibitors on the hypertension induced by new pressor protein associated with beta-factor XIIa in rats. 4315502: Renal-portal venous shunt for the correction of pressor-induced hypertension. 4319287: A study of the pressor activity in the blood of rats with experimentally induced hypertension. 5149756: [Correlation between the pressor and depressor humoral mechanisms in the pathogenesis of hypertensive disease]. 6409567: The role of pressor and depressor factors in the pathogenesis of hypertension must be comprehended in close association with the other, non-humoral mechanism of blood pressure regulation. 7016788: A deviation from the normal equilibrium among these components, with a persisting non-physiologic increase in pressor factor(s) or in the basal vascular tone and/or cardiovascular reactivity to pressor factors, leads to hypertension. 7024618: The irreversible changes of the renal juxtaglomerular apparatus and the depression of their renin synthesizing function occur with progressing hypertension, and the secondary pressor mechanisms and factors prevail in the pathogenesis of hypertension. 7453095: It focuses on the roles of various pressor factors as well as cardiovascular pressor responsiveness in the genesis of high blood pressure and in the antihypertensive mechanism of diuretic treatment. A deviation from the normal equilibrium among these components, with a persisting non-physiologic increase in pressor factor(s) or in the basal vascular tone and/or cardiovascular reactivity to pressor factors, leads to hypertension. 7662251: The pressor and subpressor models of angiotensin II-induced hypertension draw attention to the relative importance of renal and extrarenal mechanisms in the pathogenesis of hypertension. Administered dose is an important determinant of the type of hypertension produced by angiotensin II. 798489: According to this hypothesis, certain forms of experimental and human hypertension might not solely be the result of an excess in the activity of such renal pressor systems as the renin-angiotensin system and the sympathetic nervous system, but might also result from an absolute or relative deficiency of intra-renal vasodilator antihypertensive factors which might allow pressor systems to act unopposed to produce peripheral arteriolar vasoconstriction and sustained hypertension. 8576790: INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. 9797192: Hypertension induced by pressor infusion of angiotensin II increases angiotensin II type 1 messenger RNA levels both in aorta and in mesenteric resistance arteries. 12463910: We were able to obtain functional information about two proteins, Amyloid Precursor Protein and Prion Protein, that have been implicated in the etiology of Alzheimer's Disease and Creutzfeldt-Jakob Disease, respectively. 20698011: Prion protein in Alzheimer's pathogenesis: a hot and controversial issue. 20930299: The cellular form of the prion protein (PrPC) has been shown to inhibit the production of amyloid-beta which is critically involved in the pathogenesis of Alzheimer's disease (AD). 21968933: Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. 23171056: Alzheimer's disease, naturally occurring transmissible spongiform encephalopathies (TSEs) and experimental disorders caused by misfolded prion protein (PrP) generated in vitro all share an imbalance of protein synthesis, aggregation and clearance that leads to protein aggregation, prompting some to suggest that Alzheimer's disease is caused by a prion-like mechanism. 23856335: Evidence has been mounting for an involvement of the prion protein (PrP) in a molecular pathway assumed to play a critical role in the etiology of Alzheimer disease. 25869610: Our results show that Abeta activates microglia and regulates microglial protein expression in a manner similar to prions and, thus, provide new insight into the pathogenesis of AD. 25888324: Oligomeric Abeta has recently been shown to form complexes with the glycosylphosphatidylinositol (GPI)-anchored membrane protein, cellular prion protein (PrP(c)), and these complexes are believed to play an important role in the progression of AD pathogenesis. 28246183: A wealth of recent data argues that both beta-amyloid (Abeta) and tau proteins form prions that cause Alzheimer's disease, and alpha-synuclein forms prions that cause multiple system atrophy and Parkinson's disease. 29203673: Misfolding of tau proteins into prions and their propagation along neural circuits are thought to result in neurodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chronic traumatic encephalopathy, and other tauopathies. 29887525: The cellular prion protein (PrPC) can act as a cell-surface receptor for beta-amyloid (Abeta) peptide; however, a role for PrPC in the pathogenesis of Alzheimer's disease (AD) is contested. This study provides a second animal model linking PrPC expression with Abeta toxicity and supports a role for PrPC in AD pathogenesis. 31093882: Binding between Prion Protein and Abeta Oligomers Contributes to the Pathogenesis of Alzheimer's Disease. In addition, we proposed a potential mechanism to explain why infectious agents, such as viruses, conduce AD pathogenesis. 31526227: Furthermore, evidence suggests that traditional infectious agents, including certain viruses and bacteria, may trigger AD. However, amyloid beta (Abeta) or tau, which can act like infectious proteins, or prions, might induce Alzheimer's disease (AD). 32677995: These observations argue against the hypothesis that the propagation of Tau pathology in AD is caused by the prion-like templated aggregation of Tau protein, transmitted via cell-to-cell spreading of Tau. 36399277: Using cellular bioassays for prions in postmortem samples, we found that both Abeta and tau proteins misfold into prions leading to AD, which is either a sporadic or familial dementing disorder. Abeta and Tau Prions Causing Alzheimer's Disease. 38653354: miR-519a-3p, found to regulate cellular prion protein during Alzheimer's disease pathogenesis, as a biomarker of asymptomatic stages. 6381559: The similarities in the regional metabolic alterations between CJD and AD provide additional evidence for the possibility that AD may be caused by a slow infectious prion. 10608334: In contrast to adults, hypertension in children is usually secondary to an underlying disease process. 10699136: Severe systemic arterial hypertension in infants and children is usually secondary to an underlying disease process. 10950402: We conclude that the development of spontaneous and salt-induced hypertension is not associated with decreased activity of 11betaHSD. The role of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) in hypertension remains unknown even if it appears that the inappropriately decreased 11betaHSD activity might be involved in a process that leads to high blood pressure. The possible changes of 11betaHSD were therefore investigated in rats with spontaneous or salt-induced hypertension. 1117514: Divided function studies and renal vein renin determinations confirm the functional significance of this process in the etiology of hypertension. 1180979: Chronic hypertension induced by perirenal constrictive processes is known from experimental studies as well as from clinical experience. 12697744: gamma-MSH deficiency results in marked salt-sensitive hypertension that is rapidly improved with exogenous gamma-MSH through a central site of action. alpha-MSH infused at the same rate had no effect on MAP, indicating that the hypertension is a specific consequence of impaired POMC processing into gamma-MSH. 15715924: The processes of induction of hypertension, possible pathogenesis, characteristics, advantages, and limitations of these animal models are reviewed. Hypertension and related cardiovascular diseases are the leading causes of death in many countries. These models are classified as genetically-induced, environmentally-induced, pharmacologically-induced, and renal-induced hypertension according to the way of induction; the typical representatives of each of these major types of experimental hypertension are spontaneous hypertension, cold-induced hypertension, DOCA-salt-induced hypertension, and renal-induced hypertension, respectively. 15880243: PURPOSE: To evaluate the repair process in rats with experimentally induced arterial hypertension. 1630731: To understand better the ways in which these variables interact in the disease process, researchers have tried, with limited success, to produce experimental hypertension in animals by exposing them to stressful environmental paradigms. 16914965: Deciphering the relationships between these processes will enhance our understanding of the pathogenesis of hypertension. 17605504: BACKGROUND: Our understanding of the process leading to hypertension is allowing us to adopt principles of therapy that may be more beneficial for patients. 17940673: A possible mechanism of benzene-induced hypertension could be disturbance of the nitric oxide process, subsequently leading to hypertension. 20665399: Diverse processes may coexist in the pathogenesis of SAPH, and there is an overlap with mechanisms of pulmonary arterial hypertension (PAH). 21512515: Oxidative stress and endothelial dysfunction are consistently observed in hypertensive subjects, but emerging evidence suggests that they also have a causal role in the molecular processes leading to hypertension. 21689379: Underscoring the importance of proper vascular regulation, defects in these processes can lead to diseases such as hypertension, orthostatic hypotension, Raynaud's phenomenon, defective thermoregulation, hand-foot syndrome, migraine and congestive heart failure. 22205898: The loss of self-tolerance could initiate a process which ultimately results in APAH. 23012041: CONCLUSION: This study proves that all essential resources needed for hypertension care are available, but the results of process and outcome indicators show the need for the improvement of the referral system as well as good continuous constant health education programs to encourage the patients, their families and the community to observe more healthy lifestyles. 24407448: In mice, lack of corin prevents natriuretic peptide processing, causing salt-sensitive hypertension. 24431666: Although the etiology of preeclampsia (PE) is still unclear, recent studies suggest that its major phenotypes, high blood pressure and proteinuria, are due in part to the disturbed angiogenic process. 25573074: This process could contribute to the pathogenesis of hypertension. 25983299: The chronic inflammatory process is associated by many authors with the pathogenesis of coronary artery disease, endocarditis, atherosclerosis, hypertension, vasculitis, multiple sclerosis, sarcoidosis, and asthma. 26635606: Increased ROCK activity could play a pivotal role in processes leading to cardiovascular diseases such as hypertension, pulmonary hypertension, angina pectoris, vasospastic angina, heart failure, and stroke, and thus ROCK activity is a potential new biomarker for heart disease. 2691694: More basic mechanisms in the process leading to hypertension and CHD may have to be affected. 27160757: BACKGROUND: Due to the continuing increase of the elderly population in the western countries, the prevalence of the main chronic diseases (obesity, type 2 diabetes and related metabolic disorders, arterial hypertension, vascular damage due to atherosclerotic process, cancer, chronic obstructive pulmonary disease, neurodegenerative diseases, chronic kidney disease, immune-mediated diseases) is increasing. 28255250: The metabolic syndrome (MetS) is marked by abnormalities in central obesity, high blood pressure, high triglycerides, low high-density lipoprotein-cholesterol, and high fasting glucose and appears to be produced by underlying processes of inflammation, oxidative stress, and adipocyte dysfunction. 30721825: This was also associated with the occurrence of cardiovascular morbidity namely hypertension amongst the inhabitants of SIII may indicate the effect of chronic exposure to the air pollution due to e-waste processing activities, which needs to be studied further. 31302387: BACKGROUND: Small-for-gestational-age (SGA) birth bears an enhanced risk of developing hypertension, obesity, insulin resistance and mental health disorders in later life as a consequence of adaptive processes in utero. 32671677: Endothelial dysfunction is considered a primary process in the pathogenesis of hypertension and cardiovascular diseases and contributes significantly to the development and progression of the associated micro- and macrovascular complications. 3313692: Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. 35665253: Clinical studies indicate that catestatin may influence the processes leading to hypertension, affect the course of coronary artery diseases and heart failure. 37143964: Hypertension and diabetes mellitus are risk factors that make an FS poor prognosis during treatment because of the diabetes glycation process and hypertension-enhanced vascularization. 4041050: This approach has potential as an animal model of etiological processes in socially induced hypertension. 4739041: [Quantitative analyses of evoked potentials for neurophysiological characterization of defective learning processes in the pathogenesis of experimental arterial hypertension]. 6250736: Therefore, high pressure, by a negative feedback process, plays a great part in moderating the adrenergic neurotransmission responsible for the hypertension. 6553934: The diagnosis of the exact disease process responsible for hypertension in pregnancy in an individual patient is extremely difficult if based solely on clinical criteria. 7646313: To a certain degree, this process counteracts the parietal stress induced by high blood pressure. 8316786: For comparative study of vascular changes in hypertension involving SEM, cellular shrinkage due to processing should be included in the calculations in order to provide a reasonable estimate of the alterations. 8485836: Whereas the circulating endocrine RAS appears to be responsible for acute effects, the tissue RAS seems to participate in more chronic processes such as secondary structural changes and therefore may contribute to the pathogenesis of hypertension as well as other cardiovascular disorders such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. 10210631: We discuss these findings in terms of a theory of reference processing, the Informational Load Hypothesis, which views referential impairments in AD as the consequence of normal discourse processing in the context of a working memory impairment. 10349334: Although these data suggest that accumulation of A beta is an essential step in the pathogenesis of Alzheimer's disease, it still remains to be elucidated whether such process is causative for Alzheimer's disease. Recently another gene on chromosome 12 has been suggested to be involved in the development of late-onset Alzheimer's disease, and identification of the gene on chromosome 12 may bring a new insight into the pathogenesis of Alzheimer's disease. Amyloid precursor protein (APP), presenilin I (PS 1) and presenilin II (PS 2) genes have been identified as the causative genes for early-onset familial Alzheimer's disease. 10516307: Recent observations have begun to challenge this assumption by suggesting that earlier Abeta assemblies formed during the process of fibrillogenesis may also play a role in AD pathogenesis. 10616034: The fact that IL-6 is detectable in early stage diffuse plaques encourages the speculation that the acute-phase process is crucial to the pathogenesis of AD. 10818522: Our data suggest that ApoE modulates the outcome following cerebral ischemia via molecular events in common with AD pathogenesis. We propose that ischemic-reperfusion processes in brain are the fountain-head of a cycle of molecular and cellular events that have neurodegenerative consequences which finally lead to AD. 10854253: This suggests that an altered function of mutated PSs accounts for a fundamental process leading to AD. 10899439: While this suggests that oxidative stress is a proximal event in Alzheimer's disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-beta-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer's disease pathogenesis and novel therapeutic approaches. 11131295: Unregulated systemic immune processes are secondary but important as a driving-force role in AD pathogenesis. 11140685: Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). 11378240: It also suggests that synaptic loss observed in pathological conditions such as Alzheimer's disease, may be the result of the disease process and not a consequence of normal aging. 11755016: Chronic neuroinflammatory processes including glial activation may play a role in the pathogenesis of Alzheimer's disease (AD). 11771743: Oxidative stress is considered to be crucial in the pathogenesis of Alzheimer's disease-like neurodegeneration. An elevation of carbonyl compounds that are biomarkers of and leading to oxidative stress has been demonstrated in Down Syndrome (DS) and Alzheimer's Disease (AD) brains and seems to be the result of a multifactorial process. 11976212: The different categories of AD may be due to processes that augment to different degrees the innate cellular aging rate, that is, mitochondrial superoxide radical (SO) formation. 12212771: In particular, they modulate processes that govern the function and metabolism of proteins key to the pathogenesis of AD, including tau and amyloid precursor protein (APP). 12212799: Gamma-secretase processing of the amyloid-beta precursor protein (APP) releases the amyloid-beta peptide, which is widely held to be involved in the pathogenesis of Alzheimer's disease. 12392058: Because this process is a central event in the pathogenesis of AD, gamma-secretase is believed to be an excellent therapeutic target. 12435432: Fe65 modulates trafficking and processing of APP, including production of the beta-amyloid peptide that is believed to be central to the pathogenesis of Alzheimer's disease. 12436384: With the advent of further understanding of the neurodegenerative processes that cause AD, new treatments that may slow down the progression of the disease will be available. 12740808: The enigmatic proteases alpha-,beta-, and gamma-secretase are the three executioners of amyloid precursor protein processing, and disruption of their delicate balance is suspected to result in Alzheimer's disease. Despite the dramatic progress that has been made in understanding the disease, the exact cause of Alzheimer's disease is still unknown. 12751917: The evidence indicates that abnormal processing and extracellular deposition of the longer form of the beta-amyloid (Abeta) peptide (Abeta(1-42), a proteolytic derivative of the amyloid precursor protein [APP]) is implicated in the pathogenesis of Alzheimer's disease. This research strongly supports the notion that abnormal Abeta processing is essential to the pathogenesis of Alzheimer's disease and provides a crucial platform for the development and detailed testing of potential treatments in experimental models before each of these approaches can be proposed as a therapy for Alzheimer's disease. 12792666: Genetic and neuropathological studies suggest that processing of amyloid precursor protein (APP) to yield amyloid beta-protein (Abeta) plays an important role in the pathogenesis of Alzheimer's disease (AD). 1288358: The processing of the amyloid beta/A4 protein has been implicated in the pathogenesis of AD. 14501020: Calpains modulate processes that govern the function and metabolism of proteins key to the pathogenesis of Alzheimer's disease, including tau and amyloid precursor protein. 14506131: These studies demonstrate that APP processing, A beta metabolism and A beta deposition are regulated by genetic background and that analysis of these phenotypes in mice should provide new insights into the factors that regulate AD pathogenesis. 1467582: A fundamental process in the pathogenesis of Alzheimer's disease (AD) is the breakdown of the cytoskeleton. 14716023: Data suggesting that late onset AD risk factors play a role in Abeta turnover in the brain have shifted some of the research focus to the study of Abeta clearance and degradation and the impact of these processes on the etiology of Alzheimer's disease (AD). 14746246: Angiogenic brain damage and Alzheimer's disease caused by a progressing degenerative process are listed among the most frequent causes of dementia. 15342738: Alzheimer's disease (AD) may be caused by the abnormal processing of the amyloid precursor protein (APP) and the accumulation of beta-amyloid (Abeta). 15377701: CONCLUSIONS: Polymorphisms within IL-1A influence the degree of brain microglial cell activation, especially in bearers of APOE epsilon4 allele, reinforcing the importance of neuroinflammatory processes in the pathogenesis of AD, and supporting the rationale for treating the disease with inflammation modulating drugs. 15467394: Alzheimer's beta-secretase (BACE1) cleaves amyloid precursor protein to produce amyloid beta-peptide, which is a crucial initiation process of the pathogenesis of Alzheimer's disease. 15784960: Beta-amyloid (Abeta) peptides are derived from the endoproteolytic processing of amyloid precursor protein (APP) and play a key role in the pathogenesis of Alzheimer's disease (AD). 15949039: In some individuals this initially positive process becomes highly overregulated by genetic or/and epigenetic risk factors and after many years of accumulations lead eventually to AD. 16109164: These data suggest that infection can directly alter the processing of a transmembranal protein intimately linked to the aetiology of AD. 16128148: The vast number of physiological parameters involved in the poorly understood processes responsible for AD yields a large combination of parameters that can be manipulated and studied. 16251213: The reactivity of posterior cingulate and hippocampal structures to cholinergic challenge suggests a key role of the cholinergic system in the functional processes that lead to Alzheimer's disease. 16275806: It states that abnormal amyloid processing and accumulation is the primary causative factor of AD and other associated neuropathologic abnormalities are of secondary consequence. 16641106: APP also is cleaved intracytoplasmically at Asp-664 to generate a second cytotoxic peptide, APP-C31, but whether this C-terminal processing of APP plays a role in the pathogenesis of AD is unknown. 16766195: Overexpression of PCTAIRE 3 in cell culture suggests that the protein acts indirectly to stimulate phosphorylation at the pT231 and pS235 sites on tau, residues that are modified early in the process of AD pathogenesis. 16785601: Evidence in the literature suggests that gonadotropins may be involved in processes that contribute to the etiology/pathogenesis of AD such as inflammation, cholesterol homeostasis, and insulin status. 16869341: Recent understanding of this process has confirmed that interactions between AGEs and their receptor (RAGE) may play a role in the pathogenesis of diabetic complications and AD. 16884489: In this review, we summarize the arguments showing that calpains modulate processes that govern the function and metabolism of these two key proteins in the pathogenesis of Alzheimer's disease. 16892365: A central element in the pathophysiology of Alzheimer's disease (AD) is the formation of amyloid plaques, which result from abnormal processing of the amyloid precursor protein (APP). 16898674: In accord with this view, nonsteroidal anti-inflammatory drugs and antioxidants suppress early pathogenic processes leading to Alzheimer's disease, thus decreasing the risk of developing the disease. 17006763: Since these proteins are involved directly or indirectly in microtubule destabilization and hyperphosphorylation of tau, and also in APP processing we hypothesize that cell cycle disturbance may be important contributor in the pathogenesis of AD. Mild cognitive impairment (MCI) is regarded as a transition stage between the cognitive changes of normal aging and the more serious problems caused by Alzheimer's disease (AD). 17009917: Clinicians and researchers in the AD field face great challenges: the pathophysiological processes that cause AD are not well understood, definite diagnosis of AD requires autopsy, and therapeutic options are limited to treating the symptoms rather than the cause of the disease. 17047298: Numerous studies now indicate that protein synthesis and protein degradation are significantly altered in Alzheimer's disease (AD), with impairments in these two processes potentially contributing to AD pathogenesis. 17261781: Evidence from experimental and epidemiological studies suggests a role of sex hormones in the pathogenic process leading to neurodegenerative diseases, (i.e., Alzheimer's and Parkinson's disease). 17279615: Recent studies implicating Abeta oligomers and protofibrils in the neurotoxic process that ultimately leads to AD suggest that the Abeta aggregates induced by 4-HNE may be important in the pathogenesis of AD. Although it remains an open question as to whether oxidative stress is a causative factor or a consequence of AD, we show here that 4-HNE, putatively resulting from the peroxidation of lipids, covalently modifies Abeta, triggering its aggregation. 17400334: Processing of the amyloid precursor protein (APP) to produce amyloid-beta (Abeta) peptide is increasingly believed to be of central importance in AD pathogenesis. 17401045: This is in accordance with reports that lithium inhibits crucial processes in the pathogenesis of Alzheimer's disease. 17512513: OBJECTIVES: A neuroinflammatory process, triggered by amyloid-beta (Abeta)-peptide, is thought to play a central role in the neurodegenerative process leading to Alzheimer's disease (AD). 17623998: Both estimates of controlled and to a lesser extent automatic uses of memory were greater for the EC than the AD subjects, indicating that the stem completion impairment in AD may not be entirely attributable to a deficiency in controlled memory processes but also due to reduced automatic processing. 17644063: Processing of APP by BACE1 plays a crucial role in the pathogenesis of Alzheimer disease (AD). 18024114: Alzheimer's disease is a pathology putting even at the moment multiple questioning as for its etiopathogeny, which results credibly from several processes. 18081741: This process may play a significant role in the pathogenesis of AD and aging. 18299393: Presenilin 1 (PS1) plays a critical role in the gamma-secretase processing of the amyloid precursor protein to generate the beta-amyloid peptide, which accumulates in plaques in the pathogenesis of Alzheimer's disease (AD). 18410513: In this study, we evaluated the cognitive performance in rodent models of hypercholesterolemia in relation to neuroinflammatory changes and amyloid precursor protein (APP) processing, the two key parameters of Alzheimer's disease pathogenesis. 18487847: All these processes are involved in the pathogenesis of AD. 18577840: The key strategy for establishment of diagnostic and therapeutic approaches to AD is sensitive and specific detection of the incipient neuropathology characteristics of AD, combined with emerging treatments that counteract molecular processes in AD pathogenesis. 18650430: Specifically, molecular characterization of the secretases involved in Abeta production has facilitated cell biological investigations on APP processing and advanced efforts to model AD pathogenesis in animal models. 1890972: A number of neurological disorders including Alzheimer and Parkinson disease have been suggested to be caused by processes leading to lipid peroxidation. 19041409: In this review, we summarize the current understanding of the roles of lipoprotein receptors and cholesterol in APP trafficking and processing and their implication for AD pathogenesis and therapy. 19271231: Alterations in amyloid precursor protein (APP) processing and amyloid-beta (Abeta) accumulation, key molecules associated with Alzheimer;s disease pathogenesis, may therefore contribute to retinal damage. 19306098: Disruptions in Abeta processing have been hypothesised to be the major cause of AD (the amyloid cascade hypothesis). 19355848: CONCLUSIONS: The present animal imaging system would substantially facilitate establishment of a safe and effective therapeutic strategy targeting multiple key processes in the AD pathogenesis. 19357271: Understanding how APP processing is regulated under physiological conditions may provide new insights into AD pathogenesis. 19589380: The data demonstrate that VEGF may affect APP processing, at least in vitro, suggesting a role of VEGF in the pathogenesis of Alzheimer's disease. 19642202: In AD, the extracellular deposition of fibrillogenic amyloid-beta peptides (Abeta) occurs as a result of aberrant processing of the full-length Abeta precursor protein (APP). 19686046: By comparing to age-matched controls, we reasoned that such analysis could help in understanding potential mechanisms involved in upstream processes in AD pathogenesis. 20060898: In-vivo visualization of key molecular processes involved in Alzheimer's disease pathogenesis: Insights from neuroimaging research in humans and rodent models. 20061651: Our findings suggests that an imbalance in iron homeostasis is a precursor to the neurodegenerative processes leading to AD and that iron imbalance is not necessarily unique to affected regions. 20122289: This review aims to highlight the importance of the immune processes involved in AD pathogenesis based on the outcomes of the two major inflammation-relevant treatment strategies against AD developed and tested to date in animal studies and human clinical trials - the use of anti-inflammatory drugs and immunisation against Abeta. 20226030: Depression can be a risk factor for the development of AD or it can be developed secondary to the neurodegenerative process. 20463393: Mechanistically, recent reports suggest that mitochondrial fission/fusion and mitophagy are altered in AD and in in vitro models of disease, and since both processes are reported to be protective, this review will discuss the role of mitochondrial fission/fusion and mitophagy in the pathogenesis of AD. 20580938: Experimental data show that cholesterol can modulate central processes in the pathogenesis of Alzheimer's disease (AD). 20734314: The structural and mechanistic observations based on these simulations agree with the recent NMR experiments and provide the driving force and structural origin for the Abeta42 aggregation process to cause AD. 20948726: Because AD historically has been defined by neuropathologic criteria, treatment strategies have been aimed at diminishing the pathologic end result of the disease process, namely neurodegenerative changes associated with extracellular amyloid-beta-containing plaques, as well as intracellular neurofibrillary tangles of the hyper-phosphorylated microtubule protein, tau. 21085570: SIGNIFICANCE: Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. 21145918: These observations support the suggestion of a key role of the cholinergic system in the functional processes that lead to AD. 21210060: In this review, we discuss the role of metals in neurodegenerative diseases with emphasis on the utility of Caenorhabditis elegans (C. elegans) genetic models in deciphering mechanisms associated with the etiology of PD and AD. Many neurodegenerative diseases including Parkinson's disease (PD) and Alzheimer's disease (AD) are the result of neurodegenerative processes. 21257235: A recent publication suggested that hypocretin (Hcrt, orexin) may mediate the neuropathological process leading to Alzheimer's disease (AD) and that antagonism of hypocretin receptors decreases this process. 2129870: Alteration in PUFA desaturation/elongation processes and resultant membrane abnormalities may play a key role in the pathogenesis of Alzheimer's disease. 21303349: Despite the crucial role of redox active metals like copper and iron in central biological reactions, their elevated levels are involved in the pathogenesis of Alzheimer's Disease (AD). Iron, copper, and zinc are some of the metals, which intensify this process and contribute for the pathogenesis of AD. 21305033: BACKGROUND AND PURPOSE: Cognitive impairment resulting from cerebrovascular insufficiency has been termed vascular cognitive impairment, and is generally accepted to be distinct from Alzheimer's disease resulting from a neurodegenerative process. 21321391: Shift of AbetaPP processing in favor of the amyloidogenic pathway is a key event in the pathogenesis of Alzheimer's disease (AD). 21567187: Inflammation including microglial activation may contribute in AD pathogenesis, and biomarkers for this process may thus be of value to study AD pathogenesis and might facilitate development of therapies targeting these cells. 21680755: While the general notion that vascular and metabolic dysfunctions contribute to the etiology of AD is becoming accepted, recent research suggests novel mechanisms by which these/such processes could possibly contribute to AD pathogenesis. 21693162: Beta-amyloid (Abeta) is a major pathogenic peptide for Alzheimer's disease (AD) and is generated by the processing of amyloid precursor protein (APP). 21829458: Abeta peptides, generated by processing of the Amyloid Precursor Protein (APP), are thought to play a central role in the pathogenesis of AD. 21876254: Although it is still debatable whether tau aggregation is harmful or protective for the cell, detailed analysis of molecular mechanisms underlying this process seems to be of great importance for understanding AD pathogenesis. 21891862: Amyloid-beta (Abeta) aggregation is a recognized key process in the pathogenesis of Alzheimer's disease (AD). 21942868: In addition, we showed that TMS has also been used to assess neuroplasticity changes in AD supporting the notion that cortical excitability is changed in AD due to the neurodegenerative process. 21960299: While physiological function(s) of APP still remain a matter of debate, consensus exists that the proteolytic processing of this protein represents a critical event in the life of neurons and that abnormalities in this process are instrumental in Alzheimer's disease (AD) pathogenesis. Understanding neuron-specific mechanisms of APP processing would help illuminating the physiological roles of APP-derived proteolytic fragments and provide novel insights on AD pathogenesis. 2203106: This result suggests that the sprouting process may involve a reactivation of certain developmental mechanisms and that this may possibly contribute to the etiology of Alzheimer's disease. 22037310: This is illustrated by the exchange reaction between amyloid-beta (Abeta) monomers and polydisperse, NMR-invisible ('dark') protofibrils, a process of significant interest because the accumulation of toxic, aggregated forms of Abeta, from small oligomers to very large assemblies, has been implicated in the aetiology of Alzheimer's disease. 22045482: Chronic stress, associated with altered memory and other neurological processes, is thought to influence the pathogenesis of AD. 22144675: APP processing and amyloid-beta production play a central role in Alzheimer disease pathogenesis. 22170863: APP processing is linked to Alzheimer disease (AD) pathogenesis, which is consistent with a common mechanism involving toxic APP metabolites in both dementias. Processing of beta-CTF by gamma-secretase releases amyloid-beta (Abeta), which is assumed to cause AD. 22184106: The prolyl isomerase Pin1 and glycogen synthase kinase-3beta (GSK3beta) have been shown to have the opposite effects on APP processing and Tau hyperphosphorylation, relevant to the pathogenesis of AD. 22214391: The initial neurodegenerative process that causes AD is unknown. 22272623: Whether or not inflammation represents a possible cause of AD or occurs as a consequence of the disease process, or, alternatively, whether the inflammatory response might be beneficial to slow the disease progression remains to be elucidated. 22356903: Our investigation demonstrated the presence of loci of susceptibility for AD in the WD ATP7B gene, supporting a role of copper dysfunction in contributing or accelerating neurodegenerative processes leading to AD. 22450454: Four articles in the journal Alzheimer's and Dementia in 2011 describe new criteria for Alzheimer's disease (AD) dementia and mild cognitive impairment (MCI) due to the AD pathophysiological process (MCI due to AD), as well as the underlying rationale for them. 22454637: Inflammation is a complex process that has a key role to play in the pathogenesis of Alzheimer's disease. 22479317: CONCLUSIONS: Gradual saturation of gamma-secretase with its substrate can be the pathogenic process in different alleged causes of AD. Modulation of gamma-secretase activity by multiple enzyme-substrate interactions: implications in pathogenesis of Alzheimer's disease. Membrane-imbedded Abeta-bundles generated by gamma-secretase could be neurotoxic and thus crucial for our understanding of the amyloid hypothesis and AD pathogenesis. 22558227: Although the pathogenic nature of this mutation needs further confirmation, our findings suggest that the Abeta N-terminal region potentially modulates APP processing and Abeta aggregation, and further provides a genetic indication of the importance of Zn(2+) and Cu(2+) in the etiology of AD. 22594617: Interactions between miR-103 and miR-107 to genes were revealed playing a role in processes leading to AD. 22819647: Coordination of redox active metal ions such as copper or iron to the amyloid-beta (Abeta) peptide has been linked to deleterious processes encountered in the etiology of Alzheimer disease (AD), such as Abeta aggregation and reactive oxygen species (ROS) production. 22867901: Alzheimer's disease is the most common progressive neurodegenerative disorder characterized by the abnormal deposition of amyloid plaques, likely as a consequence of an incorrect processing of the amyloid-beta precursor protein (AbetaPP). 22899726: Alzheimer's disease (AD) could result from a multifactorial process involving both genetic predisposition and exposure to environmental factors like pesticides. 23020178: Processing of Abeta-precursor protein (APP) plays an important role in Alzheimer's disease (AD) pathogenesis. 23114667: CONCLUSIONS: These new criteria are immediately helpful to the practicing clinician, providing more accurate and specific guidelines for the diagnosis of AD dementia and MCI due to AD. REVIEW SUMMARY: Four articles in the journal Alzheimer's & Dementia in 2011 describe new criteria for AD dementia and mild cognitive impairment (MCI) due to the AD pathophysiological process (MCI due to AD) and the underlying rationale for them. 23131555: During the process of fibrillation, the Abeta42 takes the form of protofibrils with strong neurotoxicity, and is thus believed to play a crucial role in the pathogenesis of AD. 23142975: Cleavage of the amyloid precursor protein by enzymes commonly referred to as beta- and gamma-secretase constitute an important process in the pathogenesis of Alzheimer's disease (AD). 23166730: These processes are implicated in the pathogenesis of Alzheimer's disease (AD). 23365075: Inflammatory changes, typified by activated microglia, particularly adjacent to Abeta plaques, are also a characteristic of the disease, but it is unclear whether these contribute to the pathogenesis of AD or are a consequence of the progressive neurodegenerative processes. 23372648: Since synaptic alteration is the best pathologic correlate of cognitive dysfunction in AD, the spatial association of M/LMW Abeta peptide accumulation with pathology of MAP2 within neuronal processes and synaptic compartments early in the disease process reinforces the importance of intraneuronal Abeta accumulation in AD pathogenesis. 23623603: Amyloid beta (Abeta) plays a major role in Alzheimer's disease (AD), and neuroinflammatory processes mediated by Abeta plaque-induced microglial cells and astrocytes contribute to AD pathogenesis. 23809366: Scientists are investigating other molecular and cellular pathways and processes that contribute to AD pathogenesis. 23827971: We will shortly introduce the function of Beclin 1 interactome in autophagy and phagocytosis, review the recent evidence indicating that Beclin 1 regulates autophagy and APP processing in AD, and finally examine the potential mechanisms through which Beclin 1 dysfunction could be involved in the pathogenesis of AD. 23831375: Alzheimer's disease and prion diseases are neuropathological disorders that are caused by abnormal processing and aggregation of amyloid and prion proteins. 2386197: The focus of research on the neurofibrillary pathology (NFP) of Alzheimer disease has been not only to determine the component forming the paired helical filaments but also to determine whether they result from abnormal processes affecting a single protein. 24033439: AIMS: Phosphorylation, conformational changes and cleavage of tau protein have been widely suggested to contribute to abnormal tau processing in the pathogenesis of Alzheimer's disease, as well as in other tauopathies. 24205136: Soluble oligomeric amyloid beta peptide (Abeta) generated from processing of the amyloid precursor protein (APP) plays a central role in the pathogenesis of Alzheimer's Disease (AD) and through actions at glutamatergic synapses affects excitability and plasticity. 24279329: These processes may be important in AD pathogenesis, as proper intracellular sorting, processing and export of APP are affected by how it is glycosylated. 24333192: Converging evidence indicates that processes occurring in and around neuronal dendrites are central to the pathogenesis of Alzheimer's disease. 24463342: Brain network dysfunction in Alzheimer's disease (AD) involves many proteins (enzymes), processes and pathways, which overlap and influence one another in AD pathogenesis. 24469452: Taken together, these results suggest that Fbxo2 regulates APP levels and processing in the brain and may play a role in modulating AD pathogenesis. 24476230: Recent research has thus focused on investigating the molecular and cellular pathways and processes involved in AD pathogenesis to support the development of effective disease-modifying agents. 24478167: Many neurodegenerative diseases, like Parkinson's, Alzheimer's, or Huntington's disease, occur as a result of amyloid protein fibril formation and cell death induced by this process. 24506061: TMS has been used to assess neuroplastic changes in Alzheimer's disease (AD), corroborating findings that cortical physiology is altered in AD due to the underlying neurodegenerative process. 24516000: The amyloid precursor protein (APP) and its processing are widely believed to be central for the etiology of Alzheimer's disease (AD) and appear essential for neuronal development and cell homeostasis in mammals. 24524150: One feasible approach to improve the diagnostic and prognostic performance of AD biomarkers is to measure upstream events of amyloid precursor protein (APP) processing, which are at the core of the initial phase of AD pathogenesis. 24559299: Such interactions between Abeta and ferrihydrite shed light upon the processes of AD pathogenesis, while providing potential targets for future therapies. 24578544: A better knowledge of long-term trajectories of cognitive decline is a central feature of the study of the process leading to Alzheimer's dementia. 24735980: The impairment of the PI3K/Akt/mTOR axis in DS population might represent a key-contributing factor to the neurodegenerative process that culminates in Alzheimer-like dementia. 25045220: Alzheimer's disease (AD) is the most common form of dementia caused by neurodegenerative process and is tightly related to amyloid beta (Abeta) and neurofibrillary tangles. 25053581: Therefore, this study indicates a regulatory role of D678H in APP sorting and processing, and provides genetic evidence for the importance of APP sorting in AD pathogenesis. 25118934: All these findings suggest that APP672-699 region is critical for human wild-type APP processing and may provide new clues for the pathogenesis of sporadic AD. 25281744: Alzheimer disease (AD) is a progressive neurodegenerative disease leading to memory loss. Abeta is generated by the proteolytic processing of the amyloid precursor protein (APP), and alterations to this processing can result in Alzheimer disease. 25316600: Amyloid precursor protein processing and the subsequent generation of amyloid beta (Abeta) are central to the pathogenesis of Alzheimer's disease, as soluble, oligomeric Abeta is thought to be the toxic species driving disease progression. 25352592: On the other hand, gamma-secretase-mediated processing of amyloid precursor protein leads to the production of amyloid beta (Abeta) peptides that play an important role in the pathogenesis of Alzheimer disease. 25365422: The aggregation of amyloid-beta (Abeta) peptide and its deposition in parts of the brain form the central processes in the etiology of Alzheimer disease (AD). 25591151: Although aggregates can be functional under certain circumstances, this process often leads to the disruption of the cellular protein homeostasis (proteostasis), eventually leading to devastating diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), or transmissible spongiform encephalopathies (TSEs). 25636033: Tumor suppressor molecules play a pivotal role in regulating DNA repair, cell proliferation, and cell death, which are also important processes in the pathogenesis of Alzheimer's disease. 25727637: Such process might be important for the pathogenesis of AD, and inhibition of LPC generation could be a therapeutic target for the disease. 25766617: Disturbances in the sleep-wake cycle and circadian rhythms are common symptoms of Alzheimer Disease (AD), and they have generally been considered as late consequences of the neurodegenerative processes. 26227906: Cyclin-dependent kinase 5 (Cdk5), a unique member of the cyclin-dependent kinases (Cdks), is reported to intimately associate with the process of the pathogenesis of AD. 26242258: While the process leading to the development of AD is complex and multifactorial, and the etiology of AD is not completely known, it is nowadays clear that AD is a multifaceted illness requiring the combination of synergetic treatment strategies. 26270969: A major difference in the revised diagnostic criteria for Alzheimer's disease (AD) is the incorporation of biomarkers to support a clinical diagnosis and allow the identification of preclinical AD due to AD neuropathological processes. 26484900: CONCLUSION: Anxiety and irritability are associated with greater amyloid deposition in the neurodegenerative process leading to AD. 26519433: Most processes associated with AD pathogenesis, such as inflammation, synaptic dysfunction, and hyper-phosphorylation of tau are dependent on protein kinase activity. 26583091: Our study suggests that Abeta25-35 induces autophagy and the PI3K/AKT/mTOR/p70S6K pathway is involved in the process, which improves our understanding of the pathogenesis of AD and provides an additional model for AD research. 26629788: The conversion of soluble monomers to amyloid Abeta fibrils is a complicated process and involves several transient oligomeric species, which are widely believed to be highly toxic and play a crucial role in the etiology of AD. 26642316: To investigate whether lipid peroxidation is only a consequence or might also influence the processes leading to AD, we analyzed 7 different oxidized lipid species including 5 oxidized DHA derivatives and the lipid peroxidation products of omega-3 and omega-6 PUFAs, HNE and 4-hydroxy-hexenal, in human neuroblastoma cells and mouse mixed cortical neurons. Previously it has been demonstrated that polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid (DHA), are associated with a reduced risk of AD caused by decreased Abeta production. 26792010: The neuropathological processes eventually leading to Alzheimer's disease (AD) are thought to start decades before the appearance of clinical symptoms and the clinical diagnosis of AD dementia. 26878581: In this review, we analyze issues concerning processes of generation of two proteins (beta-amyloid peptide and Tau-protein) in the cell, which are believed to play the key role in AD genesis. 26993139: The cellular and molecular mechanisms that govern presynaptic dystrophic neurite formation are unclear, and elucidating these processes may lead to novel AD therapeutic strategies. 27012953: APP is subjected to several PTMs (proteolytic processing, glycosylation, sulfation, and phosphorylation) during its course of processing, resulting in Abeta deposition, leading to AD. 27079722: This is a reasonable assumption because amyloid-beta peptide (Abeta) accumulation and tau hyperphosphorylation are the defining histological features in AD, and because AbetaPP and tau mutations can cause AD in humans or AD-like features in animal models. Alzheimer's disease (AD) has long been viewed as a pathology that must be caused either by aberrant amyloid-beta protein precursor (AbetaPP) processing, dysfunctional tau protein processing, or a combination of these two factors. 27183464: INTRODUCTION: Neuroinflammatory processes play an important role in the pathogenesis of Alzheimer's disease (AD). 27196068: In this study, we examined the effects of ABCG1 and ABCG4 on amyloid precursor protein (APP) processing, the product of which, amyloid beta (Abeta), is involved in the pathogenesis of Alzheimer's disease. 27454922: In the absence of Abeta, hippocampal tau deposition may be insufficient for the neurodegenerative process that leads to AD. 27524794: Characteristic features of Alzheimer's disease are memory loss, plaques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofibrillary tangles and dystrophic neurites containing hyperphosphorylated tau. 27671345: BACKGROUND: It is widely accepted that neuroinflammatory processes play an important role in the pathogenesis of Alzheimer's disease (AD) and high levels of cytokines and chemokines are detected around Abeta plaques. 27713140: Although the mechanisms causing the neurodegenerative process are largely unknown, increasing evidence highlights a critical role of immunity in the pathogenesis of Alzheimer's disease. 27723573: GTM-1 is a drug that reverses Alzheimer's Disease (AD) development specifically induced by thapsgargin (TG) and endoplasmic reticulum (ER) has been reported to be a pilot process that leads to AD formation. 27856911: Our work provides insights into postsynaptic processes in AD pathogenesis and challenges a purely pathogenic role of tau phosphorylation in neuronal toxicity. 2813376: The present data extend earlier findings of abnormal processing of neurofilaments and tau protein in Alzheimer disease and, together with reported abnormal processing of cerebrovascular amyloid beta-protein, suggest that inhibition of the processing of multiple proteins is basic to the pathogenesis of Alzheimer disease, whereas formation of plaques and tangles could be merely the most striking histologic result. 28157316: In conclusion, these data suggest dysregulation of the proteins and processes identified as early events in pathogenesis of AD following Abeta accumulation. 28209190: BACKGROUND: Disturbed amyloid precursor protein (APP) processing is considered to be central to the pathogenesis of Alzheimer's disease (AD). 28569173: Together, these results indicate that an ApoE2 or ApoE3 mediated positive regulation of BDNF may be protective while ApoE4 related defects in BDNF processing could lead to AD pathophysiology. 28612181: This finding identifies a point mutation in LRP1 which slows LRP1-CT-mediated APP endocytosis and amyloidogenic processing, while enhancing APP alpha-secretase cleavage, thus demonstrating a potential novel target for slowing AD pathogenesis. 28626014: The results demonstrate that APP673 regulates APP processing and the BACE1 cleavage site selection is critical for amyloidogenesis in AD pathogenesis, and implicate a pharmaceutical potential for targeting the APP673 site for AD drug development.SIGNIFICANCE STATEMENT beta-site APP cleaving enzyme 1 (BACE1) is essential for amyloid beta protein production. The results demonstrate that APP673 regulates APP processing, and the BACE1 cleavage site selection is critical for amyloidogenesis in AD pathogenesis, and implicate a pharmaceutical potential for targeting the APP673 site for AD drug development. 28759721: The amyloid aggregation process of amyloid beta1-42 peptide is responsible for Alzheimer's disease, affecting millions of elderly people worldwide. 28812474: A number of studies demonstrated compelling evidence of the importance of oxidative processes in AD pathogenesis. 28825683: Given the importance of the GABAergic system in neuronal function and homeostasis, in the maintenance of the excitatory/inhibitory balance, and in the processes of learning and memory, such changes in GABAergic function could be an important factor in both early and later stages of AD pathogenesis. 28892789: Though the causes of Alzheimer's disease (AD) are yet to be understood, much evidence has suggested that excessive amyloid-beta (Abeta) accumulation due to abnormal amyloid-beta precursor protein (APP) processing and Abeta metabolism are crucial processes towards AD pathogenesis. 28965829: Reduced brain insulin signaling: A seminal process in Alzheimer's disease pathogenesis. 29079430: Insulin dysfunction is known as an essential process in the pathogenesis of sporadic Alzheimer's disease (AD). 29097202: However, abnormal processing of APP leads to excessive production of beta-amyloid (Abeta) in the central nervous system (CNS), an event which is regarded as a primary cause of Alzheimer's disease (AD). 29124681: However, their single actions cannot explain the extent of brain damage observed in this disorder, and the characterization of co-adjuvant involved in the early toxic processes evoked in AD is essential. 29223769: The processes involved in the pathogenesis of AD have been shown to overlap with those found in cognitive decline in patients with Obstructive Sleep Apnoea (OSA). 29277576: Amyloid precursor protein (APP) processing is central in Alzheimer's disease (AD) pathogenesis. 29407908: Dysfunctional accumulation of amyloid-beta (Abeta) protein stimulated by Cu2+ is considered as a key process in the pathogenesis of Alzheimer's disease (AD). 29410161: Minor species of amyloid beta-peptide (Abeta), such as Abeta-(1-43) and pyroglutaminated Abeta-(3-42) (Abeta-(3pE-42)), have been suggested to be involved in the initiation of the Abeta aggregation process, which is closely associated with the etiology of Alzheimer's disease. 29695619: The endoplasmic reticulum (ER) stress response is regarded as an important process in the aetiology of Alzheimer's disease (AD). 30149452: These data suggest that A?-associated clinical progression is consistent with clinical-pathological models of AD, whereas progression in the absence of elevated A? deposition may be the result of neuropathological processes other than AD that accumulate with age. 30167602: Toxic aggregation of monomeric amyloid beta (Abeta) into oligomers followed by the formation of fibrils is a causative process in the pathogenesis of Alzheimer's disease. 30200516: Considering the involvement of (mis)folding processes in AD aetiology, targeting molecular chaperones represents a promising therapeutic perspective. 30407837: The aggregation of amyloid beta-proteins (Abeta) has been recognized as a key process in the pathogenesis of Alzheimer's disease (AD), so inhibiting Abeta aggregation is an important strategy to prevent the onset and treatment of AD. 30574086: There is general agreement that the neuropathological processes leading to Alzheimer's disease (AD) begin decades before the clinical onset. 30590039: Abnormalities of the endolysosomal and autophagy systems are found in Alzheimer's disease, but it is not clear whether defects in these systems are a cause or consequence of degenerative processes in the disease. 30662636: These results suggested that SQYZ has the ability to improve the cognitive impairment and ameliorate the neural pathological changes in AD, and the therapeutic mechanism may be related to the modulation of multiple processes related to AD pathogenesis, especially anti-neuroinflammation, promotion of stress recovery and improvement of energy metabolism. 30790387: BACKGROUND: In the past few decades, it has been demonstrated with animal models and clinical studies that a chronic inflammatory process significantly contributes to Alzheimer's disease (AD) pathogenesis. 30795987: Molecular studies in rodent models suggest a direct contribution of astrocytes to neuroinflammatory and neurodegenerative processes causing Alzheimer's disease; however, these models might insufficiently mimic the human disease, because rodent astrocytes differ considerably in morphology, functionality, and gene expression. 30949921: PURPOSE OF REVIEW: Nutrition is known to modulate the immune system and may alter neuroinflammatory processes implicated in the pathogenesis of Alzheimer's disease (AD) and progression of neurodegeneration. 31058201: Alzheimer's disease (AD) is a lifelong progressive neurodegenerativa disease related with accumulation of amyloid beta peptide (Abeta) produced by processing of amyloid precursor protein (APP) in the brain. 31086058: These compounds accompany thermal processing of protein-containing foods and are known to impact on ageing, pathogenesis of diabetes mellitus and Alzheimer's disease in mammals. 31465249: In late 2016, we solicited a series of reviews covering the variety of processes that appeared to be involved in the pathogenesis of neurodegenerative disorders, particularly Alzheimer's disease (AD). 31477183: BACKGROUND: Alzheimer's disease results from a neurodegenerative process that starts well before the diagnosis can be made. 31507373: Alzheimer's disease (AD) is the most common type of dementia which characterized by a progressive loss of memory and cognitive function due to degeneration of synapses and axons. Till now, it is far from clear what role autophagy plays in AD, a causative role, a protective role, or just a consequence of the disease process itself. 31583531: In this review, we discuss the current molecular understanding of how alterations in the AS process contribute to AD pathogenesis. 31600762: Poor Diet, Stress, and Inactivity Converge to Form a \Perfect Storm\ That Drives Alzheimer's Disease Pathogenesis. It is thus likely that lifestyle and environmental factors contribute to neurodegenerative processes implicated in the pathogenesis of AD. 31704512: There are several processes which can cause AD, including mitochondrial dysfunction-mediated oxidative stress (OS), intracellular buildup of hyper-phosphorylated tau as neurofibrillary tangles (NFTs) and excessive buildup of extracellular amyloid beta (Abeta) plaques, and/or genetic as well as the environmental factors. Alzheimer's disease (AD) is a progressive, chronic and severe neurodegenerative disorder linked with cognitive and memory impairment that eventually lead to death. 31808139: Chronic cerebral hypoperfusion (CCH) is a major contributor to cognitive decline and degenerative processes leading to Alzheimer's disease, vascular dementia, and aging. 31911114: We propose that CNS APOE is involved in processes in the normal brains that in later years apply specifically to processes of AD pathogenesis. 32062666: Vascular processes even proceed AD neuropathology, implicating a causal role in the etiology of AD. 32365768: We provide a comprehensive overview of processes associated with AD pathogenesis and biomarkers, current knowledge on AD-related biomarkers derived from on human and animal brains and body fluids, comparisons of biomarkers obtained in human AD and frequently used animal AD models, and emerging body-fluid-based biomarkers. 32415525: MiR-539-5p Decreases amyloid beta-protein production, hyperphosphorylation of Tau and Memory Impairment by Regulating PI3K/Akt/GSK-3beta Pathways in APP/PS1 Double Transgenic Mice.The production of amyloid beta (Abeta) and tau hyperphosphorylation have been identified as key processes in Alzheimer's disease (AD) pathogenesis. 32418657: The convergence of pathogenic mutations on one functional pathway, the amyloidogenic cleavage of APP, strongly supports the significance of this process in AD pathogenesis. 32468556: Detecting Common Pathways and Key Molecules of Neurodegenerative Diseases from the Topology of Molecular Networks.MotivationNeurodegenerative diseases (NDs), including amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, and Huntington's disease, occur as a result of neurodegenerative processes. 32548880: Multitargeted directed ligands (MTDLs) have been considered to be a feasible way to treat AD due to the multiple neuropathological processes in AD. 32664217: Individuals residing close to busy roads are at higher risk of developing AD, and nanomaterials that are specifically generated by traffic-related processes have been detected in human brains. 33325586: The imbalance of amyloid-beta (Abeta) production and clearance causes aggregation of Abeta 1-42 monomers to form fibrils and amyloid plaques, which is an indispensable process in the pathogenesis of Alzheimer's disease (AD), and eventually leads to pathological changes and cognitive impairment. 33543132: These findings provide support for a causal relationship between two crucial processes in Alzheimer's disease pathogenesis and suggest that targeting inflammation, particularly tumour necrosis factor, may have beneficial downstream effects on ameliorating aberrant protein aggregation and accumulation. 33887256: We monitor early stages of beta-amyloid (Abeta 1-40 ) aggregation, one of key processes leading to Alzheimer's disease (AD), in the presence of high glucose concentrations by measuring Abeta 1- 40 intrinsic fluorescence. 34118718: beta-Amyloid (Abeta) triggered proteopathic and immunopathic processes are a postulated cause of Alzheimer's disease (AD). 34135909: Emerging evidence suggests that both central and peripheral immunological processes play an important role in the pathogenesis of Alzheimer's disease (AD), but regulatory mechanisms remain unknown. 34440878: Dysfunctions of both glucose metabolism and mitochondrial dynamics have been recognized as the main upstream events of the degenerative processes leading to AD. 34563212: BACKGROUND: Increasing evidence for a direct contribution of astrocytes to neuroinflammatory and neurodegenerative processes causing Alzheimer's disease comes from molecular and functional studies in rodent models. 35109055: BACKGROUND: There is a growing appreciation that systemic factors, such as chronic inflammation, metabolic disorders, vascular dysfunction and gut microbiota dysbiosis, are highly connected and traverse a complex route across multiple pathophysiological processes that play crucial roles in Alzheimer's disease (AD) pathogenesis. 35749963: Due to the central role of the amyloid aggregation process in the early phase of AD pathogenesis, we aimed at developing a lipidomic approach to evaluate the amyloid toxic effects on differentiated human neuroblastoma derived SH-SY5Y cells. 35780617: The review aims to provide a comprehensive understanding of the neuroinflammatory processes causing AD, giving a brief overview of the disease interventions. 35805958: Role of Impaired Mitochondrial Dynamics Processes in the Pathogenesis of Alzheimer's Disease. This review highlights aspects of altered mitochondrial dynamics in AD that may contribute to the etiology of this debilitating condition. 35821178: Mounting evidence indicates that intensified neuroinflammatory processes play a pivotal role in the pathogenesis of AD. 36090249: This review attempts to elucidate the process of Regulated cell death, how it gets unregulated in response to different intra and extracellular stressors, various forms of unregulated cell death, their interplay and their role in pathogenesis of Alzheimer's Disease in both human and experimental models of AD. 36464806: DISCUSSION: The identification of these novel gene-trait associations offers new perspectives into the role of rare coding variation in the distinct pathophysiological processes culminating in AD, which may lead to identification of novel therapeutic and diagnostic targets. 36551781: The processes that cause AD are still under investigation and there are no available therapies to halt it. 36702317: Liquid-liquid phase separation of protein tau: An emerging process in Alzheimer's disease pathogenesis. 37027506: This led to the alternative hypothesis that in AD, part of WMH may be secondary to AD-related processes. 37258519: Neuroinflammation is believed to be a key process in Alzheimer's disease (AD) pathogenesis. 37382195: The gene ontology (GO) analysis manifests that the included processes are close to the pathogenesis of AD. 37638691: Tau-dependent cell cycle re-entry and NiMA inhibition occur in cultured neurons within a few hours of exposure to AbetaOs, and thus may represent seminal processes in AD pathogenesis. 37759477: The results revealed that oxidative phosphorylation and mitochondrial-related pathways are significantly down-regulated in both tissues of Tg2576 mice, supporting the role of these processes in the pathogenesis of AD. 38479477: Besides this, agmatine has been shown to modulate amyloid beta (Abeta) production, aggregation, and clearance, key processes implicated in AD pathogenesis. 7745947: BACKGROUND: Dysregulation in the processing of the Alzheimer precursor protein (APP) is thought to be central to the deposition of the beta-A4 peptide and to the pathogenesis of Alzheimer's disease. 7838304: APP processing, A beta-amyloidogenesis, and the pathogenesis of Alzheimer's disease. 8122883: The persistence of abnormalities in KGDHC and particularly in its E2k component in FAD fibroblasts indicates that abnormalities of this autosomally coded nuclear component are an intrinsic part of the AD process, and the possible role of this abnormality in the pathogenesis of AD is discussed. 8157623: Based on these observations, we postulate that the accumulation of insoluble A beta N-42 in Alzheimer Disease is due to the anomalous processing of the C-terminal region. 8250938: These results implicate PLA2 in regulating APP processing and secretion, which may have important implications for understanding the pathogenesis of Alzheimer's Disease. 8326828: These data support and extend the hypothesis that complement mediated processes are related to beta-amyloid deposition and may be involved in the pathogenesis of AD. 8427604: Elucidation of the mechanisms regulating the expression of the human APP gene might therefore be an important step forward in understanding the processes leading to Alzheimer's disease. 8687017: There is mounting evidence that at least some of the neurotoxicity associated with AD is due to fragments from APP. Excessive amyloidogenic pathway of APP processing may be the final common pathway involved in the pathogenesis of AD. 8841658: Abnormal processing of beta-amyloid precursor protein (APP) and precipitation of amyloidogenic beta A4 peptide have been implicated in the pathogenesis of Alzheimer's disease (AD). 8875116: The data presented here support the hypothesis that unpaired proteolytic processes could be involved in the pathogenesis of Alzheimer's disease and suggest that the levels of urinary acid-stable inhibitors may prove to be useful markers of the disease. 8922411: apoE is involved in processes of degeneration and regeneration after nerve lesions as well as in the pathogenesis of Alzheimer's disease (AD). 9161470: Lowering of blood pressure in dementia, especially Alzheimer's disease, may be due to the dementia process itself or to the characteristics of the disease. 9199880: Reactive oxygen-mediated processes are though to contribute to the pathogenesis of Alzheimer's disease (AD). 9462872: In addition apoE has also been implicated in neural regenerative processes and in the etiology of Alzheimer's disease. 9754878: The processing of beta-amyloid precursor protein (betaAPP) and its metabolites plays an important role in the pathogenesis of Alzheimer's disease (AD) and Down's syndrome. 9809105: The pathogenic process that causes AD has not been fully delineated; however, it clearly leads to neuropathology characterized by neuritic plaques, neurofibrillary tangles, and loss of cholinergic neurons in the nucleus basalis of Meynert. 9850931: Alzheimer's disease is a neurodegenerative disorder comprising multisystem atrophies probably caused by multifactorial processes. 1936584: Insulin, prostaglandins, and the pathogenesis of hypertension. 37439351: We hypothesized that SPMs are decreased in hypertension which contributes to the acetylcholine-induced contraction in resistance arteries, which are well known to be mediated by leukotrienes and prostaglandins. 4323556: [Role of prostaglandins in the pathogenesis of arterial hypertension]. 564075: These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis. 5736738: [Prostaglandin and depressor function of the kidneys in the pathogenesis of hypertension]. 5806644: [Role of prostaglandins in the pathogenesis of hypertension]. 6255690: The depressor systems -- prostaglandins, kallikrein-kinin-system -- will in future certainly bring newer knowledge concerning their participation in the pathogenesis of arterial hypertension. 6507633: The data suggest that increased glomerular PG formation in the clipped kidneys of 2K,1C rats is involved in the pathogenesis of hypertension in this animal model. 6681580: The present results suggest that both PGE and PGF production by the uterus in patients with pregnancy-induced hypertension is increased but that catabolism of PGF by the lung is compromised; this permits larger quantities of the vasoconstrictor PG to pass into the systemic circulation, where it may cause hypertension directly or indirectly, by association with other vasoactive substances. 6739164: [Role of the prostaglandin system in the pathogenesis of spontaneous hypertension in the rat]. 6877121: Inhibition of prostaglandin synthesis: a possible mechanism for stress-induced hypertension. 7825084: Renin-sodium profile and renal prostaglandins in the pathogenesis of systemic arterial hypertension in blacks. 824936: In the unanaesthetized rabbit prolonged inhibition of prostaglandin synthesis results in hypertension. 8390504: OBJECTIVES: To clarify the involvement of prostaglandins and renal haemodynamics in the pathogenesis of salt-induced hypertension. 8870314: Ethnic differences of renin-sodium profile and renal prostaglandins in the pathogenesis of systemic arterial hypertension. 10723114: Genetic variation in adducin, a protein associated with the inner leaflet of the plasma membrane, may be in part responsible for salt-sensitive hypertension. 12169651: We have previously shown that the enhanced expression of G(i) proteins in spontaneously hypertensive rats (SHR) that precedes the development of high blood pressure may be one of the contributing factors in the pathogenesis of hypertension. 12730030: Expression of Gbeta3s, the gene product of GNB3 associated with the GNB3 825T-allele, causes increased signal transduction which may contribute to pathogenetic mechanisms ultimately resulting in hypertension and obesity. 15901525: We believe that this protein was the cause of the hypertension in the setting of aldosterone deficiency in our patient. 17691927: Restriction of food or protein during specific windows of pregnancy leads to hypertension in adult offspring. 19961262: The aim of the present study was to evaluate the role of inhibitory G (G(i)) proteins, which are involved in tonic sympathetic vasoconstriction, in the pathogenesis of NO-deficient hypertension. Influence of pertussis toxin pretreatment on the development of L-NAME-induced hypertension. 23769550: We aimed to investigate the difference of these proteins between healthy and preeclamptic pregnancies in order to help clarify their potential roles in the pathogenesis of hypertension and proteinuria in preeclampsia. 25483714: This review outlines that defects of the connexin 40 protein leads to hypertension because of dysfunction of renin secreting cells of the kidney. 29537860: With the SS- Rag1-/- rats utilized as a novel tool to explore the effects of lymphocyte deficiency, these results provide evidence that adaptive immune mechanisms contribute to the exacerbation of salt-induced hypertension and renal injury mediated by increased dietary protein intake. Rag1-null Dahl SS rats reveal that adaptive immune mechanisms exacerbate high protein-induced hypertension and renal injury. 31412635: The elevation of AGEs levels suggests that oxidative modification of proteins occurs in hypertension pathogenesis. 10079962: Approximately 30% of patients who die after a single episode of severe head injury show intracerebral deposition of beta-amyloid protein (A beta), a protein that is thought to be central to the pathogenesis of Alzheimer's disease. 10349860: These results suggest the possibility that altered presenilin gene products in stress conditions may also participate in the pathogenesis of AD. 10369525: This paper discusses the biochemical evidence that links each protein to AD, various animal and cell models that have been used in these investigations, and the putative interactions between these proteins that lead to AD. 10867209: For example, apoE can interact with amyloid beta-protein and tau, proteins central to the pathogenesis of AD. 11072133: Calsenilin was discovered by virtue of its interaction with both presenilin-1 and -2, proteins that are involved in the etiology of Alzheimer's disease. 11973456: By comparing the CSF proteome between Alzheimer disease (AD) patients and controls it may be possible to identify proteins that play a role in the disease process and thus to study the pathogenesis of AD. 12020852: Accumulation of beta-amyloid (Abeta) protein in brain is an important characteristic for the etiology of Alzheimer's disease. 12419469: These results support the hypothesis that oxidative damage to lipid, protein, and DNA is an important early event in the pathogenesis of AD. 12429067: Although the precise molecular mechanism underlying presenilin function or dysfunction remains elusive, presenilins are thought to be part of a complex of proteins that has 'gamma-secretase cleavage' activity, which is clearly central in the pathogenesis of Alzheimer's disease. 12716134: Abnormal activity of these proteins in brain may contribute to the pathogenesis of Alzheimer's disease, a neurodegenerative condition characterized by focal amyloid deposits with neurofibrillary tangles. 12893422: Since the HPC patients can be regarded as preclinical AD patients, our results suggest the accumulation of these proteins involved in the initial steps of AD pathogenesis. 12972157: Recent biological studies indicate the importance of anterior-pharynx defective-1 (APH-1) proteins in Alzheimer's disease (AD) pathogenesis. 15304237: The beta amyloid (A beta) protein is a key molecule in the pathogenesis of Alzheimer's disease (AD). 15456259: Beta-secretase (BACE) is a critical enzyme in the production of beta-amyloid, a protein that has been implicated as a potential cause of Alzheimer's disease (AD). 15663474: Increased damage to proteins by glycation, oxidation and nitration has been implicated in neuronal cell death leading to Alzheimer's disease (AD). 15686969: These findings open new perspectives for the study of the possible crosstalk between these proteins in the pathogenesis of AD. 15975080: This article will review the current knowledge of PS1 function in protein trafficking and discuss its potential role in AD pathogenesis. 16472206: After much initial debate for and against the role of amyloid in Alzheimer's disease (AD), mutations on the amyloid precursor protein (APP) and processing pathways that increase levels of the amyloid b peptide of 42 residues (Abeta42) have established that faulty function or processing of these proteins are responsible for AD pathogenesis. 16883086: By comparing the CSF proteome of AD patients and controls it might be possible to identify proteins that play a role in the disease process and thus study the pathogenesis of AD. 17369839: Polyglutamine (polyQ) diseases are classified as conformational neurodegenerative diseases, like Alzheimer and Parkinson diseases, and they are caused by proteins with an abnormally expanded polyQ stretch. 17699523: Despite the functional importance of this protein in Alzheimer disease pathogenesis, the functional correlation to the structural domain of RTN3 remained unclear. 17761554: OBJECTIVE: Serine protease inhibitors (serpins), the acute phase reactants and regulators of the proteolytic processing of proteins, have been recognized as potential contributors to the pathogenesis of Alzheimer disease (AD). 17904250: We provide evidence that normal aging involves loss of Reelin neurons, reduced production and elimination of the extracellular deposits, whereas a prenatal immune challenge or the expression of AD-causing gene products, result in earlier, higher, and more persistent levels of Reelin-positive deposits. 1791973: It has been speculated that this protein, or the lack of it, may be involved in the aetiology of Alzheimer's disease (AD). 18374273: Thus, the study of the complex interplay of proteins that are involved in or modify Abeta production is very important to gain insight into the pathogenesis of AD. 19478666: PURPOSE OF REVIEW: This article reviews recent developments in the field of amyloid imaging using PET, specifically the ability to quantify the amount and distribution of brain beta-amyloid, the protein that occupies a central position in leading theories of the pathogenesis of Alzheimer's disease. 21248114: Presenilin 1 (PS1) is an integral component of gamma-secretase and is also a protein closely linked to the etiology of Alzheimer's disease (AD). 2128596: These data suggest that an intrinsic property of AD cells is the progressive reduced ability to interact with normal biologic signals provided by proteins such as interferons which in turn may contribute to the pathogenesis of AD. 21694447: The CD147 protein interacts with other proteins such as cyclophilin A (CyPA), Cyclophilin B (CyPB), sterol carrier protein (SCP), caveolin-1 and integrins, and can influence amyloid-beta (Abeta) peptide levels, a protein that is central to Alzheimer's disease (AD) pathogenesis. 21944696: The formation and accumulation of D-aspartate residue (D-Asp) in proteins caused by oxidative stress leads to dysfunction and/or denaturation of proteins, and is consequently responsible for aging-related misfolding diseases such as cataracts, prion disease, and Alzheimer's disease. 22138302: The association between apolipoprotein E (apoE) and amyloid-beta peptide (Abeta) may significantly impact the function of both proteins, thus affecting the etiology of Alzheimer's disease (AD). 22683528: Based on the studies that have been conducted so far amyloid beta-peptide (Abeta), a protein found in senile plaques, one of the key pathological hallmarks of AD, has been reported to be critical in the pathogenesis of AD. 22926141: These observations led us to conclude that VDAC1 interacts with Abeta, and phosphorylated tau may in turn block mitochondrial pores, leading to mitochondrial dysfunction in AD pathogenesis. 22971592: The neuroprotective effects of SA in a mouse model of amyloid beta (Abeta)(1-42) protein-induced Alzheimer's disease (AD) were investigated. Neuroprotective effect of sinapic acid in a mouse model of amyloid beta(1-42) protein-induced Alzheimer's disease. 23600477: AREAS COVERED: Here, the properties and diverse functions of ubiquilin-1 protein in the context of the pathogenesis of AD and other neurodegenerative disorders are discussed. 23697802: Near-complete fragmentation of proteins up to 29 kDa is achieved with UVPD including the unambiguous localization of a single residue mutation and several protein modifications on Pin1 (Q13526), a protein implicated in the development of Alzheimer's disease and in cancer pathogenesis. 23748076: Here we have shown a novel function of Caspr in pathogenesis of Alzheimer's disease (AD). 23866266: The discovery of neuroinflammatory changes, including dramatic proliferation of activated glia overexpressing a chromosome 2 gene product--the pluripotent immune cytokine interleukin-1 (IL-1)--and a chromosome 21 gene product--S100B--in the brains of fetuses, neonates, and children with DS opened the possibility that early events in Alzheimer pathogenesis were driven by cytokines. 24028865: In summary, we provide further evidence for interactions of PrP(C) with proteins that are known to be the key players in AD pathogenesis. 24269629: In the last five years our group has been involved in unraveling the neurobiology of this protein and investigating its relationship with cellular and molecular events of functional importance in AD pathogenesis. 25108596: The neuroprotective effects of baicalin on pathological changes and behavioral deficits were explored in a mouse model of amyloid beta (Abeta)(1-42) protein-induced Alzheimer's disease (AD). 25589722: Disturbances on AbetaPP and secretases intracellular trafficking and, consequently, in their localization may affect dynamic interactions between these proteins with consequences in the AD pathogenesis. 26438529: We review the literature regarding the biological functions of these six proteins and their putative role in AD pathogenesis. 27037841: The sialylation of proteins varies during development, aging, and pathogenesis of degenerative diseases such as Morbus Alzheimer, diabetes mellitus type II, or myopathies. 28217771: Amyloid fibrils are formed by the aberrant aggregation of proteins into highly ordered beta-sheet structures and are believed to be the root cause of several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Prion diseases, etc. and have been the subject of extensive biochemical, biophysical and clinical studies. 28415805: The dysregulation of these proteins can cause diseases such as Alzheimer's disease, tumorigenesis etc. and may also lead to drug resistance. 28550247: (A?), including A?42, proteins thought critical in the pathogenesis of Alzheimer's disease (AD). 2888020: The defect in the inherited autosomal dominant form of Alzheimer's disease, familial Alzheimer's disease (FAD), has been mapped to the same approximate region of chromosome 21 by genetic linkage to anonymous DNA markers, raising the possibility that this gene product, which could be important in the pathogenesis of Alzheimer's disease, is also the site of the inherited defect in FAD (ref. 5). 29076790: Misfolded beta-sheet structures of proteins leading to neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) are in the spotlight since long. 29774507: Here we focus on CALM, a protein containing an ANTH domain, which is implicated in the pathogenesis of blood cancers and Alzheimer disease, and discuss how alteration of CALM function is involved in these diseases. 30282354: Possible Role of Chitin-Like Proteins in the Etiology of Alzheimer's Disease. 30906244: The disruption of iron metabolism and iron transport proteins have been implicated in the pathogenesis of Alzheimer's disease (AD). 31281238: Increasing evidence links proteins of the S100 family to the pathogenesis of Alzheimer's disease (AD). 31507405: Amyloid-beta (Abeta) deposits and some proteins play essential roles in the pathogenesis of Alzheimer's disease (AD). 31686372: However, the molecular mechanisms underlying the aberrant expression levels of these proteins in the pathogenesis of AD are still not completely understood. Mitochondrial dysfunctions and oxidative stress play important roles in the early pathogenesis of Alzheimer's disease (AD), which also involves the aberrant expression levels of mitochondrial proteins. 33815938: Cleavage of this protein by beta-secretase can lead to the formation of amyloid-beta (Abeta) peptide plaque, which leads to Alzheimer's disease. 33833046: Diverse gene products contribute to the pathogenesis of Alzheimer's disease (AD). 34129723: Continued evaluation of these proteins will determine to what extent they can aid in the discrimination of MCI patients with and without an underlying AD etiology, and if they have the potential to contribute to a better understanding of the AD continuum. 34627984: MATERIALS AND METHODS: 60 APP/PS1 double transgenic AD mice (Mt) and 60 Ass1-40 protein-induced AD mice (Mi) were divided into 3 groups according to the dose of BdNlRB: BdNlRB-100, BdNlRB-200 and BdNlRB-400, with 100, 200 and 400 mg/kg*weight, respectively. 35188507: Because long-lived proteins do not have the corrective regeneration capabilities of most other proteins, points of isomerism and epimerization that accumulate within the proteins can severely hamper their functions and can lead to serious diseases like Alzheimer's disease, cancer and cataracts. 35877305: Tau and beta-amyloid (Abeta) proteins are major contributors to the etiology of AD. 36983903: Since the protein is able to establish protein-protein interaction (PPI) in different contexts and aggregation-prone proteins and the PPI networks are relevant for AD pathogenesis, and due to the relevance of finding new AD markers in peripheral biofluids, we thought it was interesting to study the possible involvement of cystatin B in PPIs in saliva and to evaluate differences and similarities between AD and age-matched elderly healthy controls (HC). 36994753: This article describes the Abeta protein and its role in AD, summarizing the evidence showing that altered Abeta clearance from the brain may lead to the imbalance, toxic buildup and misfolding of the protein - triggering a cascade of cellular, molecular and systematic events that ultimately lead to AD. 37127251: Accumulating evidence indicates that impaired autophagic function for removal of damaged mitochondria and protein aggregates such as amyloid and tau protein aggregates may contribute to the pathogenesis of AD. 37454217: We aimed at validating the potential value of these proteins as new CSF biomarkers for AD and their possible involvement in AD pathogenesis, with specific interest on the preclinical phase of the disease. 37724426: Further technical advancement of glial proteomics will enable us to identify proteins within individual cells and specific cell types, thus significantly enhancing our comprehension of AD pathogenesis. 38151346: In this article, we conduct a comprehensive review on the primary functions of multiple Rab proteins and their involvement in the pathogenesis of AD. 38473975: An extensive body of genetic evidence suggests soluble aggregates of beta-amyloid (Abeta) as the primary neurotoxin in the pathogenesis of AD. New data suggest that the aggregation of misfolded native proteins initiates and drives the pathogenic cascade that leads to Alzheimer's disease (AD) and other age-related neurodegenerative disorders. Understanding the distinct roles of soluble and insoluble amyloid aggregates on AD pathogenesis has been the key missing piece of the Alzheimer's puzzle. 7542371: The results are further discussed in view of the known or anticipated physiological functions of the proteins examined and of their possible role in the etiology of Alzheimer's disease. 8856006: Two of these loci, encoding the beta-amyloid precursor protein and apolipoprotein E, have gene products that are well characterized and of evident significance in the pathogenesis of AD. 8910899: We suggest that this long transcript may alter the normal pathway for processing of amyloid precursor protein, the protein which appears to be central in the pathogenesis of AD. 9697696: A2M, LRP1 (encoding the alpha-2M receptor) and the genes for two other LRP ligands, APOE and APP (encoding the amyloid beta-protein precursor), have now all been genetically linked to AD, suggesting that these proteins may participate in a common neuropathogenic pathway leading to AD. 9804283: Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer's disease. 9838173: An indirect role for these proteins has been previously suggested in the etiology of AD. 11194914: Renal lymphangiomatosis is a very rare benign disorder that might cause abdominal pain and rarely hypertension and hematuria. 14647783: OBJECTIVE: The aim of this article is to highlight the importance of a rare disease that causes severe arterial hypertension in children. 17211315: DISCUSSION: PPH is a rare disease caused by thickening of the arteriolar walls in the pulmonary bed, which results in a right-heart hypertension with venous stasis. 26084817: BACKGROUND: Pheochromocytoma and reninoma represent two rare diseases causing hypertension. 27526338: Apparent mineralocorticoid excess (AME) is a rare autosomal recessive genetic disorder causing severe hypertension in childhood due to a deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), which is encoded by HSD11B2. 31933700: < Learning objective: Isolated unilateral adrenal medullary hyperplasia (AMH) is a relatively rare disease that causes hypertension, and is generally diagnosed only after catecholaminergic symptoms mimicking pheochromocytoma. 33952808: Pulmonary arterial hypertension (PAH) refers to a rare, progressive disorder that is characterized by occlusive pulmonary vascular remodeling, resulting in increased pulmonary arterial pressure, right-sided heart failure, and eventual death. 34707046: Mid-aortic syndrome (MAS) is a rare vascular disorder that causes refractory hypertension. 35300529: A Rare Disease Leading to Hypertension. 37160153: Primary aldosteronism (PA), once considered a rare disease, is being increasingly recognized as an important cause of hypertension. 37951648: Precise diagnosis is essential in those who have not been found to have more common identifiable causes of hypertension in adolescents, since treatment strategies for these rare conditions are specific and different from antihypertensive regimens for the other more common causes of hypertension in this age group. 10774957: There is a large body of literature describing the causative role of oxidative stress mediated by increased levels of reactive oxygen species in the pathogenesis of cardiovascular disease such as atherosclerosis, hypertension, and restenosis after angioplasty. 15277201: Recent studies have implicated reactive oxygen species (ROS) in the pathogenesis of hypertension and activation of the sympathetic nervous system (SNS). 15363831: Experimental manipulation of the redox state in vivo shows that ROS can be a cause of hypertension. 16026320: However, when there is imbalance between their occurrence and antioxidant defense mechanisms, ROS can contribute to the vascular abnormalities that lead to hypertension. Although ROS are strongly implicated in the etiology of hypertension, clinical trials with antioxidants are inconclusive regarding their effectiveness in treating the disease. 16115037: Reactive oxygen species (ROS) are proposed to induce cardiovascular diseases, such as atherosclerosis, hypertension, restenosis, and fibrosis, through several mechanisms. 16230485: METHODS AND RESULTS: To investigate the pathological role of Nox1 upregulation in vascular smooth muscle, transgenic mice overexpressing Nox1 in smooth muscle cells (TgSMCnox1) were created, and the impact of Nox1 upregulation on the medial hypertrophic response during angiotensin II (Ang II)-induced hypertension was studied. To confirm that this potentiation of vascular hypertrophy and hypertension was due to increased ROS formation, additional groups of mice were coinfused with the antioxidant Tempol. 16323976: Endothelin and reactive oxygen species have been identified as important mediators in the pathogenesis of hypertension and associated end-organ damage. 16724941: Reactive oxygen species (ROS) are proposed to induce cardiovascular diseases, such as atherosclerosis and hypertension, through several mechanisms. 16927536: The increased production of reactive oxygen species plays a role in the etiology of hypertension, but the effects of antioxidants on blood pressure are controversial. 17147922: In this review, we discuss recent evidence in support of a role for brain ROS in the pathogenesis of hypertension and summarize current studies aimed at uncovering the complex mechanisms by which brain ROS regulate blood pressure in both health and cardiovascular disease. 17645641: Interplay of reactive oxygen species and nitric oxide in the pathogenesis of experimental lead-induced hypertension. 18307745: There is increasing evidence for a role of oxidative stress and nitric oxide deficiency in experimental glucocorticoid-induced hypertension, as evidenced by increased biomarkers of oxidative stress; the effectiveness of antioxidants or reduced NADPH oxidase antagonists in lowering blood pressure; and secondary upregulation of endogenous antioxidant enzymes in response to oxidative stress. Reactive oxygen species and glucocorticoid-induced hypertension. NADPH oxidase plays a significant role in the pathogenesis of glucocorticoid-induced hypertension in the rats, but xanthine oxidase and uncoupled eNOS pathways are not important sources of reactive oxygen species in these models. 18650132: The involvement of reactive oxygen species such as superoxide is implicated in the pathogenesis of hypertension. 19069440: Specifically, the detected dysregulation of first-line antioxidative defense enzymes leads to the accumulation of different forms of active oxygen metabolites that are involved in the development of the molecular basis of the pathogenesis of AH. 19307983: These results suggest that estrogen deficiency induces endothelial dysfunction and reactive oxygen species generation, triggering endothelial damage that leads to cerebral aneurysms and that hypertension is an additional risk factor. 19807685: Oxidative stress resulting from imbalance between reactive oxygen species (ROS) generation and antioxidant mechanisms is important in the pathogenesis of cardiovascular diseases such as atherosclerosis, ischemic heart disease, heart failure, stroke, hypertension and diabetes. 21289238: Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension. 21346766: We observed that the reactive oxygen species (ROS) production increases in the RVLM in hypertensive rats, thereby enhancing the central sympathetic outflow, which leads to hypertension. 21906672: Reactive oxygen species (ROS) are strongly implicated in the pathological signaling leading to hypertension in a framework that includes renin-angiotensin system (RAS) activation, increased sympathetic activity, and cardiac remodeling. 22125211: Imbalance of antioxidants and reactive oxygen species contributes to endothelium damage and leads to hypertension. 22129514: These findings suggest that Ang II receptor activation in youth triggers the upregulation of inflammatory cytokines and the production of reactive oxygen species, thereby inducing later insulin resistance and hypertension. 22157590: Increased reactive oxygen species (ROS) in the RVLM also contribute to sympathoexcitation, leading to hypertension. 22610475: The essential role of nitric oxide (NO) in maintaining endothelial function and the relationship between NO and reactive oxygen species are discussed in the context of the etiology of hypertension. 22713144: The present review addresses the putative function of ROS in the pathogenesis of hypertension and focuses on the role of Noxs in ROS generation in vessels and the kidney. Although evidence from experimental and animal studies supports a role for oxidative stress in the pathogenesis of hypertension, there is still no convincing proof that oxidative stress is a cause of human hypertension. 22790689: Reactive oxygen species (ROS) in rostral ventrolateral medulla (RVLM) of brainstem contribute to sympathoexcitation and are critically involved in the pathogenesis of hypertension. 23600794: CRITICAL ISSUES: Although extensive experimental data support a role for increased ROS levels and altered redox signaling in the pathogenesis of hypertension, the role in clinical hypertension is unclear, as a direct causative role of ROS in blood pressure elevation has yet to be demonstrated in humans. RECENT ADVANCES: Although oxidative stress may not be the only cause of hypertension, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors, such as salt loading, activation of the renin-angiotensin-aldosterone system, and sympathetic hyperactivity, at least in experimental models. 24047403: Oxidative stress resultant from imbalance between ROS generation and antioxidant defense mechanisms is important in pathogenesis of cardiovascular diseases, such as hypertension, heart failure, atherosclerosis, diabetes, and cardiac hypertrophy. 25484552: In conclusion, the data suggest that added sugars induce atherosclerosis, hypertension, peripheral vascular disease, coronary artery disease, cardiomyopathy, heart failure, and cardiac arrhythmias and that these effects of added sugars are mediated through ROS. The mechanism by which ROS induce the development of atherosclerosis, hypertension, peripheral vascular disease, coronary artery disease, cardiomyopathy, heart failure, and cardiac arrhythmias have been discussed in detail. 27092251: This review summarizes recent work implicating immune signals and reproductive hormones, as well as gasotransmitters and reactive oxygen species in the pathogenesis of hypertension at traditional CV control centers. 27531649: In rodents, blockade of H2S synthesis by CSE, by either pharmacologic or genetic approaches, inhibited carotid body activation and hypertension induced by intermittent hypoxia. A rodent model of intermittent hypoxia that mimics blood O2 saturation profiles of patients with sleep apnea has shown that increased generation of reactive oxygen species (ROS) in the carotid body enhances the chemosensory reflex and triggers hypertension. H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea. 27659729: Reactive oxygen species (ROS) in the brain are involved in the pathogenesis of hypertension. 28320851: Therefore, TMEM16A is a positive regulator of endothelial reactive oxygen species generation via Nox2-containing NADPH oxidase, which induces endothelial dysfunction and hypertension. The knockout of endothelial-specific TMEM16A significantly lowered the blood pressure and ameliorated endothelial dysfunction in angiotensin II-induced hypertension, whereas the overexpression of endothelial-specific TMEM16A resulted in the opposite effects. 28842207: Reactive oxygen species (ROS) in the paraventricular nucleus (PVN) play a pivotal role in the pathogenesis of hypertension. 29424564: Reactive oxygen species induce vascular dysfunction and hypertension by directly interacting with nitric oxide (NO) which leads to NO inactivation. 33820956: Overproduction of reactive oxygen species (ROS) plays an important role in the pathogenesis of hypertension. 38276286: Possible Molecular Mechanisms of Hypertension Induced by Sleep Apnea Syndrome/Intermittent Hypoxia. Since SAS is linked to various serious cardiovascular complications, especially hypertension, many studies have been conducted to elucidate the mechanism of hypertension induced by SAS/IH. This review outlines the molecular mechanisms of hypertension in IH, which include the regulation systems of reactive oxygen species (ROS) that activate the renin-angiotensin system (RAS) and catecholamine biosynthesis in the sympathetic nervous system, resulting in hypertension. As hypertension is the most common complication of SAS, cell and animal models to study SAS/IH have developed and provided lots of hints for elucidating the molecular mechanisms of hypertension induced by IH. 7812826: To determine if endothelial and ROS-induced changes in hypertension, atherosclerosis, ischemia/reperfusion etc. are the primary cause of specific diseases or merely secondary effects remains to be clarified in several areas from inflammatory processes to cardiovascular diseases. 9818200: Increasing evidence implicates reactive oxygen species in the pathogenesis of hypertension and its cardiovascular complications. 10699754: Increasing evidence supports the role of reactive oxygen species (ROS) in the pathogenesis of Alzheimer's disease (AD). 10875435: The preliminary segment is an introduction to reactive oxygen species and their potential involvement in the pathogenesis of AD and the generation of an inflammatory response. 11992623: The discovery of the isoprostanes, recent studies performed in living patients, and the development of transgenic animal models of AD-amyloidosis are three important factors that are helping us to better understand and define the role that oxygen radicals might play in AD pathogenesis. 17365122: One major pathogenesis in degenerative disorders of the central nervous system (CNS), including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and ischemia, is the oxidative stress induced by reactive oxygen species (ROS). 19035781: As a result, the AbetaCu(I) complex may be a critical reactant involved in ROS associated with AD etiology. 23041154: It has been suggested that excess accumulation of reactive oxygen species, termed oxidative stress, may lead to neuronal death resulting in neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. 23417568: Identifying these differential behaviors and mechanisms of hydrogen peroxide and superoxide anion functions illuminates the possible therapeutic targets in the prevention or treatment of ROS-induced neurodegenerative diseases such as Alzheimer's disease. 24189435: Since mitochondria are also vulnerable to oxidative stress, it is likely that a vicious downward spiral involving the interactions between mitochondrial dysfunction and oxidative stress contributes to the initiation and/or amplification of reactive oxygen species that is critical to the pathogenesis of AD. 24276282: Aberrant regulation of transition metals and the resultant disregulation of neuronal reactive oxygen species (ROS) are considered significant in the etiology of Alzheimer's disease (AD). 24351276: These results indicate that dityrosine cross-links may play an important role in the pathogenesis of Alzheimer's disease and can be generated by reactive oxygen species catalyzed by Cu2+ ions. 25620241: The biology of NF-kappaB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. 27476701: We have previously shown that a specific apoE4 fragment, apoE4-165, promotes amyloid-peptide beta 42 (Abeta42) accumulation in human neuroblastoma SK-N-SH cells and increased intracellular reactive oxygen species formation, two events considered to occur early in AD pathogenesis. 28059794: While mounting evidence implicates ROS in the AD etiology, clinical trials with antioxidant therapies have not produced consistent results. 28618998: This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain. 30688256: Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. 31001602: Understanding the factors that give rise to tau aggregation and reactive oxygen species (ROS) is the key aspect in Alzheimer's disease pathogenesis. 31617375: Aims: Reactive oxygen species (ROS) generated during Alzheimer's disease (AD) pathogenesis through multiple sources are implicated in synaptic pathology observed in the disease. 33306995: The vulnerability of the brain to reactive oxygen species (ROS) is now emerging as a key detrimental factor driving AD pathogenesis. 35463198: CNDs were also found to inhibit the generation of multiple reactive oxygen species, which is an important contributor to AD pathogenesis. 37657763: Reactive Oxygen Species (ROS) and mitochondrial dysfunction are implicated in the pathogenesis of Alzheimer's disease (AD), a common neurodegenerative disorder characterized by abnormal metabolism of the amyloid precursor protein (APP) in brain tissue. 10394113: Recent papers suggested an enhanced rather than reduced activity of endogenous NO system in rats with normal renal function and rHuEpo-induced hypertension. Nitric oxide-dependent renal vasodilatation is not altered in rat with rHuEpo-induced hypertension. Further studies seem to be necessary to better clarify the exact mechanisms underlying the development of rHuEpo-induced hypertension. The exact mechanism of rHuEpo-induced hypertension has not been fully elucidated, and several possibilities have been proposed, such as a direct vascular effect of the drug with a shift in the balance of constrictor and relaxing endothelial factors (endothelins and nitric oxide (NO)). 10405199: These results suggest that the endothelin system may be involved in the pathogenesis of rhEPO-induced hypertension in uremic rats with a differential role for ET(A) and ET(B) receptors. 11482502: The pathogenesis of the rHuEPO-induced hypertension is still uncertain, though evidence of the involvement of endothelial cells has emerged. 11576916: Multiple factors are involved in rHuEPO-induced hypertension. 12558321: However, the mechanism of the r-HuEPO induced hypertension has not been fully elucidated. The results suggest that an inhibitory effect of r-HuEPO on NO production might be, at least in part, related to the r-HuEPO induced hypertension in this case. We report a case of r-HuEPO induced hypertension in an anephric patient. It is well known that chronic administration of r-HuEPO often causes hypertension in dialysis patients. A case of erythropoietin induced hypertension in a bilaterally nephrectomized patient. 12605017: Relationship between eicosanoids and endothelin-1 in the pathogenesis of erythropoietin-induced hypertension in uremic rats. Recent studies suggest a possible link between recombinant human erythropoietin (rhEPO)-induced hypertension and endothelium-derived vasoconstrictor autocoids. These results suggest that endothelium-derived vasoconstrictor autacoids (TXA and ET-1) are involved in the pathogenesis of rhEPO-induced hypertension in uremic rats. The current study was designed to evaluate the role of eicosanoids such as thromboxane (TX) A and prostacyclin (PGI ) and of endothelin-1 (ET-1) and the relationship between these vasoactive substances in rhEPO-induced hypertension in uremic rats. 12911161: Increased endothelin: nitric oxide ratio is associated with erythropoietin-induced hypertension in hemodialysis patients. These results suggest that an increase in ET-1/NOx ratio in blood, probably occurring in vascular endothelial cells, may be associated with rHuEPO-induced hypertension in HD patients. 15005270: Recombinant human erythropoietin (rHuEPO) has been reported to induce hypertension. 15728783: Recombinant human erythropoietin therapy frequently causes hypertension in humans and animals with chronic renal failure. 16049546: Cyclooxygenase inhibition with acetylsalicylic acid unmasks a role for prostacyclin in erythropoietin-induced hypertension in uremic rats. We previously reported that thromboxane (TX)A2 synthesis and receptor blockade prevented recombinant human erythropoietin (rhEPO)-induced hypertension in chronic renal failure rats. Cyclooxygenase inhibition had no effect on rhEPO-induced hypertension owing, in part, to simultaneous inhibition of both TXA2 and its vasodilatory counterpart PGI2 synthesis, whereas the vascular ET-1 overproduction was maintained. 1639525: The main results of the present studies suggest that rHu-EPO-induced hypertension might be associated with altered cellular calcium homeostasis and hyperactivity of the sympathetic nervous system. There was a close correlation between free calcium concentration in platelets and mean arterial pressure in patients developing rHu-EPO-induced-hypertension (r = 0.95). 1794212: To investigate the mechanisms of hypertension induced by recombinant human erythropoietin (rHuEPO) in patients on hemodialysis (HD), mean blood pressure (MBP), plasma renin activity (PRA), whole blood viscosity, blood volume (BV), cardiac index (CI) and total peripheral resistance index (TPRI) were measured before and after treatment with rHuEPO for 3 months in 9 patients on HD. Mechanisms of hypertension induced by erythropoietin in patients on hemodialysis. 26924494: Impaired renal endothelial nitric oxide synthase and reticulocyte production as modulators of hypertension induced by rHuEPO in the rat. Our study showed that rHuEPO-induced hypertension is present before significant hematological changes occur and, therefore, might involve direct (renal) and indirect (hematological) effects, which varies according to the dose used. 7474668: The mechanism of hypertension induced by recombinant human erythropoietin (rHuEPO) is unclear but may include an increase in peripheral vascular resistance. 7740514: It is concluded that serotonin may play a role in the development of hypertension caused by rHuEPO. The aim of this study was to investigate the mechanism of erythropoietin-induced hypertension in respect to its action on blood serotonergic system. 8015637: Endothelin may be one of the causes in rHuEPO-induced hypertension in some hemodialysis patients. 8196222: Thus, it appears that the mechanism of rHuEPO-induced hypertension may be mainly due to elevation of [Ca2+] i. 8196287: The pathogenesis of hypertension induced by recombinant human erythropoietin (rHuEPO) remains a subject of intense interest. Antiplatelet therapy and development of hypertension induced by recombinant human erythropoietin in uremic patients. Since the antiplatelet drugs used in this study did not have a significant hemodynamic effect, we infer that changes in platelet aggregability induced by rHuEPO may be involved in the pathogenesis of hypertension induced by this hormone. 8592587: The direct effect of rHuEpo on endothelial cells (EC) has been suggested as one of contributing factors of rHuEpo-induced hypertension. 8608665: Left ventricular hypertrophy (concentric and eccentric), which can be due to hypertension and anemia, is commonly observed in ESRD patients and has been shown to be a predictor of cardiac morbidity and mortality in these patients. Renal failure itself obviously is a prerequisite in the pathogenesis of r-HuEPO-induced hypertension, since it was never observed in anemic patients without renal disease. Normalization, though, is generally not achieved and in patients with r-HuEPO induced hypertension the increase of blood pressure may oppose the beneficial effects of r-HuEPO treatment on cardiac hypertrophy. 8788598: Erythropoietin (rHuEPO)-induced hypertension represents a clinical problem in hemodialysis units. 9113497: To assess the role of altered cellular calcium metabolism, resting platelet cytosolic calcium was measured in 12 previously normotensive patients with end-stage renal disease before and after 12 weeks of EPO-therapy, after 12 weeks of combined antihypertensive pharmacotherapy of EPO-induced hypertension, and after 12 weeks of concurrent administration of EPO and indomethacin. The results of the present study suggest that EPO-induced hypertension might be related to altered cellular calcium homeostasis. Antihypertensive therapy of EPO-induced hypertension resulted in a reduction of blood pressure and a reduction of platelet calcium to near normal levels (128 +/- 6 nmol/l). Hypertension induced by recombinant human erythropoietin (rHU-EPO) can be prevented by indomethacin. Patients with EPO-induced hypertension showed a significant raise in platelet calcium by comparison with calcium levels prior to EPO (179 +/- 15 vs 120 +/- 8 nmol/l), and there was a positive correlation between their blood pressure and platelet calcium levels (r = 0.9, p < 0.001). 9771008: The exact mechanism of rHuEPO-induced hypertension has not been fully elucidated, although in this paper several theories have been presented. 9829494: However there is no report on whether a change in the rate of conversion of proET-1 to ET-1 may be involved in the pathogenesis of rHuEpo-induced hypertension. BACKGROUND: The pathogenesis of rHuEpo-induced hypertension in haemodialysis (HD) patients still remains uncertain. The purpose of this study was to ascertain the potential role of ECE in the development of rHuEpo-induced hypertension. 9869008: OBJECTIVE: Plasma renin is not elevated in recombinant human erythropoietin (rhEPO)-induced hypertension but angiotensin converting enzyme inhibitors reduce blood pressure in both human and animal studies. 9925862: rHuEPO caused high blood pressure in only 1 patient that resolved spontaneously after cessation of erythropoietin treatment for a week. 10369993: Renal artery stenosis (RAS) is a treatable cause of hypertension and renal failure for which no ideal screening technique is currently available. 10396407: Renal artery stenosis is a potentially correctable cause of hypertension and renal failure, using endoluminal or, less commonly, surgical techniques. 10485378: BACKGROUND: Renal transplant artery stenosis (RTAS) continues to be a problematic, but potentially correctable, cause of post-transplant hypertension and graft dysfunction. 10533305: We report the case of a nine-year-old boy who had hypertension caused by renal arterial stenosis. 10559817: The hypertension was caused by a renal artery stenosis. 10618564: BACKGROUND: Renal artery stenosis is a common disorder and is an established cause of hypertension and renal insufficiency. 10817023: Renal artery stenosis may be a cause of hypertension and a potential contributor to progressive renal insufficiency. 1093491: Hypertension due to renal artery stenosis in transplanted kidneys. 11096658: Renal artery stenosis (RAS) is a common cause of hypertension and renal insufficiency, especially in the elderly population. 11209720: Hypertension is a frequent disease and renal artery stenosis, as a potential cause of hypertension, can be cured. 11341864: Renal artery stenosis (RAS) can accelerate or generate progressive hypertension and renal dysfunction. 11607795: BACKGROUND: Renal artery stenosis is among the most common curable causes of hypertension. 11728249: Renal artery stenosis has long been recognized as a cause of systemic hypertension, and has more recently been identified as a cause of progressive renal insufficiency. 11780674: This review focuses on the sensitivity and specificity of commonly used screening tests for renal artery stenosis and on the clinical variables that are most likely to distinguish patients with renal artery stenosis from patients with other causes of their hypertension. 11903175: Renal artery stenosis is a common, progressive cause of hypertension and renal impairment, and is frequently treated with percutaneous transluminal dilatation and stenting. 11919116: Polycythaemia and hypertension caused by renal artery stenosis. 11923791: BACKGROUND: Renal artery stenosis (RAS) is an important clinical entity that can lead to uncontrolled hypertension and progressive renal failure. 12041025: Renal revascularisation has been proved an effective treatment modality in patients with arterial hypertension or renal failure due to renal artery stenosis. 12082195: A 25-year-old female presented with uncontrolled hypertension due to renal artery stenosis, a saccular aneurysm at the mid-shaft of the right renal artery, and an arterio-venous fistula distal to the aneurysm. 12136468: BACKGROUND: Renal artery stenosis (RAS) can cause arterial hypertension and can lead to renal insufficiency. 12147876: Renal artery stenosis (RAS) is one of the important causes of correctable hypertension. 12491013: Results were better when the RADS was responsible for an ipsilateral renal atrophy or for poorly controlled hypertension. 12496538: SUMMARY BACKGROUND DATA: TRAS is an important and treatable cause of hypertension and graft dysfunction in renal allograft recipients. 12710843: Renal artery stenosis (RAS) may cause hypertension, azotemia, episodes of flash pulmonary edema and congestive heart failure. 12972481: Anecdotal evidence suggests that renal artery stenosis (RAS) may be a relevant and treatable cause of hypertension. 13669854: Revascularization of the kidney in hypertension due to renal artery stenosis. 13772830: Surgical treatment of hypertension resulting from renal artery stenosis. 13780499: [Conservative surgery in the treatment of arterial hypertension caused by renal artery stenosis]. 1385757: Use of interventional radiology for hypertension due to renal artery stenosis in children. 13859020: Hypertension due to renal artery stenosis caused by abdominal aortic aneurysm. 1387529: Transplant renal artery stenosis is a potentially treatable cause of post-transplant hypertension. 13964976: [Arterial hypertension caused by renal artery stenosis]. 13973984: [Pre- and postoperative nephrogram in hypertension caused by renal artery stenosis]. 13993701: The diagnosis and treatment of hypertension due to renal arterial stenosis. 14033738: [Hypertension due to renal artery stenosis]. 14044127: THE DIAGNOSIS AND TREATMENT OF HYPERTENSION DUE TO RENAL ARTERIAL STENOSIS. 14105033: DIAGNOSIS OF HYPERTENSION DUE TO RENAL ARTERIAL STENOSIS. 14140945: DIAGNOSIS OF HYPERTENSION SECONDARY TO RENAL ARTERY STENOSIS. 1416679: Renal artery stenosis is increasingly being diagnosed as a cause of hypertension and renal impairment. 14260841: [INTRAVENOUS UROGRAPHY AS A DIAGNOSTIC METHOD IN HYPERTENSION DUE TO RENAL ARTERIAL STENOSIS]. 14280744: [ARTERIAL HYPERTENSION CAUSED BY RENAL ARTERY STENOSIS]. 14319470: DIFFERENTIAL RENAL STUDIES IN THE DIAGNOSIS OF HYPERTENSION DUE TO RENAL ARTERIAL STENOSIS: VALIDITY OF CALCULATING COMPARATIVE URINARY VOLUME REDUCTION FROM THE COMPARATIVE URINARY CREATININE CONCENTRATIONS. 14456018: [Coarctation of the upper abdominal aorta, with reference to surgical treatment of hypertension caused by renal artery stenosis]. 14515675: UNLABELLED: Transplant renal artery stenosis (TRAS) is a cause of severe post transplant hypertension with a widely variable reported incidence from 1 to 25%. 14521202: A young infant with hypertension caused by renal artery stenosis should be controlled medically until he or she is large enough to undergo angiography and angioplasty successfully. 14628254: CONCLUSIONS: Severe hypertension can be caused by a renal artery stenosis. 14692134: Arterial hypertension in pediatric patients with neurofibromatosis type 1 (NF 1) is usually due to renal artery stenosis (RAS) mainly involving the proximal part of the vessel. 14694165: Transplant renal artery stenosis (TRAS) is a recognized, potentially curable cause of posttransplant arterial hypertension, allograft dysfunction, and graft loss. 14736540: These mechanisms importantly contribute to the pathogenesis of hypertension secondary to renal artery stenosis and end-stage renal disease. 1476271: The minimum degree of renal arterial stenosis needed to cause hypertension was identified by renal arterial angiography of anesthetized dogs. These results suggest that whether there is innervation or not, the critical degree of renal arterial stenosis that causes hypertension is more than about 70% of the diameter in the presence of renal prostaglandins; in their absence, the critical point above which hypertension occurs is 75% or more. Critical degree of renal arterial stenosis that causes hypertension in dogs. 1491910: Hypertension due to transplant renal artery stenosis was treated with percutaneous transluminal angioplasty (PTA) in 6 children. 14968343: Renal artery stenosis (RAS) leading to hypertension or ischemic nephropathy can be treated by endovascular revascularization using balloon angioplasty or stent implantation. 15012740: There are several causes of transplant renal artery stenosis, resulting in hypertension and renal dysfunction. 154170: These negative tests indicate that renal artery stenosis was not the only cause of hypertension. 15488139: BACKGROUND: Renal artery stenosis (RAS) is a known cause of hypertension and ischemic nephropathy. 15520423: BACKGROUND: Timely, accurate detection of renal artery stenosis is important because this disorder may be a potentially curable cause of hypertension and renal impairment. 15526910: BACKGROUND: Renal artery stenosis is an important cause of hypertension and renal failure. 15765911: This study evaluated the potential for transvenous ultrasonography to assess renal artery stenosis (RAS), the most common correctable cause of hypertension in the United States. 15772839: A 12-year-old girl with Alagille syndrome manifested severe hypertension caused by renal artery stenosis in a solitary functioning kidney. 15777385: Hypertension was the most common presentation (77%) and was usually a consequence of renal artery stenosis or aortic coarctation. 15900383: Severe hypertension secondary to renal artery stenosis and Cushing's syndrome. 161881: Three patients with hypertension due to renal artery stenoses were treated by percutaneous transluminal angioplasty with the coaxial-balloon-catheter system as it is used for the dilatation of coronary arteries. 16195649: The patient was admitted to our hospital after presenting with severe hypertension secondary to abdominal aortic hypoplasia and renal artery stenosis. 16251847: Clinicians need to be vigilant for evidence of unsuspected renal artery stenosis as a cause of treatment-resistant hypertension and/or renal failure. 16338259: BACKGROUND: Renal artery stenosis (RAS) is a potentially reversible cause of hypertension and renal insufficiency and is associated with poor prognosis. 16382321: Renal artery stenosis (RAS) is one of the most common causes of severe arterial hypertension in infants. We report a case of severe hypertension caused by RAS of congenital single pelvic kidney in a 4-month-old boy. 16436206: BACKGROUND: Renal artery stenosis (RAS) is one of the main causes of secondary systemic arterial hypertension. 16509936: BACKGROUND: Renal artery stenosis is a common, correctable cause of hypertension and renal impairment, with multiple screening tests available to aid diagnosis. 16802543: The clinical importance of renal artery stenosis is the induction of severe hypertension and renal dysfunction or even dialysis dependency. 16819600: BACKGROUND: Renal artery stenosis (RAS) causes significant hypertension in children. 16886129: Arterial hypertension may result from renal artery stenosis. 16892443: BACKGROUND: Renal artery stenosis (RAS) is a cause of reversible hypertension and nephropathy. 16895677: We described a 26 year-old man hospitalized for macroscopic hematuria associated with a subepithelial hematoma whose development might have been favored by arterial hypertension secondary to a renal artery stenosis. 17097949: BACKGROUND: Transplant renal artery stenosis, the prevalence of which varies from 2% to 12%, is an important cause of hypertension and allograft dysfunction. CONCLUSION: Transplant renal artery stenosis is a common cause of hypertension and renal allograft dysfunction. 17124483: The clinical importance of renovascular disease, atherosclerotic or of other origin, arises from the fact, that renal artery stenosis (RAS), if hemodynamically significant (> 70% diameter reduction), induces arterial hypertension, renal insufficiency or both. 17672905: CASE PRESENTATION: In this report, we present a relatively uncommon case of renovascular hypertension in a 35-year-old female with a history of intractable hypertension as a result of fibromuscular dysplasia involving an accessory renal artery. BACKGROUND: Renovascular hypertension is defined as hypertension caused by renal artery stenosis. 179157: The hypertension was the result of renal artery stenosis. 18037777: Since RAS is an underlying cause of hypertension and renal failure, it is important to consider the presence of RAS in patients with severe CAS. 1828297: Renal artery stenosis (RAS) is a rare cause of hypertension. Normalization of the blood pressure can be achieved by intervention (operation, percutaneous transluminal renal angiography; PTRA), in cases of prolonged RAS-induced hypertension long-term preservation of the organ function is most important. 18292612: Renal computed tomography angiography excluded renal artery stenosis as a cause of hypertension but disclosed many distended collateral blood vessels in the musculus rectus abdominis and in the upper abdominal area. 18365815: BACKGROUND: Renal artery stenosis may produce hypertension, and this condition is referred to as renovascular hypertension (RVH). 18593803: RAS leads to activation of the renin-angiotensin-aldosterone system and may result in hypertension, ischemic nephropathy, left ventricular hypertrophy and congestive heart failure. 1894119: Renal artery stenosis is the most common surgically or interventionally curable cause of hypertension. 19003743: Because renal artery stenosis is a potentially correctable cause of hypertension and ischemic nephropathy, early identification of this entity may lead to proper hypertension control and improved renal function and survival. 19096816: The challenge of treating these patients is to find the evidence proving that the RAS is responsible for hypertension and/or renal dysfunction. 19112228: Transplant renal artery stenosis (TRAS) is a recognized and potentially curable cause of post transplant arterial hypertension, allograft dysfunction, and graft loss. 19129856: Renal artery stenosis (RAS) is an important cause of arterial hypertension and chronic kidney disease. 19575169: Renal artery stenosis is a well accepted cause of hypertension or at least deterioration of blood pressure control as well as the cause of a progressive course of renal insufficiency if of an atherosclerotic nature. 1959243: Detection of a renal artery stenosis (RAS) as a cause of arterial hypertension is of great practical importance because dilatation of the stenosis frequently results in an improvement or cure of the hypertension. 19616971: Renal artery stenosis (RAS) is a progressive disease that may cause hypertension and chronic renal insufficiency. 19621837: Up to 5 percent of all occurrences of hypertension are caused by renal artery stenosis, equating to as many as 3.5 to 4 million occurrences in the United States. 19649626: A 12-year-old boy presented with severe arterial hypertension due to a severe subsegmental renal artery stenosis. Severe hypertension due to renal polar artery stenosis in an adolescent treated with coil embolization. 20184703: CASE PRESENTATION: A 30-year-old white female patient with resistant hypertension caused by a severe renal artery stenosis attributed to fibromuscular dysplasia, was submitted to conventional balloon angioplasty without success. 20339816: BACKGROUND: Renal artery stenosis (RAS) is a potentially correctable cause of hypertension and ischemic nephropathy. 2108582: Renal artery stenosis (usually proximal), intraparenchymal renal arterial abnormalities, and coarctation of the abdominal aorta often lead to hypertension. 21173521: We report the case of a 65-year-old woman with a solitary kidney who developed hypertension due to renal artery stenosis caused by fibromuscular dysplasia. 21326078: Transplant renal artery stenosis (TRAS) is a potentially curable cause of posttransplant arterial hypertension, allograft dysfunction and graft loss. 2137541: Severe hypertension developed secondary to renal artery stenosis in 11 of 229 children who received a renal allograft. 2147849: Hypertension due to renal artery stenosis in pregnancy--the use of angioplasty. 21558950: John is taking amlodipine and hydrochlorothiazide for hypertension due to renal artery stenosis. 21559256: Transplant renal artery stenosis (TRAS) is a well-known cause of posttransplant hypertension accompanied by possible graft dysfunction and is potentially curable when is diagnosed early. 21566313: Renal artery stenosis is an important cause of uncontrolled hypertension and progression to chronic kidney disease. 21915167: BACKGROUND: Transplant renal artery stenosis (TRAS) is an important cause of hypertension and renal allograft dysfunction occurring in kidney transplant recipients. 2193862: In 10 kidneys removed for hypertension due to renal artery stenosis, the histological appearances varied from negligible ischaemic damage to end-stage ischaemic atrophy. 2243982: Renal artery stenosis (RAS) is the most common correctable cause of hypertension. 22569449: We report here two interesting cases of successful transplantation of kidneys from live related kidney donors with hypertension due to renal artery stenosis who became normotensive with good graft function in the recipient. 22577447: BACKGROUND: Renal artery stenosis is one of the important causes of hypertension and end stage renal failure. 22724464: Renal artery stenosis (RAS) is a cause of hypertension and ischemic nephropathy. 22891616: Two had PV, five had severe hypertension, one of them because of renal artery stenosis, and two had diabetes mellitus. 22901822: Pheochromocytoma and renal artery stenosis are two common causes of surgically correctable childhood hypertension that may coexist. 23023722: Renovascular hypertension (hypertension induced by renal artery stenosis) is a form of secondary hypertension caused by overactivation of the renin-angiotensin system by the ischemic kidney. 23348540: [Hypertension caused by renal artery stenosis: new view on a difficult clinical problem]. 235218: The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. 23587124: Renal artery stenosis is causative in 2 - 5% patients with hypertension and accounts for 3 - 15% cases of chronic kidney disease (CKD). 23590038: BACKGROUND: Although RAS is a relatively uncommon cause of hypertension, it is the most common form of correctable hypertension. 23671537: Transplant renal artery stenosis (TRAS) is a potentially treatable cause of allograft dysfunction, hypertension and graft loss. 23986869: The indications for considering intervention include uncontrolled hypertension due to renal artery stenosis, severe symptomatic coronary artery or cerebrovascular disease, severe aortic regurgitation, stenotic or occlusive lesions resulting in critical limb ischemia, and aneurysms at risk of rupture. 24122504: Renal artery stenosis can cause renal failure, hypertension, and heart failure, leading to a poorer life prognosis. If renal artery stenosis is found as a cause of acute renal failure, severe hypertension, or heart failure, it is useful to perform revascularization as soon as possible. 24197551: Renal artery stenosis is the narrowing of the renal artery which causes hypertension and atrophy of the affected kidney, ultimately leading to renal failure if not treated and most often caused by atherosclerosis or fibromuscular dysplasia. 24305958: BACKGROUND: Transplant renal artery stenosis (TRAS) is an increasingly recognised cause of post-transplant hypertension. 24625996: Renal artery stenosis (RAS) is one of the main correctable causes of secondary systemic arterial hypertension. 24678641: CONCLUSIONS: NF1 may present with hypertension due to renal artery stenosis in children. 24754495: Renal artery stenosis as the cause of resistant arterial hypertension: an unusual technique for revascularization. 2510517: The vascular changes in children with NFvR are mostly asymptomatic; however hypertension secondary to renal artery stenosis and/or Moya-moya disease have been reported infrequently. 25220318: Renal artery stenosis (RAS) is one of the most common causes of severe hypertension (approximately 1-5% of all patients with hypertension). 2526394: Renal artery stenosis may be the cause of hypertension and reduced renal function. 25353610: [Urgent revascularisation can preserve renal function in a patient with severe hypertension because of renal artery stenosis]. 25704353: Transplant renal artery stenosis is an important, potentially treatable cause of hypertension. 25852907: A consistent percentage of patients affected by ECD develop renal failure and hypertension as a consequence of renal artery stenosis and hydronephrosis. 2596648: Renal artery stenosis is an uncommon, but curable cause of systemic hypertension. 26193229: Remarkably, this variant was associated with an area of proximal arterial stenosis, which produced signs and symptoms of hypertension secondary to renal arterial stenosis. 26564026: It is a potentially treatable cause of hypertension, and is often caused by renal artery stenosis (RAS). 27398034: We report a case of a female in her mid 20s who developed hypertension due to RAS with no evidence of FMD or underlying renal dysfunction and underwent successful angioplasty and stenting. 27528003: Spontaneously Resolving Hyperreninemic Hypertension Caused by Accessory Renal Artery Stenosis in a 13-Year-Old Girl: A Case Report. 27641455: Renal artery stenosis is a potentially reversible cause of hypertension, and transcatheter techniques are essential to its treatment. 28205351: We report a 10-month-old girl with arterial hypertension caused by right-sided renal artery stenosis detected by Doppler ultrasound. 28265213: Revascularization in a 17-Year-Old Girl with Neurofibromatosis and Severe Hypertension Caused by Renal Artery Stenosis. 28554696: Vascular changes lead to the main complications, including hypertension, most often due to renal artery stenosis or, more rarely, stenosis of the suprarenal aorta. In 54% of cases, hypertension was due to a renal artery stenosis. 2858047: Patients had both non-vascular symptoms (arthralgias in 56%, fever in 44%, weight loss in 38%) and symptoms of vascular stenosis such as arm claudication (47%) and hypertension due to renal artery stenosis (41%). 28760595: Thus, smoking can contribute to the development of atheromatous renal artery stenosis, which is an aggravating cause of hypertension. 2878759: Systemic hypertension secondary to renal artery stenosis is a common complication of Takayasu's disease. 28814591: Renal Artery Stenosis (RAS) is an important cause of treatment-resistant hypertension. 28902735: A positive captopril renography indicates that patient's hypertension is renin dependent, most commonly caused by renal artery stenosis. 2936215: Percutaneous transluminal angioplasty (PTA) was done in a 58-year-old man with hypertension due to a left-sided renal artery stenosis. 2936692: Percutaneous transluminal renal angioplasty (PTRA) has been infrequently used in the treatment of children with hypertension due to renal artery stenosis. 29373648: BACKGROUND: Renal artery stenosis (RAS) in isolation or in conjunction with middle aortic syndrome (MAS) are important vascular causes of childhood hypertension. 2944021: Furthermore, the extremely low overall cure rate of 6% (4/67) suggests that renal artery stenosis due to atherosclerosis is rarely a sole cause of hypertension, but more likely is an atherosclerotic complication of essential hypertension that develops in patients who are cigarette smokers. 29578191: Background & objectives: Renal artery stenosis (RAS) is an important cause of severe hypertension in patients with chronic kidney disease (CKD). 2967149: Five of 24 non-insulin-dependent patients had unilateral renal artery stenosis but functional tests did not clearly suggest that renal artery stenosis was causing the hypertension in these cases. 29800631: However, when the tumor arises near the renal hilum, hypertension may also be secondary to renal artery stenosis, which can occur via several purported mechanisms. Classically, pheochromocytomas and paragangliomas result in hypertension secondary to an excess release of catecholamines. 2982541: Enalapril 10-40 mg per day orally has shown efficacy comparable to that of captopril in treating patients with mild, moderate, and severe hypertension, hypertension caused by renal-artery stenosis, and in congestive heart failure resistant to digitalis and diuretics. 30064025: CONCLUSIONS: The anomaly of supradiaphragmatic origin of the renal artery is rare but may be associated with renal artery stenosis, which may then result in hypertension. 3007062: Efficacy in treating congestive heart failure and hypertension secondary to renal artery stenosis has also been demonstrated for both angiotensin converting enzyme inhibitors. 30121120: BACKGROUND: Renal artery stenosis (RAS) is a leading cause of hypertension, renal failure, pulmonary edema, and loss of renal mass. 30430513: Resistant hypertension secondary to coexisting primary hyperaldosteronism and renal artery stenosis. 30791890: BACKGROUND: Renal artery stenosis is one of the secondary causes of pediatric hypertension. 3139898: Hypertension as a result of proximal renal artery stenosis has been described in patients with neurofibromatosis, but a review of the English language literature showed no familial incidence of renovascular lesions in association with neurofibromatosis. 31614781: Renal artery stenosis (RAS) induces renal ischemia and hypertension and leads to loss of kidney function, but whether RAS alters renal endogenous repair mechanisms, such as STCs, remains unknown. 31672102: CONCLUSIONS: NF1 vasculopathy is a rare condition that most often presents with hypertension due to renal artery stenosis. 32277359: Although renal artery stenosis and pheochromocytoma are well-known causes of HTN in NF1, this case demonstrates that HTN can be caused by AUK in patients with NF1. 32309529: Background: Renal artery stenosis (RAS) can lead to hypertension and renal failure. 32399343: Renal hypoperfusion from renal artery stenosis (RAS) activates the renin-angiotensin system, which in turn causes volume overload and hypertension. 32702156: Hypertension secondary to renal artery stenosis(RAS, 59.4%) or mid-aorta stenosis(MAS, 14.5%), heart failure(21.7%), claudication(21.7%) were leading clinical hints for interventions. 329938: Renal autotransplantation in the treatment of hypertension and uraemia due to renal artery stenosis. 33151345: MATERIALS AND METHODS: All patients 0-18 years of age who underwent CT angiography for evaluation of RAS as a cause of hypertension between January 2012 and May 2019 were identified for the study. 3336930: She had been treated for severe hypertension due to renal artery stenosis. 33826107: While renal artery stenosis (RAS) is considered one of the causes of hypertension with MMD, most hypertension causes remain unexplained. 34374838: BACKGROUND: Renal artery stenosis is an important cause of hypertension in children, accounting for 5-10% of cases. 34601043: CONCLUSIONS: In patients selected by clinical indicators and DUS, reaching a translesional systolic gradient <=10mmHg or reduced by at least 80% after angioplasty, promotes a high success rate for PTRA in hypertension due to FMD RAS. 34703193: Background: Renal artery stenosis is a common cause of hypertension in children; however, infectious causes of renal artery stenosis are rare. 34930129: Refractory hypertension secondary to renal artery stenosis with a honeycomb-like structure. 35014584: Hypertension was induced by renal artery stenosis. 35028279: Hypertension secondary to renal artery stenosis is typically managed with lifestyle and pharmacological interventions and less commonly with angioplasty or stenting, although exact treatment varies depending on the cause. 3511391: A number of variables, including status of the diseased native kidneys, steriod therapy, rejection, recurrence of original disease, activation of the renin-angiotensin system, sodium and calcium metabolism, and transplant renal artery stenosis may play a role in the etiology of hypertension after transplantation. 35288289: OBJECTIVES: Renal artery stenosis (RAS) is an uncommon cause of pediatric hypertension. 3555143: Renovascular hypertension is more common in hypertensive children than in hypertensive adults, and renal artery stenosis is second only to coarctation of the thoracic aorta as a cause of surgically correctable hypertension. 35687907: In conclusion, galangin attenuated hypertension, renin-angiotensin system activation, cardiorenal damage and oxidative stress induced by renal artery stenosis in rats. 35887726: RAS induces hypertension or reduces renal function. 35937747: This short report demonstrates an uncommon presentation of intracranial bleeding and sixth nerve palsy in a child with systemic hypertension due to long-standing unilateral renal artery stenosis of unknown etiology that resulted in contracture of the affected kidney and compensatory hypertrophy of the contralateral kidney. 36647988: Renal artery stenosis-induced HTN can occur in the presence of unilateral or bilateral narrowing and a solitary kidney with stenotic artery, which may subsequently lead to renal insufficiency (e.g., ischemic kidney disease) or pulmonary edema. 36780709: Differently, TAK patients had longer delay to diagnosis from the beginning of symptoms (p = 0.048), they presented more frequently with loss of pulses of large arteries (p = 0.0001), vascular bruits (p = 0.001), limb claudication (p = 0.003), myocardial infarction/angina (p = 0.03), and hypertension induced by renal artery stenosis (p = 0.001). 3690389: In renal artery stenosis severe enough to cause hypertension, angiotensin II maintains glomerular filtration rate (GFR) both in the initial high renin phase of hypertension and later when plasma levels are normal. 371469: The first episode of hypertension was caused by renal artery stenosis and was surgically corrected; the second was caused by a sizable pseudoaneurysm at the site of arterial anastomosis which was resected, and arterial continuity was successfully re-established. 37164809: Next, we present the case of a kidney transplant patient with well-controlled arterial hypertension with worsening secondary to renal artery stenosis and development of PRES. 37760104: Background: Moderate renal artery stenosis (50-70%) may lead to uncontrolled hypertension and eventually cause irreversible damage to renal function. 378492: Renal artery stenosis was an infrequent but significant cause of hypertension and was found in 10 of 29 arteriograms performed. 3895907: Subsequent follow-up has revealed chronic rejection or renal artery stenosis as a probable cause of hypertension for 11 of the 33 patients. 3899070: We used renal artery stenosis (two-kidney, one clip model) to produce hypertension associated with elevated plasma renin activity, and used cellophane wrapping of both kidneys (bilateral perinephritis model) to produce hypertension with normal renin activity. 390647: [Autotransplantation of the kidney in treatment of arterial hypertension caused by renal artery stenosis]. 3959261: Coarctations of the abdominal aorta are often associated with renal artery stenosis resulting in hypertension, which is commonly the presenting symptom. 400733: 18-OH-DOC was normal in 2 cases of hypertension due to renal artery stenosis, in 1 patient with nephrosclerosis, and in 1 patient with horseshoe kidney. 5015558: [Diagnosis and surgical treatment of renal artery stenosis leading to arterial hypertension]. 5178869: Hypertension secondary to renal artery stenosis; processes and principles. 5179472: Hypertension secondary to renal artery stenosis; a patient with renal artery stenosis. 5321025: Salt loading in hypertension due to renal artery stenosis. 5425276: It is concluded that experimental hypertension of renal origin or induced by DCA treatment can develop even though most of the sympathetic nervous system has been destroyed. Experimental hypertension in the rat, induced either by renal artery stenosis or by treatment with deoxycorticosterone acetate (DCA) developed maximally over a period of 8 weeks. 5443497: [2 cases of arterial hypertension caused by renal artery stenosis and solitary kidney]. 564075: These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis. 5646095: Results of surgery in hypertension due to renal artery stenosis. 5664628: [Arterial hypertension in a child caused by renal artery stenosis]. 5808212: Surgical treatment of hypertension secondary to renal artery stenosis. 5889121: [How can one verify the fact that renal artery stenosis is the cause of arterial hypertension?]. 5896841: Hypertension due to renal artery stenosis. 5909049: Renal arterial reconstruction in the treatment of hypertension due to renal artery stenosis. 5960988: [Arterial hypertension in a child due to a retroperitoneal tumor and renal artery stenosis]. 6064531: Surgical treatment of hypertension secondary to renal artery stenosis. 6097566: The serum converting enzyme activity (SCEA) was measured in 86 healthy individuals (1.44 +/- 0.82 u, mean +/- SD), 39 patients with essential hypertension (1.53 +/- 0.71 u), 7 patients with hypertension due to renal artery stenosis (1.76 +/- 0.77 u), 14 patients with chronic renal failure (2.10 +/- 0.57 u), 7 patients with renal failure and hypertension (2.62 +/- 0.35 u), 22 normotensive pregnant women (1.02 +/- 0.26 u) and 6 hypertensive pregnant women (1.1 +/- 0.3). 6114724: Because the mortality is low, we think that patients whose blood pressures are resistant to medical management should be examined carefully for renal artery stenosis as the cause of their hypertension. 6224607: Two clinical cases are described in which percutaneous transluminal dilatation (PTD) determined the correction of hypertension and renal hypoperfusion due to renal artery stenosis of the transplanted kidney. 6343903: The patient developed hypertension in the posttransplant period due to renal arterial stenosis. 6370156: Operative repair should be offered to patients with renal artery stenosis leading to unmanageable hypertension or renal dysfunction, but withheld from those with documented chronic rejection regardless of major arterial compromise. 6441543: High blood pressure (BP) was due to renal artery stenosis in 22 patients, to diffuse vascular lesions (mainly due to chronic rejection) in 13, to high-dose corticosteroid treatment in the early phase in 11, and to various or unknown causes in 10 patients. 6441547: Acute renal failure has been reported during captopril therapy of hypertension due to renal artery stenosis with a single kidney or bilateral renal artery stenosis. 6460123: The present study was done to investigate the relation between the prognosis and hypertension, especially hypertension due to renal arterial stenosis, atypical coarctation of the aorta and aortic regurgitation in patients with aortitis syndrome. 6507762: Ten patients had therapeutic renal artery reconstruction for isolated renal artery stenosis causing severe hypertension, nine patients had therapeutic renal artery reconstruction for severe hypertension combined with simultaneous aortic reconstruction, and nine patients had prophylactic renal artery reconstruction for renal artery stenosis combined with simultaneous aortic reconstruction. 6697556: Role of angiotensin II in the hypertension induced by renal artery stenosis. 6708226: Split renal vein renin studies and angiography showed that hypertension was caused by renal artery stenosis in 1 patient. 6806: Hypertension due to renal arterial stenosis was observed in 18 cases. 6976710: Evidence has accumulated from clinical experience that the hypertensive urogram is not a satisfactory screening test for differentiating hypertension due to renal artery stenosis from essential hypertension. 7037338: The effect of a continuous 12-hour infusion of a saline solution of the angiotensin II antagonist, [Sar1, Ile8] angiotensin II, on mean arterial pressure was studied in 11 conscious New Zealand white rabbits with hypertension induced by renal artery stenosis and contralateral nephrectomy, and in 11 normotensive control rabbits. 7164729: In order to prove that the functional activity of the renal artery stenosis is the real cause of high blood pressure, we have introduced to our Department a method of renal vein catheterization by which renin activity id determined. Therefore, before venturing surgery on renal vessels, with the aim to cure renovascular hypertension, it is necessary to prove that the angiographically verified changes really cause high blood pressure. 7344205: In addition, the prevalence of hypertension caused by renal artery stenosis appears quite low, in the range of 1-3%. Clinical experience indicates that hypertensive excretory urography is not a satisfactory screening examination to detect patients having hypertension due to renal artery stenosis. 7369807: In most cases the mechanism of hypertension is elevated blood renin levels secondary to associated renal artery stenosis. Coarctation or hypoplasia of the abdominal aorta is a rare cause of life-threatening hypertension. 7748147: We conclude that hypertension is one of the most common manifestation of Takayasu's arteritis in these patients and renal artery stenosis is the most common cause of hypertension. 7749342: Graft renal artery stenosis is one of the causes of hypertension after kidney transplantation. 7753462: These data indicate that chronic ACEi or recent ACEi medication reduces the effectiveness of ACEi renography in diagnosing hypertension due to a moderate renal-artery stenosis. 7938730: Particularly, Doppler US is the method of choice to study renal artery stenoses, which are among the most frequent causes of arterial hypertension in children, in both renal allografts and native kidneys. 805524: A child with neurofibromatosis and hypertension also demonstrated renal artery stenosis, the most common cause of hypertension in children with neurofibromatosis; abdominal coarctation, which has previously been described; and thoracic coarctation, which to our knowledge, has not been previously reported. 8090896: CONCLUSION: PTRA should be considered the first-line treatment for hypertension due to renal branch artery stenosis in fibromuscular disease. 8263891: Percutaneous transluminal renal angioplasty (PTRA) is an accepted method of treatment of hypertension resulting from renal artery stenosis. 8278881: The authors report 2 cases of patients with single functioning kidney and severe hypertension caused by renal artery stenosis who were treated by percutaneous transluminal angioplasty (PTA). 857106: In contrast, when risk factors are severe, operative management is undertaken only when hypertension is difficult to control or deterioration of renal function is thought to be secondary to the renal artery stenosis. 857317: In 4 female patients (0.5%) the hypertension was caused by oral contraceptives. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone-producing adenoma of the adrenal gland, and oral contraceptives). In 4 females (.5%) hypertension was caused by oral contraceptives. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone producing adenoma of the adrenal gland and oral contraceptives). 8720085: Ischemic nephropathy is defined as hypertension and a defect in renal function and/or loss of renal parenchyma caused by hemodynamic changes secondary to a renal artery stenosis. 8763016: A renal artery stenosis is definitely responsible for hypertension when the correction of stenosis has resulted in the cure of hypertension. [How to prove the role of renal artery stenosis as a cause of arterial hypertension]. 8766086: CONCLUSIONS: RAS is a potentially reversible cause of hypertension post-transplantation. 8768916: In conclusion, renal artery stent placement is a technically and clinically effective treatment for hypertension and azotemia due to renal artery stenosis. 8884105: Captopril-induced changes in ERPF can differentiate patients with native-kidney-induced hypertension from those with hypertension secondary to transplant renal artery stenosis in patients without evidence of rejection. 8979004: Renal artery stenosis is an important cause of hypertension and progressive renal insufficiency. 8983584: Renal artery stenosis (RAS) is the commonest secondary cause of hypertension and may result in renal ischaemia with resultant renal failure. 9064793: Renal artery stenosis is a potentially curable cause of hypertension. 920587: Systemic hypertension is the physiologic consequence of significant renal artery stenosis. 9308605: Renal artery stenoses can cause hypertension and renal failure. 9342100: Renal artery stenosis is an important and potentially curable cause of hypertension. 9426277: Twenty percutaneous transluminal renal angioplasties were performed on 16 children (mean age 8.7 years) with hypertension secondary to renal artery stenosis (RAS). 9807033: Renal transplant artery stenosis is a potentially treatable cause of post-transplant hypertension and several techniques such MRT angiography, Doppler sonography and conventional angiography are available. 9841602: BACKGROUND: Renal artery stenosis is a rare cause of hypertension. 10618564: BACKGROUND: Renal artery stenosis is a common disorder and is an established cause of hypertension and renal insufficiency. 15053272: This prospective study on assessment of renal insufficiency in pregnancy induced proteinuric hypertension was carried out on 104 cases, in Bangabandhu Sheikh Mujib Medical University (former IPGM&R), Dhaka during period of August 1997 to September 1998. 16298268: More frequent causes of hypertension were essential hypertension (26%), hypertension secondary to renal insufficiency (16%), and diabetes (10%). 3023736: Endogenous digitalis-like factors have been implicated in the adaptations that accompany renal insufficiency and in the pathogenesis of hypertension. 32972183: These are namely arterial hypertension, present in majority of patients after transplantation, frequently caused by persisting renal dysfunction of various degree and effect of immunosuppressants, post transplant diabetes mellitus, dyslipidaemia, which is our focus because chronic kidney disease is considered a coronary heart disease risk equivalent, and anaemia. 34285027: Renal impairment frequently results in hypertension due to increased activity of the tubuloglomerular feedback system and renin-angiotensin-aldosterone axis. 36026870: OBJECTIVE: Hypertension and kidney injury are two of the major adverse effects of the targeted anti-tumor drug apatinib, it was suspected that hypertension may be the result of renal dysfunction in some of the previous studies. 36264884: NEW & NOTEWORTHY The findings of our study are significant in several ways: 1 ) loss of an amino acid chaperone in the proximal tubule is sufficient to cause hypertension, 2 ) the results in global and proximal tubule-specific collectrin knockout mice support the notion that vascular dysfunction is required for salt sensitivity or that impaired renal tubule function causes hypertension but is not sufficient to cause salt sensitivity, and 3 ) our study is the first to implicate a role of collectrin in human hypertension. 6246305: [Cyclic 3,5-adenosine monophosphate content and calcium transport in the aorta in hypertension due to experimental renal insufficiency]. 7967780: RESULTS: Renovascular disease is an important cause of resistant hypertension and progressive renal insufficiency, particularly in the elderly population. 11206681: Hypertension due to renal artery occlusion in a patient with antiphospholipid syndrome. 13201450: Thromboendarterectomy for hypertension due to renal artery occlusion. 13510726: A case of hypertension due to renal artery occlusion. 1358485: Patterns of renal function in hypertension due to unilateral renal artery occlusion. 13998530: Recognition of renal artery occlusion as a cause for hypertension is resulting in a systematic search for the patient with a potentially curable vascular lesion. 14111744: HYPERTENSION DUE TO RENAL ARTERY OCCLUSION SIMULATING PRIMARY ALDOSTERONISM. 14413475: Hypertension caused by renal artery occlusion simulating primary aldosteronism. 21528765: We present the case of a 59-year old female patient with recently diagnosed arterial hypertension due to renal artery occlusion through intimal fibromuscular dysplasia. 25439445: Resistant hypertension due to unilateral renal artery occlusion as the first presentation of antiphospholipid syndrome. 25883516: OBJECTIVE: The objective of this study was to investigate the antihypertensive activity of naringin in RAO induced hypertension in rats. BACKGROUND: Renal artery occlusion (RAO) induced hypertension is a major health problem associated with structural and functional variations of the renal and cardiac vasculature. 27882189: CASE REPORT: A 54-year-old woman affected by paranoid schizophrenia with a history of hypertension and chronic renal failure due to renal artery occlusion was treated by endovascular recanalization and stent placement that resulted in improvement of renal function and control of hypertension. 5912374: The surgical relief of hypertension due to renal artery occlusion. 1032446: Hypertension due to renal infarction. 13172514: Nephrectomy in hypertension due to renal artery infarction with superinfection of streptococcal endocarditis by fungus. 13702297: Hypertension due to renal infarction: report of a case. 16877969: CONCLUSION: Kidney infarction is a rare cause of hypertension, usually associated with renal artery lesions. 21431897: Hypertension was considered secondary to renal infarction caused by paradoxical embolism through PFO. 35509677: Self-limited Hypertension Due to Kidney Infarction. 4564096: Role of the kidney in hypertension due to renal infarction in the rat, determined by renal transplantation. 5701458: [A case of arterial hypertension caused by kidney infarction]. 5771841: Renal infarction as cause of hypertension developing in patients after corrective surgery for renal artery stenosis. 6111849: Cerebral aneurysms were induced in rats treated with unilateral ligation of the common carotid artery and hypertension produced by renal infarction with or without beta-aminopropionitrile, one of the lathyrogens. In this experiment, cerebral aneurysms developed more frequently than in the previous experiments in which hypertension induced by deoxycorticosterone and salt had been used. 6398333: It is therefore suggested that hypertension due to renal infarction, unlike that caused by fibromuscular dysplasia, may be managed by prolonged medical treatment. 796491: Role of the kidney in the development and maintenance of hypertension caused by renal segmental infarction in the rat. 8367004: The pathophysiology of hypertension secondary to renal infarction is discussed. 9732840: [Arterial hypertension secondary to renal infarction in primary antiphospholipid syndrome]. 13328693: [Hypertension due to renal ischemia]. 13617842: Unilateral renal ischemia as a cause of hypertension. 13619203: [Ion exchange resins in hypertension induced by renal ischemia in rats]. 13775175: Hypertension secondary to unilateral renal ischemia. 13809202: On the occurrence of vascular lesions in the kidneys of dogs with hypertension due to renal ischemia. 13969548: [Electrocardiographic study of experimental arterial hypertension due to renal ischemia in the rabbit]. 14023915: Hypertension due to primary renal ischemia: a correlation of juxtaglomerular cell counts with clinicopathologic finding in 25 cases. 14023916: Hypertension due to primary renal ischemia: a correlation of juxtaglomerular cell counts with clinicopathological findings in twenty-five cases. 14062876: STUDIES ON SEGMENTAL RENAL ISCHEMIA IN THE ETIOLOGY OF HYPERTENSION. 14104412: STUDIES ON SEGMENTAL RENAL ISCHEMIA IN THE ETIOLOGY OF HYPERTENSION. 14209384: HYPERTENSION DUE TO RENAL ISCHEMIA. 14301255: [AORTOGRAPHY AND SELECTIVE RENAL ARTERIOGRAPHY IN DIAGNOSIS OF HYPERTENSION DUE TO UNILATERAL RENAL ISCHEMIA]. 14419871: Renal ischemia as a cause of hypertension. 14475878: [Apropos of 3 cases of hypertension caused by renal ischemia]. 14482964: [The diagnosis and treatment of hypertension due to unilateral renal ischemia]. 14634967: Renal ischemia as cause of hypertension in dogs opened a new chapter in the connection between kidney circulation and blood pressure elevation. 16105047: BACKGROUND: Cellophane wrapping of the kidneys (Page kidney) induces perinephrits and hypertension, assumed to be due to renal ischemia resulting from parenchymal compression by the fibrous hull surrounding the kidneys. 16490915: The central proposition of both papers was the same: Renal ischemia causes persistent hypertension. 16824832: The consequences of renal ischemia are neuroendocrine activation, hypertension, and renal insufficiency that can potentially result in acceleration of atherosclerosis, further renal dysfunction, myocardial infarction, heart failure, stroke, and death. 1685246: Changes in alpha 2-adrenoceptors on vascular smooth muscle and neural membranes following hypertension induced by renal ischemia. 19312072: Experimental Hypertension Induced by Renal Ischemia: Harvey Lecture, May 19, 1938. 19475351: The hypertension is due to renal ischemia. 19870597: It is also in agreement with the work of Page (8), and of Collins (9), who showed that in dogs excision of the extrinsic renal nerves alone does not prevent experimental hypertension due to renal ischemia. 19870681: THE EFFECT OF SECTION OF ANTERIOR SPINAL NERVE ROOTS ON EXPERIMENTAL HYPERTENSION DUE TO RENAL ISCHEMIA. 19870955: This procedure did not interfere with the development of hypertension produced by renal ischemia. There was no significant difference between the levels of hypertension due to renal ischemia in animals with both carotid sinuses previously excised and in those with both carotid sinuses intact. The carotid sinus has no demonstrable influence upon hypertension caused by renal ischemia, although in such animals it probably plays the same part in the regulation of blood pressure as it does in normal animals (7). In one of three animals with hypertension due to renal ischemia, in which the elevated blood pressure had gradually subsided, there was a slight and only temporary reelevation of pressure after excision of both carotid sinuses. THE EFFECT OF EXCISION OF THE CAROTID SINUSES ON EXPERIMENTAL HYPERTENSION PRODUCED BY RENAL ISCHEMIA. 19871029: THE DEPRESSOR EFFECT OF SPLENO-RENO-PEXY ON HYPERTENSION DUE TO RENAL ISCHEMIA. 19871059: THE ETIOLOGY OF HYPERTENSION DUE TO COMPLETE RENAL ISCHEMIA. 20645250: These heavily calcified plaques grow into the lumen and can cause significant stenoses, leading to malperfusion of the lower limbs, visceral ischaemia or hypertension due to renal ischaemia. 22477301: These heavily calcified plaques grow into the lumen and can cause significant stenoses, which may lead to malperfusion of the lower limbs, visceral ischemia or hypertension due to renal ischemia. 22788095: The prototype hypertension caused by renal ischaemia is renal artery stenosis. 27227941: In addition, hypertension secondary to renal ischemia and activation of renin-angiotensin-aldosterone system may also occur. 367458: Hypertension was induced by renal ischemia using Goldblatt's technique. 4353885: Renin-angiotensin system in human hypertension due to segmental renal ischemia. 4541540: Seven cases of hypertension due to segmental renal ischemia. 4737133: [7 cases of hypertension caused by renal segmental ischemia]. 5525130: Difficulties in the evaluation of hypertension secondary to renal ischemia. 6826962: The development of hypertension secondary to renal ischemia that can occur as a complication of certain types of aneurysmal disease is well recognized. 8203370: We report a case of hyponatremia, polyuria-polydipsia, hypokalemia, nephrotic syndrome, and hypertension caused by unilateral renal ischemia, and the resolution after nephrectomy of the ischemic kidney. 841806: This is a report of hypertension caused by stenosis of a segmental renal artery and cured by simple ligation of the stenotic artery. Hypertension secondary to segmental renal ischemia caused by segmental renal artery stenosis has been relieved by nephrectomy, partial nephrectomy, excision of atrophic segments, or repair of the segmental vessels. 844262: Blood pressure and plasma renin activity were studied after bilateral nephrectomy in groups of rats with hypertension caused by unilateral renal ischaemia with the opposite kidney left intact. 847859: Major complications include rupture or thrombosis of the renal artery, and hypertension due to renal ischemia; the latter is best diagnosed by renin determination in renal venous blood collected by selective catheterization. 8919222: Thus, the hypertension in our patient was probably due to renal ischemia extrinsically compressed by a non-functioning retroperitoneal paraganglioma (Page kidney). 916991: [Reversible hypertension caused by local renal ischemia]. 9877520: These data show that NO plays a key role in the maintenance of renal function during the evolution of hypertension induced by chronic renal ischemia. 10957653: PURPOSE: This retrospective review describes the surgical management of consecutive patients with severe hypertension and ischemic nephropathy due to atherosclerotic renovascular disease. 11338095: Atheromatous renovascular disease (ARVD) is a common cause of hypertension and chronic renal failure (CRF). 11416740: Renovascular disease is an important cause of hypertension in children and is associated with considerable morbidity and mortality risks. 11771866: CONCLUSIONS: Although symptoms are relatively uncommon. renovascular disease is a frequent cause of severe hypertension in childhood. 11956860: In patients with neurofibromatosis, hypertension is mainly caused by renovascular disease, whereas in tuberous sclerosis (TSC) reasons for hypertension are renoparenchymal lesions, such as angiomyolipoma or cysts. We report on a girl with TSC and hypertension due to unilateral renal artery stenosis associated with aneurysmatic changes of internal carotid artery. 12046025: Atherosclerotic renovascular disease (ARVD) commonly causes renal failure and hypertension and is accompanied by high cardiovascular comorbidity and mortality. 12087578: BACKGROUND: Renovascular disease is a common cause of renal impairment and hypertension, particularly in the older population. 12616031: ARVD is a common cause of hypertension and chronic renal failure (CRF), and it is one of the most common renal diagnoses in elderly patients accepted on to dialysis programmes with end-stage renal failure (ESRF). 1290088: The assessment of the renal arteries is particularly important in the detection of a renovascular cause of the arterial hypertension. 13126725: Hypertension resulting from unilateral renal vascular disease and its relief by nephrectomy. 1329461: Renovascular disease, one of the most common secondary causes of hypertension, is usually the result of atherosclerosis in older patients and the result of fibromuscular dysplasia in younger patients. 13872876: Renal vascular disease as a cause of hypertension. 13900415: [Arterial hypertension caused by renal vascular disease in children]. 14023143: Renal-vascular disease as a cause of hypertension. 14228117: HYPERTENSION DUE TO UNILATERAL RENAL VASCULAR DISEASE. 14974369: Renovascular etiology of hypertension may be suggested by abrupt onset of hypertension, resistant and malignant hypertension or recurrent pulmonary edema of unknown etiology. 14978868: The confirmation of a renovascular disease as the cause of a child's hypertension is based on the elevation of the peripheral plasma renin level, the captopril tests, possibly the renal vein renin determinations and the imaging studies. 16359595: The child developed hypertension due to renal vascular disease. 16990369: We report three infants with severe, early hypertension due to unilateral renovascular disease, whose cardiovascular changes, or polycythaemia, or both, indicated they had been affected as fetuses. 17974355: Regular diagnostic procedures confirmed the renovascular aetiology of the existing hypertension, and percutaneous transluminal angioplasty of the narrow segment of the right upper renal artery made the necessary replacement therapy possible. 18320238: However, secondary causes of hypertension such as renal parenchymal diseases, congenital abnormalities and renovascular disorders still remain the leading cause of pediatric hypertension, particularly in children under 12 years old. 1833057: In elderly patients with uncontrolled hypertension or increasing azotemia caused by renovascular disease, hepatorenal or splenorenal bypass procedures are helpful alternatives. 18440428: Renovascular disease is an uncommon but important cause of hypertension in children. 19595533: Atherosclerotic renovascular disease (aRVD) is an increasingly recognized cause of severe hypertension and declining kidney function. 19685045: BACKGROUND: Renovascular disease is an uncommon but important cause of hypertension in children. 19856000: Renovascular disease (RVD) is an important cause of hypertension in children, as it often is amenable to potentially curative treatment. 20108080: In children, up to 10% of the cases of arterial hypertension may be caused by a renovascular disease. 20924335: Atherosclerotic renovascular disease is an increasingly recognized cause of severe hypertension and declining kidney function. 21118836: Flash pulmonary edema (FPE) is a severe renovascular disease that leads to acute recurring pulmonary edema and acute systemic hypertension. 21326543: As a result, screening for renovascular causes of hypertension is rarely done. 22330627: AIM: Renovascular disease may cause arterial hypertension and decreases renal function, which both impair endothelial function. 24522941: Renovascular disease is a cause of hypertension in 10 % to 15 % of prepubertal children. Interventions to address hypertension and causes of renovascular disease continue to advance. 26430136: Renovascular disease (RVD) can lead to hypertension and chronic kidney disease (CKD). 2686992: Thus the combination of the two methods seems to be a reasonable diagnostic approach to hypertensive patients with the aim of selecting those with curable hypertension due to renal vascular disease. 30642276: Acting upon literature evidence suggesting renovascular disease as a cause of IDH, we referred her to an interventional radiologist for evaluation of the renal arteries. 31045658: PURPOSE OF REVIEW: Renovascular disease (RVD) remains an important cause of hypertension and renal dysfunction. 31061719: This suggested a renovascular etiology of hypertension causing the initial presentation of acute heart failure. 3160766: We conclude that the RVRR is of no prognostic value in the surgical treatment of hypertension due to unilateral renovascular disease. 3545608: A nine-year-old child was referred for a routine renal dynamic study to detect a renal and/or renovascular cause for hypertension. 4738846: [Case of juvenile hypertension caused by unilateral renovascular disease and contralateral hypoplastic kidney]. 4959458: Hypertension due to unilateral renal vascular disease. 6249611: In childhood hypertension due to renovascular disease or pyelonephritic scarring peripheral plasma renin is increased. 6419807: The results of the investigations of all patients who underwent renal arteriography for hypertension due to renovascular disease over a three and a quarter year period prior to January 1st 1981 are reviewed and discussed. 693862: Renovascular disease often leads to hypertension in children. 7103302: These two cases stress the problem of the respective responsibility of both pheochromocytoma and renovascular disease in hypertension genesis. 7553835: Although renovascular disease may cause hypertension and/or renal insufficiency, it may also occur in the absence of the usual clinical markers that suggest renovascular hypertension. 7667614: Renovascular hypertension (RVH) remains a leading cause of potentially curable hypertension. Advances in percutaneous transluminal renal angioplasty (PTRA) have renewed interest in developing better noninvasive screening tests for identifying patients with potentially correctable hypertension or renal impairment due to renovascular disease caused by either fibromuscular dysplasia (FMD) or arteriosclerosis. 7743162: Renal vascular disease as a cause of hypertension. 7967780: RESULTS: Renovascular disease is an important cause of resistant hypertension and progressive renal insufficiency, particularly in the elderly population. 8351926: Under the current conditions of improved pharmacological therapy of arterial hypertension there is a danger that the physician may overlook considering the possibility of underlying renovascular causes for the hypertension. 8404957: This work suggests that a screening investigation with a low radiation burden can be carried out at most institutions; if the investigation is positive, there will be a high index of suspicion that renovascular disease is the cause of the hypertension. In children over 1 year of age, renal disease is the commonest cause of hypertension. 8586940: Renovascular disease is the leading cause of surgically-curable arterial hypertension and one of the few cause of reversible chronic renal failure, but its exact prevalence remains unknown. 8723806: Renovascular disease is a frequent cause of severe hypertension in children and may result in significant morbidity or mortality. 908239: With modern specific diagnostic studies like isotope renography, angiotensin-infusion-test, peripheral venous renin assay, comparative assays of the renin activity in the individual renal veins, and angiography the renal and renovascular causes for hypertension become more and more significant. When it has been shown that the hypertension is caused by a constriction of the renal arteries, instant operative therapy is indicated. 9203196: Renovascular disease is an important cause of remediable hypertension in childhood. 9423201: Renovascular disease is an important cause of hypertension in children because it is potentially treatable by surgical or angioplasty techniques. 9536103: The anatomic presence of atherosclerotic RVD as a threat to renal function has become a more pressing concern than that of hypertension secondary to RVD. 9568855: BACKGROUND: Renovascular disease is the most frequently encountered secondary cause of hypertension and is one of the few potentially reversible causes of chronic renal failure. 18802431: Hypertension due to a renin-secreting juxtaglomerular cell tumor. 19403544: Most secrete renin, causing hypertension and hypokalemia due to secondary hyperaldosteronism. 19663191: SLE activity enhancement was associated with renal dysfunction and growth of plasmic renin leading to AH resultant from activation of the renin-angiotensin-aldosteron system (RAAS), sympathico-adrenal system (SAS) and suspended by endothelial dysfunction. 20515792: These studies with decoy peptide including the \handle\ sequence have focused on the association of the (pro)renin receptor and prorenin in the pathogenesis of diabetes and hypertension. 2189028: A 41 year old man with severe hypertension due to a renin-secreting retroperitoneal leiomyosarcoma is described. 22681982: In order to explore this, we used RenTgKC mice overexpressing renin into the liver, leading to an increased plasma angiotensin II and thus induction of severe hypertension, and AS mice overexpressing aldosterone synthase (AS) in cardiomyocytes which have a doubled intracardiac aldosterone concentration. [Hypertension-induced fibrosis: a balance story]. 25611839: Here we present the first reported case in Argentina of a 21-year-old patient with arterial hypertension and hypokalaemia due to a renin-secreting juxtaglomerular cell tumour, which was diagnosed after seven years of development. Juxtaglomerular cell tumour as a curable cause of hypertension: case presentation. 3028117: These findings have led us to speculate that aberrant tissue renin, angiotensinogen gene expression(s) or abnormalities in the regulation of the local renin-angiotensin system may result in such cardiovascular disorders as vasospasm, hypertension and cardiac hypertrophy. 30797056: The renin level was elevated, likely indicating a secondary cause for the HTN. 34419773: During the late phase of severe COVID-19, compensatory secretion of renin and ACE enzymes are subsequently upregulated, leading to inflammation, hypertension and thrombosis, which further sustain ACE2 and ADAM17 upregulation. 35904033: Yet, in particular, for the treatment of hypertension, the number of patients with uncontrolled hypertension continues to rise, either due to patient noncompliance or because of the significant renin rises that may, at least partially, overcome the effect of RAS blockade (RAS escape). 4296172: Hirano J, Masson GM: Effects of dietary sodium on hypertensive disease caused by renin. 490476: Eleven cases of hypertension due to a renin secreting renal tumor have been reported since 1967. 6060417: Hypertension due to a renin-secreting renal tumour. 6202006: Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. 762618: Hypertension secondary to a renin-producing juxtaglomerular cell tumor. 11593508: OBJECTIVE: To determine the function of, in vivo, renin and its role in the pathogenesis of hypertension. 1186102: This may or may not indicate a role for renin in the cause of spontaneous hypertension. 1209189: Arterial hypertension due to a renin-producing renal carcinoma. 1316398: Such transgenic work has also shown that the renin gene can cause hypertension. 1325502: OBJECTIVE: To evaluate the significance of locally synthesized renin in the pathogenesis of hypertension, we investigated modulation of the renin gene expression in extrarenal tissues. 1396991: These results suggest that rh-renin can stimulate the rat renin-angiotensin system, thereby producing hypertension. 1405319: Elevated levels of active renin in renal cysts may be linked to the pathogenesis of hypertension in ADPKD. 15225806: Mice lacking the Vitamin D receptor (VDR) have elevated production of renin and angiotensin (Ang) II, leading to hypertension, cardiac hypertrophy and increased water intake. 17083061: Genetic clamping of renin gene expression induces hypertension and elevation of intrarenal Ang II levels of graded severity in Cyp1a1-Ren2 transgenic rats. 1813878: Participation of catecholamines and renin in the pathogenesis of hypertension in KTP is not dominant. 18653711: Overexpression of renin in Ren2 rats results in hypertension, insulin resistance, and cardiovascular and renal damage. 1875502: Elevated plasma renin activity in the renal vein of the affected side and biochemical investigations demonstrated that the resected segment of the renal cortex was the source of the renin leading to hypertension by activation of the renin-angiotensin-aldosterone system. 21239248: These include the isolation of cDNA and genomic clones for interspecific renin genes, the demonstration of primary expression in tissues where only renin activity data were previously reported, and, more recently, the development of tools to examine specifically the mechanisms of renin transcription and regulation, and to define the role played by the renin-angiotensin system in the pathogenesis of hypertension. 22775989: Renin is the rate-limiting step of the renin-angiotensin system (RAS) and can induce hypertension and cardiovascular diseases (CVDs) through the over-activated renin-angiotensin-converting enzyme (ACE)-angiotensin (Ang) II-Ang II type 1 receptor (AT(1)R) axis. 2544716: These findings suggest that hypertension secondary to increased tumour associated renin production is a feature of congenital mesoblastic nephroma. 26132761: DISCUSSION: Reninoma is a rare juxtaglomerular cell tumour (JGCT) producing excessive amounts of renin resulting in severe hypertension. 28695400: Current active investigations are aimed at elucidating the mechanisms regulating renin in the distal nephron segments and understand its role in the pathogenesis of hypertension. 31551925: Together with altered vascular reactivity to Ang peptides, the iRAS causes hypertension, renal damage and secondary changes in the neurohumoral control of the maternal circulation and fluid and electrolyte balance, which contribute to the pathophysiology of preeclampsia. Experimental studies in animals have shown that placental renin, when released into the maternal circulation, can cause hypertension. 3531004: Modulation of kidney renin messenger RNA levels during experimentally induced hypertension. 4812744: Interrelationship of volume and renin in the pathogenesis of hypertension. 57338: Slowly acting mechanisms, probably initiated by hypersecretion of renin, may be responsible for the hypertension. 598208: The interrelation between the two renin systems in NaCl hypertension could not be evaluated, since exogenous factors (Na), which interfere with the kidney renin system, play a considerable role in the pathogenesis of NaCl hypertension. 6266727: It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. 6343641: Since the renin content in the kidney distal to the shunt was higher than in the kidney of the sham operated rats and since there was a positive correlation between renal renin content and blood pressure in hypertensive animals, it is suggested that an activation of the renin angiotensin system in the ipsilateral ischemic kidney is responsible for hypertension. 6357559: Whilst these studies suggest therefore that renin taken up by the arterial wall is an important determinant of blood pressure, they provide no evidence that accumulation of renin locally produces hypertension in the presence of normal or low plasma renin activity. 6400106: However, we have no evidence for the hypothesis that selective accumulation of renin in the resistance vessel walls causes hypertension when circulating levels of renin are normal. 7599751: The etiology of hypertension in nonrenovascular unilateral renal disease--two cases of renin induced hypertension in congenital renal dysplasia. 7721420: A survey of the medical literature revealed a number of clinical cases in which hypertension was caused by renin-secreting pulmonary tumors and a fairly widespread occurrence of immunoreactive renin in banked pulmonary tumors of diverse origin. 8398651: Hypertension secondary to renin-secreting juxtaglomerular cell tumor: case report and review of 38 cases. 9746116: Renin- and Ang II-induced chronic hypertension are identically sustained by very small increases in plasma Ang II. 31902262: Here, the effects of CGA on beta-amyloid protein (Abeta)-induced cell models were investigated, aiming to provide a direction for Abeta-induced AD. 31922154: This new analytical strategy allows the direct detection and identification of all possible Asp, isoAsp, and Ser stereoisomers in Abeta, and may contribute to a better understanding of the pathogenesis of AD. 31969500: Methods: After estradiol (E2) treatment in Abeta-induced AD cell model, reactive oxygen species (ROS), TXNIP, and apoptosis levels were detected. 32023927: Genetic studies, biochemical data, and animal models have suggested that Abeta is responsible for the pathogenesis of AD (i.e., the amyloid hypothesis). 32212051: Taken together, the results of this meta-analysis clarified circulating autoantibodies to Abeta levels in AD patients and suggested that endogenous IgG and IgM-class antibodies to Abeta may play a role in the pathogenesis of AD. 32341098: Beta-amyloid (Abeta) is thought to play a critical role in Alzheimer's disease (AD), and application of soluble oligomeric forms of Abeta produce AD-like impairments in cognition and synaptic plasticity in experimental systems. 32355946: In this review, emerging evidence highlights the importance of the Abeta cascade hypothesis and indicates a significant role of Abeta and its aggregates as biomarkers in the pathogenesis of AD; we present an up-to-date summary on Abeta-based biosensor systems. 32375443: Conclusion: The inhibitor of mTOR rapamycin can improve the cognitive dysfunction of mice with AD induced by Abeta(1-42) and reduce deposition of Abeta(1-42) in the hippocampus, and the possible mechanism is rapamycin depressing the phosphorylation of mTOR as the same as Up-regulation the expression level of Homer3. 32377164: A beta plays an important role in the pathogenesis of AD. 32430275: The deposition of Abeta in the brain due to impaired Abeta clearance is considered as an important cause of AD. 32479003: The aim of this study was to investigate the proximate and functional composition of P. eryngii, and evaluate the cognitive effects of low (LPE), medium (MPE), and high (HPE) P. eryngii dosages in an Abeta-induced Alzheimer's disease C57BL/6J mouse model. Effect of the King Oyster Culinary-Medicinal Mushroom Pleurotus eryngii (Agaricomycetes) Basidiocarps Powder to Ameliorate Memory and Learning Deficit in Ability in Abeta-Induced Alzheimer's Disease C57BL/6J Mice Model. Effect of the King Oyster Culinary-Medicinal Mushroom Pleurotus eryngii (Agaricomycetes) Basidiocarps Powder to Ameliorate Memory and Learning Deficit in Ability in Abeta-Induced Alzheimer's Disease C57BL/6J Mice Model.One of the major causes of Alzheimer's disease (AD) is oxidative stress, which accelerates beta-amyloid peptide (AP) plaque and neurofibrillary tangle accumulation in the brain. 32496898: Abeta (1-42) was injected intracerebroventricularly to healthy male mouse to induce AD-like behavioral manifestations on Day-1 (D-1) of the experimental protocol. 32531337: Ion channel formation by N-terminally truncated Abeta (4-42): relevance for the pathogenesis of Alzheimer's disease. 32556928: As AD develops and progresses, mitophagy diminishes insoluble Abeta, and mitochondrial dysfunction seems to be a determining factor in the pathogenesis of AD. 32587293: Such findings strongly implicate Abeta in the altered iron handling and increased oxidative stress observed in AD pathogenesis. 32592731: Activation of cannabinoid receptor 2 protects rat hippocampal neurons against Abeta-induced neuronal toxicity.Alzheimer's disease (AD) is a dementing, neurodegenerative disorder characterized by increased accumulation of beta-amyloid peptides (Abeta), degeneration of hippocampal neurons and the gradual development of learning and memory deficits. 32599696: We also summarize the characteristics and pathogenicity such as the size, morphology and cytotoxicity of dimers, trimers, Abeta*56 and spherical oligomers, and suggest that Abetaos may play a different role at different phases of AD pathogenesis, resulting in differential consequences on neuronal synaptotoxicity and survival. 32790274: Synthetic and biophysical studies on the toxic conformer in amyloid beta with the E22Delta mutation in Alzheimer pathology.The toxic conformer of the 40- or 42-mer-Abeta (Abeta40, Abeta42) with a turn at positions 22 and 23 plays a role in oligomer formation, leading to neurotoxicity as part of the pathogenesis of Alzheimer disease (AD). 32827351: DISCUSSION: Refining the molecular mechanisms connecting tau, Abeta, and apoE with cerebrovascular pathologies is critical for greater understanding of AD pathogenesis and establishing effective therapeutic interventions for the disease. 32950104: Melatonin Induction of APP Intracellular Domain 50 SUMOylation Alleviates AD through Enhanced Transcriptional Activation and Abeta Degradation.The amyloid precursor protein (APP) intracellular domain (AICD) is implicated in the pathogenesis of Alzheimer's disease (AD), but post-translational modification of AICD has rarely been studied and its role in AD is unknown. 33665647: Despite a wealth of experimental and genetic evidence implicating both Abeta and tau in the pathogenesis of AD, the precise molecular links between these two pathological hallmarks have remained surprisingly elusive. Here, we review emerging evidence for a critical nexus among Abeta, tau, and the lysosomal protease cathepsin D (CatD) that we hypothesize may play a pivotal role in the etiology of AD. Future research into these novel mechanistic links among Abeta, tau and CatD promises to expand our understanding of the etiology of AD and could potentially lead to novel therapeutic approaches for combatting this devastating disease of brain and mind. 33912008: Evidence implicates elevated soluble oligomeric Abeta as one of the primary triggers during the prodromic phase leading to AD, effected largely via hyperphosphorylation of the microtubule-associated protein tau. 33953832: Oral Administration of Gintonin Protects the Brains of Mice against A beta -Induced Alzheimer Disease Pathology: Antioxidant and Anti-Inflammatory Effects. 34214643: Moreover, the concurrence of neuroinflammation and Abeta dyshomeostasis, which by reciprocal interactions drive the vicious cycle of neurodegeneration, contradicts Abeta as the primary trigger of AD. 34272583: Our data indicate an essential role for intracellular prion-like Abeta and its synaptic spread in the pathogenesis of AD. 34356865: AD has two significant pathological hallmarks: extracellular senile plaques composed of amyloid beta-peptide (Abeta) and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein, and the aggregation of Abeta, which starts in earlier stages, is usually claimed to be the primary cause of AD. 34371202: Can platelet activation result in increased plasma Abeta levels and contribute to the pathogenesis of Alzheimer's disease? 34435574: Moreover, the mechanism of action of L7 on improving Abeta-induced AD was preliminarily investigated, and the results uncovered that the neuroprotective effects of L7 was might exerte via intervening Abeta-induced pyroptosis through NLRP3-caspase-1-GSDMD axis and ameliorating neuronal apoptosis by mitochondrial apoptosis pathway. 34608607: However, intermediate soluble oligomers of Abeta are now recognized as initiators of the pathogenic cascade leading to AD. 34655726: Genetic studies, biochemical data, and animal models have suggested that Abeta is a critical species in the pathogenesis of AD. 34672433: CONCLUSIONS: Our findings confirmed that 6D11 has a therapeutic effect in APP/PS1 transgenic AD mouse model and Abeta-induced AD cell model, and the effect exerted via increase of neurogenesis and cell differentiation by transduction of Abeta peptide signal. 34810230: Therefore, the predominant processing of C99 and enrichment of Abeta in late endosomes and lysosomes may be critical events in the molecular cascade leading to AD. 34946712: The complete characterization of the copper complexes made with phenHH, phenHGH and H'phenH' is reported, along with the ability of ligands to remove Cu from Abeta, and to prevent the formation of reactive oxygen species catalyzed by Cu and Cu-Abeta, including in presence of zinc, the second metal ions important in the etiology of Alzheimer's disease. 35098860: The mouse model of AD and the cell model induced by Abeta were established. 35181336: CBD was found to alleviate the progression of Abeta-induced AD but not tau protein-induced AD or alpha-syn-induced Parkinson's disease. 35292372: Abeta (1-42) was injected into the hippocampus of the animals to induce AD-like pathology. 35452628: We found that: 1) Recognition memory impairment in Abeta-induced Alzheimer's disease model was associated with the reduction in TREM2 which induced microglial activation and neuroinflammation; 2) Exercise activated the TREM2 pathway, which was necessary for inhibiting microglial activation and neuroinflammation, leading to improved recognition memory in the Alzheimer's disease model. 35453040: Amyloid beta peptide (Abeta) is produced through the proteolytic processing of amyloid precursor protein (APP), and Abeta accumulation in the brain is proposed to be an early toxic event in the pathogenesis of AD. 35786817: CONCLUSION: The tau deletion mutation significantly improved the synaptic damage caused by Abeta, and tau protein played an indispensable role in the synaptic dysfunction caused by Abeta, suggesting that Abeta and tau have close interactions in the pathogenesis of AD. 35865745: Opinions are divided about whether there is enough evidence to definitely consider Abeta as a causative substance of AD. 35956985: Anti-Inflammatory Activity of 4-(4-(Heptyloxy)phenyl)-2,4-dihydro-3 H -1,2,4-triazol-3-one via Repression of MAPK/NF-kappaB Signaling Pathways in beta-Amyloid-Induced Alzheimer's Disease Models. In this study, the neuroprotective effects of 4-(4-(heptyloxy)phenyl)-2,4-dihydro-3 H -1,2,4-triazol-3-one (W112) against beta-amyloid (Abeta)-induced AD pathology and its possible mechanism were explored both in vitro and in vivo. The results showed that W112 exhibits a neuroprotective role against Abeta-induced cytotoxicity in PC12 cells and improves the learning and memory abilities of Abeta-induced AD-like rats. 36074939: According to the amyloid cascade hypothesis, Abeta is the critical early initiator of AD pathogenesis. 36120034: More importantly, 1c could ameliorate the impaired learning and memory in Abeta-induced AD mice. 36200197: Flavonoids from Stems and Leaves of Scutellaria baicalensis Georgi Improve Composited Abeta-induced Alzheimer's Disease Model Rats' Memory and Neuroplasticity Disorders. 36233130: Abeta and its isoforms are important factors in the Alzheimer's disease (AD) pathogenesis. 36321205: Hippocampal injection of Abeta was used to induce AD. Abeta induced AD by Abeta plaques formation and increasing step-through latency time. 36399096: Modulation of the effect of the epsilon4 alleles by TOMM40 and APOC1 variants indicates the potential genetic mechanism of differential roles of Abeta and tau in AD pathogenesis. 36399277: Using cellular bioassays for prions in postmortem samples, we found that both Abeta and tau proteins misfold into prions leading to AD, which is either a sporadic or familial dementing disorder. Abeta and Tau Prions Causing Alzheimer's Disease. 36549596: Naringin enhances long-term potentiation and recovers learning and memory deficits of amyloid-beta induced Alzheimer's disease-like behavioral rat model. However, the effect of naringin in AD caused by Abeta has not been clearly studied, and there are few studies on the electrophysiological aspect. 36809522: The present research aimed to investigate the possible protective effect of RJ on learning and memory in a rat model of Abeta-induced AD. 36856542: The exact pathogenic mechanisms linking Abeta to AD pathogenesis remain however not fully understood. 36899831: Of note, miRNA-146a-5p was exclusively dysregulated in the Abeta-induced AD model. 37179042: Minocycline effects on memory and learning impairment in the beta-amyloid-induced Alzheimer's disease model in male rats using behavioral, biochemical, and histological methods. This study investigated the effect of minocycline on the changes in learning and memory functions, activities of blood serum antioxidant enzymes, neuronal loss, and the number of Abeta plaques after AD induced by Abeta in male rats. 37264159: Extensive studies indicate that beta-amyloid (Abeta) aggregation is pivotal for Alzheimer's disease (AD) progression; however, cumulative evidence suggests that Abeta itself is not sufficient to trigger AD-associated degeneration, and whether other additional pathological factors drive AD pathogenesis remains unclear. 37342418: However, whether Abeta itself is a key toxic agent in AD pathogenesis and the precise mechanism of Abeta-elicited neurotoxicity are still debated. 37372012: Reactive oxygen species (ROS) and lipid peroxidation (LPO) assays were performed and showed that the levels of ROS and LPO were markedly reduced in the caffeic acid-treated mice, as compared to Abeta-induced AD mice brains. 37401257: However, the histidine behaviors of Abeta(1-42) are unconfirmed, which is the key point to understanding the pathogenesis of Alzheimer's disease. 37849639: Within the framework of the ACH2.0, AD is triggered by amyloid-beta protein precursor (AbetaPP)-derived intraneuronal Abeta ( i Abeta) and is driven by i Abeta produced in the AbetaPP-independent pathway and retained intraneuronally. 37858630: Examples include the self-assembly of phenylalanine, which causes phenylketonuria; Abeta, which causes Alzheimer's disease; the tau protein, which causes both Alzheimer's and Parkinson's diseases; and alpha-synuclein, which causes Parkinson's illness. 37886704: Retracted: Oral Administration of Gintonin Protects the Brains of Mice against A beta -Induced Alzheimer Disease Pathology: Antioxidant and Anti-Inflammatory Effects. 38008888: We reported that UA treatment significantly alleviated memory decline in Abeta-induced AD model mice and APP23/PS45 double transgenic AD model mice. 38178136: And the relation between the peripheral blood Abeta and tau tangles of brain, another crucial pathologic factor contributing to the pathogenesis of AD, is also ambiguous. In the present review, we summarize recent studies on the roles of peripheral blood Abeta and the peripheral innate immune cells in the pathogenesis of AD. More recently, the anti-Abeta monoclonal antibodies are approved for treatment of AD patients through declining the peripheral blood Abeta mechanism of action to enhance plasma and central nervous system (CNS) Abeta clearance, leading to a decrease Abeta burden in brain and improving cognitive function, which clearly indicates that the levels of the peripheral blood Abeta impacted on the Abeta burden in brain and involved in the pathogenesis of AD. 38434588: This observation, along with the failure of previous clinical trials targeting Abeta or Tau and the modest success of recent trials using Abeta monoclonal antibodies, has led to a reappraisal of the view that Abeta accumulation is the sole factor in the pathogenesis of AD. 38559176: It is well known that Abeta and tau proteins are deposited stereotypically in brain regions to cause Alzheimer's disease. 38612434: In conclusion, we have identified DDX24 as a protein with a potential role in Abeta-induced AD pathology. 38612514: Interestingly, as AD progresses, less Abeta42 is detectable in the plasma, a phenomenon thought to result from Abeta becoming more aggregated in the brain and less Abeta42 and Abeta40 being transported from the brain to the plasma via the CSF. Alzheimer's disease (AD) is the fifth leading cause of death among adults aged 65 and older, yet the onset and progression of the disease is poorly understood. 15620565: However, in chronic lesioned rats, hypertonic saline induced sustained hypertension. 16500513: METHODS: Mice rendered hypertensive by Ang II infused intravenously at 30 ng/min for 6 h or by osmotic minipump at 0.9 mug/h for 7 or 14 days, were compared to saline-infused normotensive controls and to mice with hypertension induced by subtotal nephrectomy and 1% saline as drinking water. 2828469: Central catecholamines and alpha-adrenoceptors in acute hypertension induced by intracerebroventricular hypertonic saline. 28567090: SUBJECTS AND METHODS: We used three different hypertensive animal models: (i) Wistar-Kyoto rats (n=8) and spontaneously hypertensive rats (SHR; n=8), (ii) mice infused with saline or angiotensin II to induce hypertension, via osmotic mini-pump for 2 weeks, and (iii) mice that were allowed to drink L-NG-nitro-L-arginine methyl ester (L-NAME) to induce hypertension. 3284820: We investigated the status of circulating kinins in rats with severe hypertension caused by drinking 1% NaCl (saline) and treatment with deoxycorticosterone (DOC, 25 mg/kg/wk s.c.) for 5 weeks. 3894143: CRL or saline on artificially induced biliary tree hypertension was studied in 7 patients with a T-tube common bile duct drainage. 4459300: Reduction by coenzyme Q10 of hypertension induced by deoxycorticosterone and saline in rats. 514639: Arterial lesions and hypertension induced by saline, unilateral nephrectomy, and deoxycorticosterone in spontaneously hypertensive SHR rats. 7285865: In mononephrectomized rats, the daily administration of 1 mg/day quickly caused an enhanced consumption of 1% saline and induced severe hypertension within 3-4 weeks. 8927496: Intracerebroventricular injection of hypertonic saline induces experimental hypertension. 9887018: To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. 30571226: Recently, mathematical models of human integrative physiology, derived from Guyton's classic 1972 model of the circulation, have been used to investigate potential mechanistic abnormalities mediating salt sensitivity and salt-induced hypertension. 30593397: Deficiency of vitamin D has several health consequences and some of them have been proposed by other authors as important for the spreading of cystic fibrosis mutations: rickets/osteomalacia; susceptibility to diarrheal diseases and tuberculosis and salt induced arterial hypertension. 30595123: We found that PP242 not only completely prevented but also reversed salt-induced hypertension and kidney injury in salt-sensitive rats. In the present study, we, therefore, determined the effect of mTORC2 inhibition with compound PP242 on salt-induced hypertension and renal injury in salt-sensitive rats. Therapeutic Suppression of mTOR (Mammalian Target of Rapamycin) Signaling Prevents and Reverses Salt-Induced Hypertension and Kidney Injury in Dahl Salt-Sensitive Rats. mTORC1 has been implicated in pathological conditions, such as cancer and type 2 diabetes mellitus in humans, and inhibition of this pathway with rapamycin has been shown to attenuate salt-induced hypertension in Dahl salt-sensitive rats. 30595125: Together, these data demonstrate the influence of the parental diet in determining the salt-induced hypertension, renal damage, and inflammatory phenotype of the offspring. The current study sought to compare salt-induced hypertension, renal damage, and immune cell infiltration in the offspring of breeders fed either a casein- or gluten-based diet, with the hypothesis that offspring from gluten-fed breeders would fail to develop these SS phenotypes. 30631160: In conclusion, we produced a new miso with potent ACE inhibitory activity that reduced spontaneous and salt-induced hypertension. Similarly, in a salt-induced hypertension model with Dahl rats, the 5% nenrin miso solution attenuated the rising SBP observed in the salt solution group. 30668283: BACKGROUND: Salt is important in the pathogenesis of hypertension (HT). 30670332: Fueling Ketone Metabolism Quenches Salt-Induced Hypertension. (Cell Reports 2018;25:677-689) discovered that supplementation with a metabolic precursor produced beta-hydroxybutyrate (BHB), counteracting the pathological effects of high-salt diet-induced hypertension, suggesting a new treatment modality. 30681096: Therefore, it provides evidence that HW confers an antioxidant effect on high-salt induced hypertension and dramatically alters the metabolic patterns of SS rats, and the antihypertensive ingredients of HW also further indicate that it may be used as a nutritional supplemental therapeutic drug to protect against high-salt induced hypertension in the renal medulla. High salt causes hypertension in Dahl salt sensitive (SS) rats, while HW can effectively attenuate high-salt induced hypertension, and, various antihypertensive ingredients of HW have also been successfully identified using GC/MS. The protective role of hawthorn fruit extract against high salt-induced hypertension in Dahl salt-sensitive rats: impact on oxidative stress and metabolic patterns. 30703746: Our systemic study clearly supports the modulation of CSRP3 by a polyphenol-rich berries diet as an efficient cardioprotective strategy in hypertension-induced heart failure. The capacity of a polyphenol-enriched diet (i.e., blueberries, blackberries, raspberries, strawberry tree fruits and Portuguese crowberries berries mixture) to promote animal survival and protect cardiovascular function from salt-induced hypertension was evaluated in a chronic salt-sensitive Dahl rat model. 30783421: Mice with high-salt diet-induced hypertension were divided into four groups: Control (standard diet alone for 8 weeks), model (diet containing 8% NaCl for 8 weeks and intragastric administration of distilled water for the last 4 weeks), XJEK + high-salt-treated (diet containing 8% NaCl for 8 weeks and intragastric administration of XJEK for the last 4 weeks) and irbesartan + high-salt-treated (diet containing 8% NaCl for 8 weeks with intragastric administration of irbesartan for the last 4 weeks). Therefore, XJEK exerted protective effects against high salt-induced hypertension and cardiovascular remodeling in mice via improving ED, restoring pro- and anti-inflammatory factor balance and decreasing oxidative stress. 30797659: L-arginine supplementation lowers blood pressure, protein excretion and plasma lipid profile in experimental salt-induced hypertension in pregnancy: Relevance to preeclampsia. 30866441: New preclinical data demonstrates the activation of the renal sympathetic nerves in fructose-induced salt-sensitive hypertension, and reductions of blood pressure after renal nerve ablation. This review further demonstrates the interplay between sodium handling by the kidney, the renin-angiotensin-aldosterone system, and activation of the renal sympathetic nerves as important mechanisms in fructose and salt-induced hypertension. 30894696: In conclusion, SIK1 activity is necessary to prevent the development of salt-induced high blood pressure and associated SNS overactivity. 30917704: Given that leafy green and root vegetables contain large amounts of inorganic nitrate, these findings raise the possibility that fortification of salty food products with small amounts of a nitrate-rich vegetable concentrate may provide a simple method for reducing risk for salt-induced hypertension. In the current studies in a widely used model of salt-induced hypertension, the Dahl salt-sensitive rat, we found that supplemental dietary sodium nitrate confers substantial protection from initiation of salt-induced hypertension when the molar ratio of added nitrate to added salt is only ~1:170. Thus, new strategies that reduce the risk of salt-induced hypertension without requiring major changes in dietary habits would be of considerable medical interest. To reduce the risk of salt-induced hypertension, medical authorities have emphasized dietary guidelines promoting high intakes of potassium and low intakes of salt that provide molar ratios of potassium to salt of >=1:1. 30925093: In this study, we investigated the involvement and mechanisms of the PVN-PRR in DOCA-salt-induced hypertension, a mouse model of hypertension. 31037602: High salt-induced hypertension is relevant to the levels of pro-inflammatory cytokines (PICs) and oxidative stress in the hypothalamic paraventricular nucleus (PVN). We concluded that exogenous or endogenous CO attenuates high salt-induced hypertension by regulating PICs and oxidative stress in PVN. We explored whether CO in PVN can attenuate high salt-induced hypertension by regulating PICs or oxidative stress. Carbon Monoxide Attenuates High Salt-Induced Hypertension While Reducing Pro-inflammatory Cytokines and Oxidative Stress in the Paraventricular Nucleus. 31240902: BACKGROUND: The purpose of this study was to estimate the effects of 9-week swimming training on cardiodynamic parameters and coronary flow in a rat model of high salt-induced hypertension with a special focus on the role of oxidative stress. 31257672: OBJECTIVES: To study the promotive effect of salt-induced hypertension on crystal deposition and urolithiasis using a salt-sensitive rat hypertension model. Hypertension was induced by a high-salt diet. 31401881: It suggests that enhancing TRPM5 function might antagonize excessive salt intake and high salt-induced hypertension. 31411073: Nitric oxide inhibition with Nomega-nitro-l-arginine methyl ester (l-NAME), along with salt overload, leads to hypertension, albuminuria, glomerulosclerosis, glomerular ischemia, and interstitial fibrosis, characterizing a chronic kidney disease (CKD) model. 31476910: With previous work eliminating the involvement of genetic differences, grain-fed SS rats from Charles River Laboratories (SS/CRL; 5L2F/5L79) were less susceptible to salt-induced hypertension and renal damage compared with purified diet-fed SS rats bred at the Medical College of Wisconsin (SS/MCW; 0.4% NaCl, AIN-76A). SS/CRL rats were protected from salt-induced hypertension (116.5+/-1.2 versus 141.9+/-14.4 mm Hg), albuminuria (21.7+/-3.5 versus 162.9+/-22.2 mg/d), and renal immune cell infiltration compared with SS/MCW. These functional and transcriptomic T-cell differences between SS/MCW and SS/CRL show that dietary components in addition to salt may influence immunity and the infiltration of immune cells into the kidney, ultimately impacting susceptibility to salt-induced hypertension and renal damage. 31579948: METHODS: Hypertension was induced by deoxycorticosterone-acetate (DOCA) and salt administration in uni-nephrectomized rats for 12 weeks. 31634913: Strategies Are Needed to Prevent Salt-Induced Hypertension That Do Not Depend on Reducing Salt Intake. 31641986: Salt-sensitive rats were given a high salt diet for 10 weeks to induce hypertension. Toll-like receptor 4 (TLR4) and cellular Src (c-Src) are closely associated with inflammatory cytokines and oxidative stress in hypertension, so we designed this study to explore the exact role of c-Src in the mechanism of action of the TLR4 signaling pathway in salt-induced hypertension. Blockade of c-Src Within the Paraventricular Nucleus Attenuates Inflammatory Cytokines and Oxidative Stress in the Mechanism of the TLR4 Signal Pathway in Salt-Induced Hypertension. 31679420: Together, these findings provide new insight into how EP receptors in both the central nervous system and peripherally on DCs promote inflammation in salt-induced hypertension. 31809906: Hypotensive activity in normotensive and antihypertensive activity against DOCA-salt induced hypertension in rats were evaluated at doses 0.03 mg/Kg and 0.1 mg/Kg, i.p of Iloperidone. 31838911: Lastly, inhibition of DNA methyltransferases blunted salt-induced hypertension and renal damage in the SS/MCW rats providing a functional role for methylation. 31886193: Salt sensitivity and salt concentration were two key factors for the induction of hypertension. 32063725: Although l-arginine is an established vasodilator, the mechanism by which it modulates vascular reactivity in salt-induced hypertension is not clearly understood. Background: Abnormal vascular reactivity and reduced expression of endothelial nitric oxide synthase ( eNOS ) gene are hallmark of salt-induced hypertension in rats. 32078445: We found that HSD induced hypertension in Wistar rats. Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension. Intestinal flora has been reported to be associated with high salt-induced hypertension (hSIH). 32154868: Dietary sodium can upregulate mTORC1 signaling in cardiac and renal tissue, and inhibition of mTOR can prevent aldosterone associated, salt-induced hypertension. 32179848: (-)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats. However, its effects on salt-induced hypertension and renal injury remain unclear. 32303962: Herein we found that bitter melon extract (BME) and cucurbitacin E (CuE), a major compound in BME, lowered high salt-induced hypertension. 32428209: However, the causal relationship between vascular dysfunction and salt-induced hypertension remains controversial. Notably, the overt salt-induced hypertension in S-P467L mice was not driven by higher cardiac output, implying elevations in peripheral vascular resistance. 32437928: Our findings provide a vision about the metabolic responses of hypertensive rats to a (poly)phenol enriched diet, which may contribute to the understanding of the beneficial effects of (poly)phenols in salt-induced hypertension. 32475313: Here, we explored the hypothesis that elevations of H 2 O 2 by NOX4 in high-salt fed SS rat stimulate mTORC1 for the full development of salt-induced hypertension and renal injury. Given the direct activation of mTORC1 by H 2 O 2 and absence of any further protection from salt-induced hypertension in rapamycin-treated SS Nox4 -/- rats, we conclude that NOX4-H 2 O 2 is a major upstream activator of mTORC1 that contributes importantly to salt-induced hypertension and renal injury in the SS rat model. To determine the in vivo relevance of NOX4/H 2 O 2 /mTORC1 in the salt-induced hypertension, SS- Nox4 knockout (SS Nox4 -/- ) rats were daily administrated with vehicle/rapamycin fed a high-salt diet for 21 days. NOX4/H 2 O 2 /mTORC1 Pathway in Salt-Induced Hypertension and Kidney Injury.We have reported that a high-salt (4.0% NaCl) dietary intake activates mTORC1 and inhibition of this pathway with rapamycin blunts the chronic phase of salt-induced hypertension and renal injury in Dahl salt-sensitive (SS) rats. NOX4/H 2 O 2 /mTORC1 Pathway in Salt-Induced Hypertension and Kidney Injury. Rapamycin treatment of SS Nox4-/- rats had shown no augmented effect on the salt-induced hypertension nor upon indices of renal injury. 32508113: A recent study reported that increasing levels of beta-hydroxybutyrate levels by administration of its precursor, 1,3-butanediol, decreased salt-induced HTN in male Dahl salt-sensitive (S) rats. 32592815: The effect of L-NAME on phosphorylated NCC was blocked by both the SPAK inhibitor STOCK2S-26016 and the superoxide dismutase mimetic TEMPO which also attenuated salt-induced hypertension. 32597829: Salt causes aging-associated hypertension via vascular Wnt5a under Klotho deficiency. 32601353: Author Correction: (-)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats.An amendment to this paper has been published and can be accessed via a link at the top of the paper. Author Correction: (-)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats. 32856709: The Relationship between Urine Uromodulin and Blood Pressure Changes: the DASH-Sodium Trial.BACKGROUND: Uromodulin modulates the sodium-potassium-two-chloride transporter in the thick ascending limb of the loop of Henle, and its overexpression in murine models leads to salt-induced hypertension. 32880753: While prior studies have mainly focused on the brain, kidney, and vasculature as playing a role in salt-induced hypertension, the gut is the first and largest location for Na + absorption. RECENT FINDINGS: The innate and adaptive immune systems are involved in the genesis of salt-induced hypertension. Recent studies suggest that alterations in the gut microbiome contribute to salt-induced hypertension. Research from our group and others strongly suggests that the gut microbiome contributes to salt-induced inflammation and hypertension. 32905820: Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats. High salt intake elicited a significant increase in BP in the control group, while in the anti-DbetaH-SAP group the depletion of TH + neurons prevents the salt-induced hypertension. 33046522: Role of opioid signaling in kidney damage during the development of salt-induced hypertension. 33052061: The Dahl salt-sensitive (SS) rat is a classical model of salt-induced hypertension and associated kidney injury. 33061560: Discussion: Thus, short-term consumption of high fructose plus high salt diet by rats results in modest hypertension, insulin resistance, diminished aortic and renal artery compliance, and left ventricular diastolic dysfunction. Existing studies show that a rat model reflecting a diet of fructose and salt consumed by the upper 20th percentile of the human population results in salt-sensitive hypertension mitigated by treatment with an antioxidant. 33080347: Dietary supplementation of Huangshan Maofeng green tea preventing hypertension of older C57BL/6 mice induced by desoxycorticosterone acetate and salt. The current study investigated the effect and mechanism of dietary supplement of Huangshan Maofeng green tea (HSMF) on prevention of hypertension induced by deoxycorticosterone acetate (DOCA) and salt in old C57BL/6 mice. 33252422: Cardiac and renal protective effects of 2,5-dimethylcelecoxib in angiotensin II and high-salt-induced hypertension model mice. 33282868: Gut Microbiota-Related Evidence Provides New Insights Into the Association Between Activating Transcription Factor 4 and Development of Salt-Induced Hypertension in Mice. We conclude that ATF4 plays an important role in regulating gut microbiota and VK2 production, providing new insights into the association between ATF4 and development of salt-induced hypertension in mice, meanwhile contributing to the development for a new preventive strategy of hypertension. 33327798: Ablation of TRPV1-positive nerves exacerbate salt-induced hypertension and tissue injury in rats after renal ischemia-reperfusion via infiltration of macrophages. Conclusions: These data suggest that degenerating TRPV1-positive nerves exacerbates salt-induced hypertension and tissue injury in rats after renal I/R injury via macrophages-mediated renal inflammation. This study tested the hypothesis that degeneration of transient receptor potential vanilloid 1 (TRPV1)-positive nerves exacerbates salt-induced hypertension and renal injury after I/R via enhancing renal macrophage infiltration. 33665515: The combination of a Western diet and 11-deoxycorticosterone acetate salt-induced hypertension in the Gottingen miniswine led to the development of a novel large animal model of HFpEF that exhibited multiorgan involvement and a full spectrum of comorbidities associated with human HFpEF. 33775129: As a proof of concept, we experimentally validated the gene regulatory effect of a 3'-tRF (3'-tRF-ProTGG-19) that was dysregulated in both salt-induced hypertension in rats ( P =0.002) and hypertensive nephrosclerosis in humans ( P =1.7*10 -05 ). 33783375: OBJECTIVE: Pregnancy-associated plasma protein-A2 (PAPP-A2) is the homolog of PAPP-A in the vertebrate genome and its role in protecting against salt-induced hypertension in salt-sensitive rats has been confirmed. 33790341: PP242, an inhibitor of mTORC1/2 pathways exhibits potent natriuretic actions and completely prevented salt-induced hypertension in SS rats. 33797275: These observations should motivate research on the impact of the new dietary potassium guidelines on racial disparities in salt sensitivity, the risks and benefits of potassium-containing salt substitutes or supplements, and methods for increasing consumption of foods rich in nutrients that protect against salt-induced hypertension. 33857222: The results demonstrated that L-phenylalanine supplementation significantly enhanced the serum nitrite levels and attenuated the high salt-induced hypertension in SS rats. Thus, we hypothesized that a defect in amino acids may contribute to the development of salt-induced hypertension. L-phenylalanine attenuates high salt-induced hypertension in Dahl SS rats through activation of GCH1-BH4. 33898454: Commentary: Gut Microbiota-Related Evidence Provides New Insights Into the Association Between Activating Transcription Factor 4 and Development of Salt-Induced Hypertension in Mice. 34488433: IL-18 (Interleukin-18) Produced by Renal Tubular Epithelial Cells Promotes Renal Inflammation and Injury During Deoxycorticosterone/Salt-Induced Hypertension in Mice. 34569287: IsoLGs are immunogenic and contribute to salt-induced hypertension. 34623176: Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension. 34679745: Effects of Black Garlic Extract and Nanoemulsion on the Deoxy Corticosterone Acetate-Salt Induced Hypertension and Its Associated Mild Cognitive Impairment in Rats. Organosulfur compounds, phenolic acids and flavonoids in raw and black garlic were determined, and followed by preparation of black garlic nanoemulsion for studying their effects on deoxycorticosterone acetate-salt-induced hypertension and associated mild cognitive impairment in rats. 34684578: In a previous study, we demonstrated that melatonin prevents kidney damage in a salt-induced hypertension model by decreasing oxidative stress. 34689582: Conclusions Our data support the concept that renal vasodysfunction contributes to blood pressure salt sensitivity in Dahl SS rats, and that genes on rat chromosome 1 play a major role in modulating renal hemodynamic responses to salt loading and salt-induced hypertension. 34708426: Protein-rich almond supplementation might prevent the development of salt-induced hypertension by restoring arginine and NO regeneration and alleviating salt-induced oxidative stress. Dietary functional foods probably could help to improve salt-induced hypertension. Effects of almonds on ameliorating salt-induced hypertension in Dahl salt-sensitive rats. 34756849: Dietary Supplementation of Huangshan Maofeng Green Tea Preventing Hypertension of Older C57BL/6 Mice Induced by Desoxycorticosterone Acetate and Salt: Green Tea Preventing Senior Hypertension. The current study investigated the effect and mechanism of dietary supplement of Huangshan Maofeng green tea (HSMF) on prevention of hypertension induced by deoxycorticosterone acetate (DOCA) and salt in old C57BL/6 mice. 34819446: Background Intake of excess salt can lead to high blood pressure a leading cause of cardiovascular diseases (CVDs). 34836378: However, consuming too much salt can lead to high blood pressure, heart disease and even disruption of circadian rhythms. 34862465: Finally, joint public genome-wide association study data and our single-cell RNA-sequencing data showed the expression of hypertension susceptibility genes in ECs, SMCs, and fibroblasts and revealed 21 genes involved in the initiation and development of high-salt-induced hypertension. 34864872: Corrigendum to: LCZ696, Angiotensin II Receptor-Neprilysin Inhibitor, Ameliorates High-Salt-Induced Hypertension and Cardiovascular Injury More Than Valsartan Alone. 35113090: A combined intake of high fructose and high salt induced salt-sensitive hypertension and maternal high-fructose consumption induced programmed hypertension in adult offspring. 35153813: Salt-induced hypertension and fructose-induced hypertension are manifested in different mechanisms, including Inflammation, aldosterone-mineralocorticoid receptor pathway, aldosterone independent mineralocorticoid receptor pathway, renin-angiotensin system (RAS), sympathetic nervous system (SNS) activity, and genetic mechanisms. This review describes the evolution of hypertension and cardiovascular diseases (CVDs) in Lebanon and aims to elucidate potential mechanisms where salt and fructose work together to induce hypertension. These mechanisms increase salt absorption, decrease salt excretion, induce endogenous fructose production, activate fructose-insulin-salt interaction, and trigger oxidative stress, thus leading to hypertension. High intakes of salt and sugar (mainly fructose from added sugars) have been linked to the etiology of hypertension, and this may be particularly true for countries undergoing the nutrition transition, such as Lebanon. 35181841: Exogenous H 2 S Ameliorates High Salt-Induced Hypertension by Alleviating Oxidative Stress and Inflammation in the Paraventricular Nucleus in Dahl S Rats. These findings suggest that exogenous H 2 S attenuates hypertension caused by an HSD by ameliorating oxidative stress, inflammation, and apoptosis in the PVN. 35204171: Bilateral PVN microinjection of NKA alpha2 shRNA not only improved Na + /K + -ATPase activity and ADP/ATP ratio but also suppressed PKC gamma-dependent oxidative stress and TLR4-dependent inflammation in the PVN, thus decreasing sympathetic activity in rats with salt-induced hypertension. CONCLUSIONS: NKA alpha2 in the PVN elicits PKC gamma/Rac1/NAD (P)H-dependent oxidative stress and TLR4/MyD88/NF-kappaB-induced inflammation in the PVN, thus increasing MAP and sympathetic activity during the development of salt-induced hypertension. Therefore, we hypothesized that NKA alpha2 regulates oxidative stress and inflammation in the PVN in the context of salt-induced hypertension. Na + /K + -ATPase Alpha 2 Isoform Elicits Rac1-Dependent Oxidative Stress and TLR4-Induced Inflammation in the Hypothalamic Paraventricular Nucleus in High Salt-Induced Hypertension. 35310038: Preventive Potential of the Aqueous Extract of the Mixture of Bidens pilosa (Asteraceae) and Cymbopogon citratus (Poaceae) Aerial Parts on Hypertension Induced by a Chronic Salt and Alcohol Consumption on the Rats. 35312067: NPY in the hypothalamic arcuate nucleus (Arc) is best known for its control in appetite and energy homeostasis, but it is unclear whether it is also involved in the development of salt-induced hypertension. Arcuate NPY is involved in salt-induced hypertension via modulation of paraventricular vasopressin and brain-derived neurotrophic factor. 35439285: Blockade of Microglial Activation in Hypothalamic Paraventricular Nucleus Improves High-salt Induced Hypertension. Blockade of PVN microglial activation inhibits inflammation and oxidative stress, therefore attenuating the development of hypertension induced by high-salt diet. METHODS: High-salt diet was given to male Dahl salt-sensitive rats to induce hypertension. 35452099: Accordingly, efforts to identify and correct the nutrient deficiencies that promote salt sensitivity hold promise for decreasing population risk of salt-induced hypertension without requiring reductions in salt intake. High-salt diets are a major cause of hypertension and cardiovascular (CV) disease. Suboptimal nutrient intake is a common cause of the hemodynamic disturbances mediating salt-induced hypertension. Mechanism-based strategies to prevent salt sensitivity and salt-induced hypertension. 35466690: The goal of this study was to determine whether SGLT2 inhibition alters blood pressure and kidney function via affecting the Renin-Angiotensin-Aldosterone System (RAAS) and sodium channels/transporters along the nephron in Dahl Salt-Sensitive (SS) rats, a model of salt-induced hypertension. Administration of dapagliflozin (Dapa) at 2 mg/kg/day via drinking water for 3 weeks blunted the development of salt-induced hypertension as evidenced by lower blood pressure and a left shift of the pressure natriuresis curve. Our data suggest that SGLT2 inhibition in a non-diabetic model of salt-sensitive hypertension blunts the development of salt-induced hypertension by causing glucosuria and natriuresis without changes in RAAS and expression or activity of studied Na + channels and transporters. 35493997: While both male and female E-Cul3?9 mice developed salt-induced hypertension and renal injury, the pressor effect of salt was greater in female mutants. Endothelial Cullin3 Mutation Impairs Nitric Oxide-Mediated Vasodilation and Promotes Salt-Induced Hypertension. Because NO deficiency contributes to salt-induced hypertension, we tested the salt-sensitivity of E-Cul3?9 mice. 35534373: They also impair salt and water excretion, leading to edema and hypertension. 35551760: We then tested the effect of ROCK2 inhibition in vivo on DOCA (deoxycorticosterone) salt-induced hypertension. 35551857: Angiotensin AT2 Receptor Activation during Ischemic Injury Protects against High Salt-Induced Hypertension and Proteinuria in the Long-term: Role of IL-17A Cells. 35553531: To examine the role of K ir 7.1 in renal electrolyte handling and the development of salt-induced hypertension, we generated a knockout of Kcnj13 on the Dahl salt-sensitive (SS) rat background. SS Kcnj13+/- rats were further used to measure blood pressure and electrolyte handling changes during the development of salt-induced hypertension. 35553536: Interestingly, genetic deletion of CD14 in the Dahl SS rat (SS CD14-/- ) confers a significant exacerbation of salt-induced hypertension and associated renal disease that is specific to females. 35555027: Therapeutic effects of L-lysine in Dahl SS rats, a Model of Salt-Induced Hypertension. 35555364: CONCLUSION: Together, implementation of this methodology will provide key insights and be valuable in further predicting the emergent properties of complex metabolic interactions in the kidney of rats during the development of salt-induced hypertension. 35555627: Adult diabetic db/db mice were salt loaded (4% NaCl) for 7 days to induce hypertension. 35556281: Dahl Salt-Sensitive (SS) rat, a model for salt-induced hypertension, was used to test this hypothesis in a hypertensive, non-diabetic environment. We found that administration of dapagliflozin at a concentration of 2 mg/kg/day via drinking water during 3 weeks blunts the development of salt-induced hypertension with no changes in the heart rate. Therefore, our data suggest that SGLT2 inhibition blunts the development of salt-induced hypertension, causes glucosuria and natriuresis but does not affect RAAS and expression and activity of Na + channels and transporters in a model of non-diabetic, salt-sensitive hypertension. 35557199: Assessment of Mitochondrial Respiratory Function in Isolated Nephron Segments of Dahl SS Rats in Salt Induced Hypertension. We hypothesized that mitochondrial function of proximal tubules (PT) and medullary thick ascending limbs (mTAL) is altered during the development of salt induced hypertension in the Dahl salt-sensitive (SS) rat. CONCLUSION: These observations demonstrated that renal tubular mitochondrial respiratory function is altered in SS rats during the development of salt-induced hypertension and that both PT and mTAL exhibit an increased respiratory capacity in response to HS feeding. 35674015: RESULTS: Gastrin-SiO 2 microspheres treatment prevented the high salt-induced hypertension and increase in urine Na concentration by inhibiting intestinal Na +/ H + exchanger 3 trafficking and activity, increasing stool sodium without inducing diarrhea. 35700961: The list of most often applied animal hypertension models reviewed here includes variants of salt-induced hypertension, the models with genetic background: such as spontaneously hypertensive rats (SHR) and Dahl salt sensitive (SS/SR) rats, Goldblatt 2K-1C hypertensive rats, and also the pharmacologically-plus-dietary salt-induced model known as DOCA-salt hypertension. 35705768: Citrulline, as one of the important component in ME, could attenuate salt-induced hypertension by increasing endogenous synthesis of arginine and NO. Thus, the present study indicated that feeding Momordica charantia could avoid high-salt-induced hypertension in DSS rats. Dietary Momordica charantia may be an alternative approach to avoid salt-induced hypertension. Identifying functional foods that can help prevent mechanistic abnormalities mediating salt-induced hypertension is an issue of considerable nutraceutical and scientific interest. 35904193: Conclusions We define a previously unrecognized role of TRPC3/NCX1 mediated vascular calcium dysfunction in the development of high-salt-induced hypertension, which can be improved by canagliflozin treatment. Canagliflozin treatment significantly reduced high-salt-induced hypertension and this effect was not totally dependent on urinary sodium excretion in salt-sensitive hypertensive rats. 35947845: In the present study, we hypothesized that anthocyanins from HS may attenuate salt-induced hypertension in rats by suppressing the components of renin-angiotensin-aldoslestrone system (RAAS). 35986807: Genistein Alleviates Oxidative Stress and Inflammation in the Hypothalamic Paraventricular Nucleus by Activating the Sirt1/Nrf2 Pathway in High Salt-Induced Hypertension. Our results demonstrated that PVN infusion of Gen could inhibit the progression of hypertension induced by an HS diet by activating the Sirt1/Nrf2 pathway. Hypertension caused by a high-salt (HS) diet is one of the major causes of cardiovascular diseases. This study investigates genistein's (Gen) role in HS-induced hypertension and the underlying molecular mechanism. 36017217: In this study, traditional Chinese medicine (TCM) syndrome of hypertension caused by high salt had been diagnosed and the pathogenesis of hypertension was explored from the perspective of intestinal microecology. Hypertension induced by a high salt diet belongs to liver-Yang hyperactivity syndrome. Rats in a high salt diet-induced hypertension group (CG) and normal group (CZ) were compared by 16S rRNA gene full-length sequencing and liquid chromatography and mass spectrometry to identify differences in the bacterial community structure, metabolites, and metabolic pathways. These findings suggest that a high salt diet induces hypertension of liver-Yang hyperactivity syndrome by mediating the microbiota associated with the glutamate/GABA-glutamine metabolic cycle via the gut-brain axis. 36314446: Benincasa hispida extracts positively regulated high salt-induced hypertension in Dahl salt-sensitive rats: Impact on biochemical profile and metabolic patterns. The objective of this study was to investigate the potential role of Benincasa hispida extracts on high salt-induced hypertension in Dahl-salt sensitive (D-SS) rats and to find out the metabolic and biochemical pattern involved in the reduction of hypertension. Salt-induced hypertension is one of the major issues worldwide and one of the main factors involved in heart and kidney failure. The antihypertensive components malic acid, aspartic acid, and glycine of extract can be used as therapeutic drugs to protect kidneys from salt-induced hypertension. 36458162: However, its role in the progression of hypertension induced by high salt diet (HSD) has not been elucidated. Together, our results offer evidence that the dietary uptake of glutamine may be associated with attenuating the development of high salt-induced hypertension and slightly alleviating the degree of left ventricular hypertrophy in hypertensive rats. The association of dietary glutamine supplementation with the development of high salt-induced hypertension in rats. 36564179: Neurons of the median preoptic nucleus contribute to chronic angiotensin II-salt induced hypertension in the rat. 36583382: A detailed understanding of the environmentally-induced epigenetic modulations related to salt-induced hypertension could be promising for developing preventive and therapeutic approaches to hypertension. 36685421: Further experiments were conducted to verify the effect and mechanism of drugs on cold and high salt in an induced-hypertension rat model. 36700429: In the EC fraction, HS-induced hypertension significantly altered protein mediators of contractility, metabolism, mechanotransduction, renal function, and the coagulation cascade. METHODS: We performed systematic molecular characterization of the endothelial glycocalyx and EC proteomes in mice with HS (8%) diet-induced hypertension versus healthy control animals. 36715005: Although there are several animal models in which to study salt-induced hypertension with prolonged exposure to a high-sodium diet, here we sought to investigate whether the increase in arterial blood pressure of rats subjected to a short exposure to high salt, with 2% NaCl drinking solution instead of water, relies on changes in the circulating blood volume. 36830842: We evaluated the blood pressure reducing ability of metformin in salt-induced hypertension and progression of nephropathy in db/db mice. 36982271: Early renal biochemical alterations due to salt-induced hypertension in Dahl/salt-sensitive rats were monitored by Fourier-Transform Infrared (FTIR) micro-imaging. 37076133: The involvement of Ang II-AT1 and PGE2-EP1 systems in HS-induced hypertension and neuronal and behavioral impairments was examined by treatment with losartan, an AT1 receptor blocker (ARB), or EP1 gene knockout. 37123470: Our studies indicate that extracellular Na + enters APCs via ENaC leading to inflammation and salt-induced hypertension. Targeting extra-renal ENaC may provide new drug therapies for salt-induced hypertension. 37318990: Interestingly, chronic infusion of ML418 significantly increased sodium and chloride excretion after 14 days of high salt but did not alter salt-induced hypertension development. 37377160: The adenosine A2A receptor (A2AR) is expressed in lymphatic endothelial cells (LECs), while the roles and mechanisms of LEC-A2AR in skin lymphangiogenesis during salt-induced hypertension are not clear. 37454306: Bilateral PVN infusion of anthocyanin attenuated NLRP3-dependent inflammation (NLRP3, caspase-1, IL-1beta and TNF-alpha) and ROS production, reduced AT 1 R expression and function in PVN and lowered peripheral sympathetic nerve activity and blood pressure in rats with salt-induced hypertension. Whether anthocyanin can reduce salt-induced hypertension and the related mechanisms remain unclear. Anthocyanin attenuates high salt-induced hypertension via inhibiting the hyperactivity of the sympathetic nervous system. 37518960: CONCLUSION: Pre-electroacupuncture tends to lower blood pressure, improve cardiac function and reduce myocardial fibrosis in high-salt-induced hypertension rats, which may be associated with inhibiting inflammatory response. [Effects of pre-electroacupuncture on blood pressure and cardiac function in high-salt-induced hypertension rats]. 37532951: Our study revealed a considerable effect of TRPV4 channels in smooth muscle-dependent contraction in mice during high-salt induced hypertension. These results suggested that TRPV4 channels regulate smooth muscle-dependent contractions in high salt-induced hypertension, and this contraction involves increased [Ca 2+ ] i , IP 3 R2, and IRF7 activity. Whole-transcriptome analysis by RNA-seq and western blot assays revealed the involvement of interferon regulatory factor 7 (IRF7) in TRPV4-IRF7-IP 3 R2 signaling in HSD-induced hypertension. Aortic smooth muscle TRPV4 channels regulate vasoconstriction in high salt-induced hypertension. 37559717: In recent years, it has been found that the ENaC can lead to immune cell activation, endothelial cell dysfunction, aggravated inflammation involved in high salt-induced hypertension, cystic fibrosis, pseudohypoaldosteronism (PHA), and tumors; some inflammatory cytokines have been reported to have a regulatory role on the ENaC. 37592043: Vascular smooth muscle TRPV4 channel: a promising therapeutic target for salt-induced hypertension? 37646962: These findings suggest that barley supplementation exerted protective effects against high salt-induced hypertension by an antioxidant, anti-inflammatory, and vasodilating effects and restoring neurochemical alterations. 37805298: There is insufficient evidence that high salt (sodium) intake early in life might lead to hypertension or salty diet preference in adults. 37909169: Irrespectively of the mouse strain used, the number of renal regulatory T cells was not decreased in Ang II as well as in deoxycorticosterone salt induced hypertension. 37932290: The result showed that administration of Dapa for 3 weeks prevented the progression of salt-induced hypertension in female rats, similar to its effects in male SS rats. Dapagliflozin (Dapa) blunted the development of salt-induced hypertension by causing glucosuria and natriuresis without changes in the Renin-Angiotensin-Aldosterone System. Effect of SGLT2 inhibition on salt-induced hypertension in female Dahl SS rats. Our data suggest that SGLT2 inhibition in a non-diabetic model of salt-sensitive hypertension blunts the development of salt-induced hypertension independent of sex. 38186979: CONCLUSIONS: This study demonstrates that tempol down-regulates epithelial transport mechanisms in each segment of the nephron and normalizes salt-induced high blood pressure in diabetic animals presumably in a PKC dependent manner. 38545789: We hypothesized that PT fructose reabsorption by SGLT5 initiates a genetic program enhancing Ang II-stimulated oxidative stress in males and females, thereby causing fructose-induced salt-sensitive hypertension. CONCLUSIONS: SGLT5-mediated PT fructose reabsorption is required for FHS to augment Ang II-stimulated proximal nephron O 2 - production, and increases in PT oxidative stress likely contribute to FHS-induced hypertension. SGLT4 (sodium glucose-linked cotransporters 4) and SGLT5 are implicated in PT fructose reabsorption, but their roles in fructose-induced hypertension are unclear. Knocking Out Sodium Glucose-Linked Transporter 5 Prevents Fructose-Induced Renal Oxidative Stress and Salt-Sensitive Hypertension. 38581621: CONCLUSION: The combination of zinc deficiency and high salt causes hypertension. 38673987: Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension. 16128149: In this study, we hypothesized that a quantitative EEG (qEEG) method for measuring EEG variability combined with specific psychophysical tasks could improve the classification accuracy of subjects with normal aging vs. mild cognitive impairment (MCI) or mild dementia due to Alzheimer's Disease and Related Disorders (ADRD). 17006763: Since these proteins are involved directly or indirectly in microtubule destabilization and hyperphosphorylation of tau, and also in APP processing we hypothesize that cell cycle disturbance may be important contributor in the pathogenesis of AD. Mild cognitive impairment (MCI) is regarded as a transition stage between the cognitive changes of normal aging and the more serious problems caused by Alzheimer's disease (AD). 19647374: Taken together with other phenomena such as cell cycle re-activation and ectopic re-expression of cyclins and cyclin dependent proteins, we propose that AD is an oncogenic phenotype leading to accelerated aging of the affected brain. 20413856: Additional work is required, but such associations suggest that reduced cardiac output may be a risk factor for Alzheimer's disease (AD) and abnormal brain aging through the propagation or exacerbation of neurovascular processes, microembolism due to thrombosis, and AD neuropathological processes. 21514249: The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. 22343502: UNLABELLED: In the recently revised diagnostic criteria for Alzheimer disease (AD), the National Institute on Aging and Alzheimer Association suggested that confidence in diagnosing dementia due to AD and mild cognitive impairment (MCI) due to AD could be improved by the use of certain biomarkers, such as (18)F-FDG PET evidence of hypometabolism in AD-affected brain regions. 22594104: METHODS: The rat model of Alzheimer's disease (AD) was established using D-galactose to cause subacute aging combined with Meynert nucleus damage. 22773365: To this effect, the Alzheimer's Association and the National Institute on Aging have developed a new classification scheme that has categorized AD into a preclinical phase (research category), MCI due to AD, and dementia of Alzheimer's type. 23026363: Recently, the National Institute on Aging and the Alzheimer's Association identified specific structural and functional neuroimaging findings as valuable markers of biological processes occurring in the human brain, especially processes that herald impending dementia caused by Alzheimer's disease (AD) in its prodromal form. 23138093: Currently, healthcare costs associated with aging at home can be prohibitive if individuals require continual/periodical supervision and assistance because of Alzheimer's disease. 23760360: Early identification of persons at risk for cognitive decline in aging is critical to optimizing treatment to delay or avoid a clinical diagnosis of mild cognitive impairment (MCI) or dementia due to Alzheimer's disease (AD). 27025083: The Natinal Institute on Aging and the Alzheimer's Association proposed AD dementia, mild cognitive impairment due to AD, the preclinical stage of AD. 27071083: To address this problem in a systematic manner, we performed a meta-analysis of about 1,600 microarrays from human central nervous system tissues to identify transcriptional changes upon aging and as a result of Alzheimer's disease. 27567815: Both healthy and pathological aging due to Alzheimer's disease (AD) are associated with decreased brain grey matter volume (GMV) and disrupted white matter (WM) microstructure. 29316249: Aging is a major driving force underlying dementia, such as that caused by Alzheimer's disease (AD). 30777767: Beyond episodic memory: Semantic processing as independent predictor of hippocampal/perirhinal volume in aging and mild cognitive impairment due to Alzheimer's disease. 33164934: CONCLUSION: These findings extend previous observations in cognitively normal aging, demonstrating that entorhinal tau continues to be closely associated with hippocampal hyperactivity and memory performance in MCI and mild dementia due to AD. 33816761: Association between regional tau pathology and neuropsychiatric symptoms in aging and dementia due to Alzheimer's disease. 34655980: Brain atrophy occurs in aging even in the absence of dementia, but it is unclear to what extent this is due to undetected preclinical Alzheimer disease. 35908596: In a society where the global population is gradually ageing, the health threats and financial burdens caused by AD are becoming increasingly severe since AD often occurs in old age. 36223647: AD overture proposes that sAD is: (i) a multifactorial and progressive neurodegenerative biological process, (ii) characterized by the early appearance of 3R + 4Rtau NFTs, (iii) later deposition of beta-amyloid and SPs, (iv) with particular non-overlapped regional distribution of NFTs and SPs, (v) preceded by or occurring in parallel with molecular changes affecting cell membranes, cytoskeleton, synapses, lipid and protein metabolism, energy metabolism, neuroinflammation, cell cycle, astrocytes, microglia, and blood vessels; (vi) accompanied by progressive neuron loss and brain atrophy, (vii) prevalent in human brain aging, and (viii) manifested as pre-clinical AD, and progressing not universally to mild cognitive impairment due to AD, and mild, moderate, and severe AD dementia. 36876565: One theory claims that AD is due to brain aging affecting mainly the functions of mitochondria, therefore, the factors leading to mitochondrial ageing should lead to the development of Alzheimer's disease. 37422287: DISCUSSION: Amyloid beta deposition and striatal dopaminergic depletion contribute to regional perfusion changes, clinical symptoms, and cognition in the spectrum of normal aging and cognitive impairment due to AD and/or LBD. 38645748: As such, CR may slow aging and reduce the risk of all diseases of aging, including dementia due to AD. 15141356: Especially cerebral microangiopathy is strongly associated with Alzheimer's dementia, it triggers the vicious circle which leads to amyloid deposition. 23945233: For example, FDG-PET demonstrates hypometabolic regions in the posterior cingulate gyri, precuneus, and parietotemporal association cortices, while amyloid PET indicates amyloid deposition in Alzheimer disease and mild cognitive impairment due to Alzheimer disease. 2566117: However, since increased levels of PreA4 are not present in Alzheimer's disease, additional factors must account for the amyloid deposition in that disorder. 2682324: Advances in our knowledge of the normal posttranslational processing of the amyloid precursor protein may help to elucidate the defect in Alzheimer's disease that leads to amyloid deposition. 28124588: Cellular Model of Alzheimer's Disease: Abeta1-42 Peptide Induces Amyloid Deposition and a Decrease in Topo Isomerase IIbeta and Nurr1 Expression. 28304292: The aim was to evaluate brain amyloid-beta (Abeta) deposition in patients with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) using amyloid PET imaging and clarify the relationship between the annual change in Abeta deposition and disease progression. 31068220: AQP4 redistribution has been proposed to impair bulk Abeta clearance in AD, resulting in increased amyloid deposition in the brain; however, this finding is controversial. 33883492: Asymmetric Amyloid Deposition as an Early Sign of Progression in Mild Cognitive Impairment Due to Alzheimer Disease. 35328176: Amyloid positron emission tomography (PET) scan is clinically essential for the non-invasive assessment of the presence and spatial distribution of amyloid-beta deposition in subjects with cognitive impairment suspected to have been a result of Alzheimer's disease. 7724603: The data demonstrate that both apoE epsilon 4/AD and trisomy 21/AD lead to increased amyloid deposition, but by apparently different mechanisms. 12899186: Alzheimer's disease (AD) results in atrophy of limbic structures, whereas normal aging relatively spares limbic regions but affects prefrontal areas. 19955375: Thus, it is possible that the accelerating atrophy with increasing age is due to preclinical AD. 21674695: BACKGROUND: Alzheimer's disease (AD) and mild cognitive impairment (MCI) affect the limbic system, causing medial temporal lobe (MTL) atrophy and posterior cingulate cortex (PCC) hypometabolism. 22383167: CONCLUSION: Our results suggest that (i) hippocampal and amygdala but not entorhinal cortex, volumes differ between AD and LBD and (ii) factors other than current markers of neurodegenerative pathological change are responsible for atrophy of medial temporal lobe structures in AD and LBD. 23024883: Clinicians and researchers alike are in need of quantitative and robust measurement tools to assess medial temporal lobe atrophy (MTA) due to Alzheimer's disease (AD). 24167442: Conversely, patients with hippocampus atrophy due to Alzheimer's disease, but not patients with Fronto-Temporal Dementia, were less inclined to favor options that required mental simulation. 24787913: Our results demonstrated that subjects with increased medial temporal atrophy (MTA) severity on VSRAD, increased Cho/Cr, MI/Cr ratio, and decreased NAA/Cr and NAA/MI ratio on 1H MRS at baseline were at risk of dementia due to AD. 25082631: In conclusion, automated MRI brain tissue segmentation differentiates shunt-responsive NPH with high accuracy from atrophy due to AD and normal aging. To better characterize NPH, we test the hypothesis that a prediction model based on automated MRI brain tissue segmentation can help differentiate shunt-responsive NPH patients from cerebral atrophy due to Alzheimer disease (AD) and normal aging. 25120483: Medial temporal lobe (MTL) atrophy resulting from AD lesions and cerebrovascular lesions [i.e., white matter lesions (WML), lacunar strokes, and strokes] are often revealed concurrently on magnetic resonance imaging (MRI) in MCI subjects. 25260848: In a previous report, we proposed a method for combining multiple markers of atrophy caused by Alzheimer's disease into a single atrophy score that is more powerful than any one feature. 25324775: Glucose hypometabolism and gray matter atrophy are well known consequences of Alzheimer's disease (AD). 25750526: BACKGROUND: An increased electroencephalographic (EEG) upper/lower alpha power ratio has been associated with less regional blood perfusion, atrophy of the temporoparietal region of the brain, and reduction of hippocampal volume in subjects affected by mild cognitive impairment due to Alzheimer's disease as compared with subjects who do not develop the disease. 29420642: Inner retina in Alzheimer's Disease (AD) may experience neuroinflammation resulting in atrophy. 29844294: Alzheimer's disease (AD) represents the prevalent type of dementia in the elderly, and is characterized by the presence of neurofibrillary tangles and amyloid plaques that eventually leads to the loss of neurons, resulting in atrophy in specific brain areas. 31054405: In this study, we assessed whether patients with hippocampal atrophy due to Alzheimer's disease (AD) are still able to retrieve overlearned arithmetic facts from memory. 33407913: BACKGROUND: Alzheimer's disease (AD) and behavioral variant frontotemporal dementia (bvFTD) cause distinct atrophy and functional disruptions within two major intrinsic brain networks, namely the default network and the salience network, respectively. 35068451: CONCLUSION: Data suggest that less atrophy of the Ch1/2 area and younger age are associated with a more significant cholinergic deficit in MCI due to AD. 35109316: BACKGROUND: Alzheimer's disease (AD) is a progressive neurological disease that leads to atrophy of the brain and cognitive decline. 35770026: Multiple experiments were performed to get the data from three lamb brain phantoms that realistically mimic the whole-brain atrophy due to Alzheimer's disease. 36038918: This alteration persists throughout AD progression and leads to generalized dendritic atrophy at late stages of the disease. 36410182: AD is characterized by two cardinal pathological mechanisms: amyloid beta (Abeta) plaques and neurofibrillary tangles (NFTs), leading to atrophy of the brain. 18280925: RATIONALE AND OBJECTIVES: An automated method for identification of patients with cerebral atrophy due to Alzheimer's disease (AD) was developed based on three-dimensional (3D) T1-weighted magnetic resonance (MR) images. 20157252: Although it is established that Alzheimer's disease (AD) leads to cerebral macrostructural atrophy, microstructural diffusion changes have also been observed, but it is not yet known whether these changes offer unique information about the disease pathology. 22011258: Abstract Posterior cortical atrophy (PCA) is a visual-cognitive syndrome caused by Creutzfeldt-Jakob disease (CJD), Alzheimer's disease (AD), or subcortical gliosis. Clinical manifestations of PCA caused by AD included visual agnosia, cortical blindness, optic apraxla, delusions, hallucinations, agitation, depression, amnestic deficit, Wernicke's aphasia, acalculia, and left/right disorientation. Posterior cortical atrophy produced by AD can be demonstrated on magnetic resonance imaging, positron emission tomography, and electroencephalography; determination of the etiology requires tissue examination. 22265212: The progressive neurodegeneration affecting parietal, occipital, and occipitotemporal cortices that underlies PCA is attributable to Alzheimer's disease in most patients. 23138762: Overlap in the linguistic profiles of PCA and LPA, which are both most commonly caused by Alzheimer's disease, further emphasises the notion of a phenotypic continuum between typical and atypical manifestations of the disease. 2428577: Comparison with records of 22 patients, with cortical atrophy due to Alzheimer's disease but with only mild to moderate dementia, showed a similar low frequency of non-specific abnormalities. 25082631: In conclusion, automated MRI brain tissue segmentation differentiates shunt-responsive NPH with high accuracy from atrophy due to AD and normal aging. To better characterize NPH, we test the hypothesis that a prediction model based on automated MRI brain tissue segmentation can help differentiate shunt-responsive NPH patients from cerebral atrophy due to Alzheimer disease (AD) and normal aging. 25589715: Left temporal lobe epilepsy revealing left posterior cortical atrophy due to Alzheimer's disease. 25869784: AD and LLD led to brain atrophy in networks only partially overlapping. 27180794: Therefore, the PCA was considered to be a result of AD. 28116234: We investigated the association between RAVLT scores (RAVLT Immediate and RAVLT Percent Forgetting) and the structural brain atrophy caused by AD. 28394771: BACKGROUND: Flortaucipir (tau) positron emission tomography (PET) binding distinguishes individuals with clinically well-established posterior cortical atrophy (PCA) due to Alzheimer disease (AD) from cognitively normal (CN) controls. 2872473: These volumes were measured in 4 patients and the results were: 11.0 ml ventricular volume, 68.7 ml total cranial CSF in the patient with benign intracranial hypertension; 606.6 ml ventricular, 174.1 ml total in the patient with hydrocephalus due to a blocked ventriculo-peritoneal (V-P) shunt; 83.4 ml ventricular, 108.5 ml total in the patient with normal pressure hydrocephalus; and 52.7 ml ventricular, 181.0 ml total in the patient with cerebral atrophy due to Alzheimer's disease. 30425798: A patient with posterior cortical atrophy due to Alzheimer's disease. 30568088: Our proposed method would be useful for the accurate evaluation of cerebral atrophy caused by Alzheimer's disease. 32603972: Influence of plasma matrix metalloproteinase levels on longitudinal changes in Alzheimer's disease (AD) biomarkers and cognitive function in patients with mild cognitive impairment due to AD registered in the Alzheimer's Disease Neuroimaging Initiative database.OBJECTIVE: The present study investigated the effects of plasma matrix metalloproteinases (MMPs) on longitudinal changes in Alzheimer's disease (AD)-related biomarkers in cerebrospinal fluid (CSF), brain atrophy, and cognitive function in patients with mild cognitive impairment due to AD (MCI-AD). 36419215: INTRODUCTION: Carrying out a randomized controlled trial to estimate the causal effects of regional brain atrophy due to Alzheimer's disease (AD) is impossible. 37370645: Alzheimer's disease (AD) is a progressive neurological problem that causes brain atrophy and affects the memory and thinking skills of an individual. 37930972: N = 43 patients were studied of whom n = 13 had DLB or PD with Dementia (PDD); n = 13 had PD; n = 12 had typical, memory-onset Alzheimer's Disease (tAD); and n = 5 had Posterior Cortical Atrophy (PCA) due to Alzheimer's disease. 9613493: PURPOSE: In the older patient with dilated ventricles, it is often difficult to differentiate normal pressure hydrocephalus (NPH) from cerebral atrophy caused by Alzheimer disease (AD). 10404929: CONCLUSIONS: Although Alzheimer's disease is widely regarded as a leading cause of death, dementias are reported on the death certificates of only a quarter of demented individuals in the population at large. 10459279: The trend likely reflects changes in attitudes of physicians and the public about attributing Alzheimer's disease as a cause of death as well as the availability of improved diagnostic procedures; the recent leveling in mortality trends from this condition may signal that death certificate diagnoses for Alzheimer's disease are more reliable now. Physicians report that Alzheimer's disease caused the death of 21,397 persons in 1996 and contributed to the death of 21,703 additional persons. Alzheimer's disease is a major cause of death, which exhibits variations by age, sex, race, and geographic area. 10681274: Alzheimer disease is one of the leading causes of death among older individuals. 10822478: CONCLUSIONS: In recognition of the importance of the condition as a major public health problem, Alzheimer's disease was added to the list of causes eligible to be ranked as leading causes of death in the United States beginning with mortality data for 1994. Overall, Alzheimer's disease was the 14th leading cause of death in 1995; for people 65 years of age or older, it was the 8th leading cause of death. OBJECTIVE: To describe the scope of mortality from and trends in Alzheimer's disease, to show how Alzheimer's disease ranks as a leading cause of death, to describe a methodological change regarding ranking, and to discuss issues related to the reporting of Alzheimer's disease on death certificates. Alzheimer's disease as a cause of death in the United States. RESULTS: Alzheimer's disease has increasingly been reported as a cause of death on death certificates in the United States; however, this increase may represent a variety of factors including improved diagnosis and awareness of the disease or changes in the perception of Alzheimer's disease as a cause of death. 10934557: Alzheimer's disease (AD), by far the most common form of dementia in the elderly, is clinically characterized by gradual, progressive loss in cognitive functioning and changes in personality, ultimately leading to death. So far, three genes have been identified in which mutations cause autosomal-dominant AD: the amyloid precursor protein (APP) gene on chromosome 21, the presenilin 1 (PSEN1) gene on chromosome 14, and the homologous presenilin 2 (PSEN2) gene on chromosome 1. 10993580: Alzheimer's disease type dementia is a growing health problem and is one of the leading causes of death among elderly people. 11182240: (6) AD is associated with a reactivation of developmental programmes that are incompatible with a differentiated cellular background and, therefore, lead to neuronal death. 11279271: beta-Amyloid (A beta) has been strongly implicated in the pathophysiology of Alzheimer's disease (AD), but the means by which the aggregated form of this molecule induces neuronal death have not been fully defined. 11400868: Alzheimer's disease is a neurodegenerative condition that affects approximately 5 million people and is the fourth leading cause of death in America. 11433428: beta-amyloid peptide (Abeta) has been implicated in the pathogenesis of Alzheimer disease and has been reported to induce apoptotic death in cell culture. 11726544: Mutant ubiquitin expressed in Alzheimer's disease causes neuronal death. 11803006: Alzheimer's disease was the 11th leading cause of death. 12410910: Only 13% of a group of patients receiving the AD therapy donepezil had AD as the primary diagnosis, and AD is rarely included as a primary or secondary DRG diagnosis when the condition precipitating admission to the hospital is caused by AD. In addition, AD is often not mentioned on death certificates, although it may be the proximate cause of death. 12861345: Potential therapeutic strategies for AD treatment include palliative treatment with nonspecific neuroprotecting agents, symptomatic treatment with psychotropic drugs for noncognitive symptoms, cognitive treatment with cognition enhancers, substitutive treatment with cholinergic enhancers to improve memory deficits, multifactorial treatment using several drugs in combination and etiopathogenic treatment designed to regulate molecular factors potentially associated with AD pathogenesis. In our opinion, the pharmacological treatment of AD should rely on a better understanding of AD etiopathogenesis in order to use current drugs that protect the AD brain against deleterious events and/or to develop new drugs specifically designed to inhibit and/or regulate those factors responsible for premature neuronal death in AD. 12907842: Among neurodegenerative diseases, Alzheimer's disease (AD) is a leading cause of death in elderly individuals. 14769384: Amyloid beta-peptide (Abeta) contributes to the pathogenesis of Alzheimer's disease (AD), causing neuronal death through apoptosis. 15519530: Alzheimer's disease is the fourth largest cause of death for people over 65 years of age. 15526713: Humanin and its analogues have been shown to protect cells against death induced by various Alzheimer's disease genes and amyloid-beta-peptides in vitro: the analogue [Gly14]-humanin has also been shown to be potent in reversing learning and memory impairment induced by scopolamine in mice in vivo. 15639804: Neurodegenerative diseases such as Huntington's disease, ischemia, and Alzheimer's disease (AD) are major causes of death. 15825927: Alzheimer's disease is the fourth leading cause of death among seniors but its insidious onset makes it difficult to distinguish from age-related decline and little is known about how much knowledge and fear people entertain about this disease. 15883266: BACKGROUND: Alzheimer disease (AD) is considered a leading cause of death, but few studies have examined the contribution of AD to mortality based on follow-up of representative US cohorts. 16189900: Alzheimer's disease was the eighth-leading cause of death in 2001. 16199521: Alzheimer's disease (AD) is a neurodegenerative disease with an insidious onset and progressive course that inevitably leads to death. 16712493: In addition to Abeta pathology, an invariant trait of Alzheimer's disease, disruption of tau processing is a necessary event in the neurotoxic cascade which eventually leads to neuronal death and subsequent dementia. 16787840: In the slowly progressive neurodegenerative disorders like Parkinson's disease and Alzheimer's disease very different neuronal populations undergo degenerative processes, although the cascades of cellular events leading to death are supposed to be similar. 17017864: Although oxidative stress and mitochondrial dysfunction have been linked to neurodegenerative diseases such as Alzheimer's disease (AD), it remains unclear how mitochondrial oxidative stress may induce neuronal death. 17115369: Alzheimer's Disease (AD) is the most common neurodegenerative disorder in western societies affecting up to 15 million individuals worldwide.It leads to death after a progressive memory deficit and cognitive impairment accompanied by the appearance of two pathological hallmarks in specific brain areas: neurofibrillary tangles and amyloid plaques. 17192682: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairments that become severe enough to interfere with the daily activities of patients and eventually lead to death (Chung and Cummings, 2000). 17401657: Alzheimer's disease is an irreversible, progressive neurodegenerative disorder leading invariably to death, usually within 7-10 years after diagnosis and is the leading cause of dementia in the elderly. 18042001: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterised by severe cognitive impairment that ultimately leads to death. 1830977: Alzheimer's disease, a devastating, irreversible and progressive degenerative disease of unknown cause or cure, is the fourth leading cause of adult death. 18322383: Structural and functional genomics studies demonstrate that genomic factors, probably induced by environmental factors, cerebrovascular dysfunction, and epigenetic phenomena, might be responsible for AD pathogenesis leading to premature neuronal death. 18406539: Recent studies have indicated that amyloid beta peptide, which is implicated in the progression of Alzheimer's disease, may be also responsible for retinal ganglion cells death in glaucoma. 18488798: Every 72 seconds, someone in the United States develops Alzheimer's disease, an incurable affliction that kills at least 66,000 people annually, making it the nation's seventh leading cause of death. 18631956: Alzheimer's disease is the seventh leading cause of all deaths in the United States and the fifth leading cause of death in Americans older than the age of 65 years. 18647630: Humanin (HN) and its analogues have been shown to protect cells against death induced by various Alzheimer's disease (AD) genes and amyloid-beta-peptides in vitro; the analogues [Gly(14)]-HN and colivelin have also been shown to be potent in reversing learning and memory impairment induced by scopolamine or quinuclidinyl benzilate (QNB) in mice or rats in vivo using the Y-maze or multiple T-maze tests. 18800967: Alzheimer's disease, the most common neurodegenerative disorder, and cerebral ischaemia, the most common cause of neurological death, are used to illustrate our current understanding of death signalling in neurodegenerative diseases. 19036982: Alzheimer's disease (AD) is the most prevalent form of dementia, resulting in progressive neuronal death and debilitating damage to brain loci that mediate memory and higher cognitive function. 19177976: AD is the seventh-leading cause of death in the United States (Centers for Disease Control 2006). 19426951: Alzheimer's disease (AD) is the sixth leading cause of all deaths in the United States, and the fifth leading cause of death in Americans aged 65 and older. Whereas other major causes of death have been on the decrease, deaths attributable to AD have been rising dramatically. 19864195: In the United States, Alzheimer's disease (AD) is the leading type of dementia and was the fifth and eighth leading cause of death in women and men aged > or = 65 years, respectively, in 2003. 19897016: Alzheimer's disease (AD) is the most common form of dementia, which is one of the four leading causes of death in developed nations. 19903243: The cellular pathology of Alzheimer's disease is progressive and protracted leading eventually to considerable neuronal death. 19912228: Chronic degenerative inflammatory diseases, such as chronic obstructive pulmonary disease and Alzheimer's dementia, afflict millions of people around the world, causing death and debilitation. 20064601: The neurodegenerative disorder Alzheimer's disease (AD) is the 6th leading cause of death in the USA. 20298981: AD is the fifth leading cause of death in Americans aged 65 and older. Although other major causes of death have been on the decrease, deaths because of AD have been rising dramatically. 20345790: Our study suggests that decedents >65 years of age in an ME practice are afflicted by common causes of dementia such as AD and FTLD which could contribute wholly or in part to their causes of death. 20383807: Currently AD is the major form of dementia and the fourth leading cause of death in aged population. 20615444: Beta-amyloid (Abeta) peptide, the hallmark of Alzheimer's disease (AD), invokes a cascade of oxidative damages to neurons and eventually leads to neuronal death. 20664211: Whereas other major causes of death have been decreasing, the number of deaths due to Alzheimer's disease is rising. 20667675: RESULTS: In France, in 2006, AD or dementia was reported as the underlying cause or a multiple cause of death on 45,597 death certificates. 20739349: beta-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. 20926742: More than 5 million people in the United States are afflicted with Alzheimer disease, a condition that is the seventh leading cause of death in the nation. 21155625: Alzheimer's disease (AD) is characterized by dysfunctional intracellular and extracellular biochemical processes that result in neuron death. 21238939: Alzheimer's Disease, the most common neurodegenerative disorder, and cerebral ischemia, the most common cause of neurologic death, are used to illustrate our current understanding of death signaling in neurodegenerative diseases. We will examine the current understanding of caspase function in developmental neuronal death and then illustrate the role of caspases in neuronal death in disease employing two diseases of neuronal loss, Alzheimer's Disease (AD), which is the most common chronic neurodegenerative disorder, and cerebral ischemia/stroke, the third most common cause of death in Western society, which is an acute neuronal disorder with chronic sequelae. 21374507: Alzheimer's disease (AD) is the fourth commonest cause of death in the United States; the recent outbreak of new variant Creutzfeldt-Jakob disease (nvCJD) has raised the specter of a large population being at risk to develop this prionosis. 21414557: Alzheimer's disease (AD) is the sixth leading cause of all deaths in the United States and is the fifth leading cause of death in Americans aged >=65 years. Although other major causes of death have been on the decrease, deaths because of AD have been rising dramatically. 21694457: Synapse loss is considered to be the best correlate of cognitive impairments in Alzheimer's disease (AD), and growing evidence supports the notion that certain events that trigger neuronal death in AD can be initiated by the local activation of caspases within the synaptic compartment. 21695038: We analyzed the US multiple cause of death files for 2005-2006 and 1999-2000 US deaths with Alzheimer's Disease (International Classification of Disease 10th revision code G30) and other dementias (codes F01, F02, R54) coded as underlying or contributing cause of death based on the death certificate. 21766442: Alzheimer's disease (AD) is the fourth leading cause of death in adults, characterized by hallmark neuritic plaques and neurofibrillary tangles. 21793014: In view of this complex pathogenic mechanisms, and the successful treatment of chronic diseases such as HIV or cancer, with multiple drugs having complementary mechanisms of action, the concern is growing that AD could better be treated with a single compound targeting two or more of the pathogenic mechanisms leading to neuronal death. 21840361: Alzheimer's disease (AD) is the 6th leading cause of death in United States afflicting >5 million Americans. 21920373: Alzheimer Disease (AD) is the most prevalent form of dementia and the sixth leading cause of death in developed world. 22133718: Alzheimer's disease (AD) is the only leading cause of death for which no disease-modifying therapy is currently available. 22212311: Alzheimer's disease (AD) is the most common form of dementia, and one of the principal causes leading to death around the world. 22254735: AD is a neurodegenerative disorder characterized by neurofibrillary plaques and tangles in the brain that leads to neuronal death and dementia. 22265578: The characterization of AD as a leading cause of death among the elderly was crucial to sustaining the movement, but also operated as a \double edged sword\. 2231117: Senile dementia and Alzheimer's disease (often considered a single process) rank as the fourth most common cause of death in the United States and outrank in cost to the nation the three leading causes of death combined. 22404854: Although the proportions of deaths due to other major causes of death have decreased in the last several years, the proportion due to AD has risen significantly. AD is the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age >=65 years. 22543304: AD is a complex multifactorial disorder with a number of genetic, epigenetic and environmental factors which ultimately lead to premature neuronal death. 22681044: Alzheimer's disease is a fatal neurological disorder that is a leading cause of death, with its prevalence increasing as the average life expectancy increases worldwide. 22696871: In AD, neurons have been shown to enter the cell cycle inappropriately without the ability to complete it fully and the aberrant re-entry leads to its death. 22778828: Alzheimer's disease (AD), an age-related neurodegenerative disorder, is the most common form of dementia, and the seventh-leading cause of death in the United States. 22888398: Alzheimer's disease (AD) is the most common neurodegenerative disease featuring progressive impairments in memory, cognition, and behavior and ultimately leads to death. 23106978: Tacrine-6-ferulic acid, a novel multifunctional dimer against Alzheimer's disease, prevents oxidative stress-induced neuronal death through activating Nrf2/ARE/HO-1 pathway in HT22 cells. 23113839: Because of the toxicity caused by the heme redox-active iron proteins, their elevated levels, localization, and accumulation in the brain, many forms of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, occur as a result of which the brain becomes vulnerable to oxidative stress, ultimately resulting in neuronal death. 23161037: Alzheimer's disease (AD) is the sixth leading cause of all deaths in the United States, and the fifth leading cause of death in Americans aged 65 and older. During the past years, several agents have been approved that enhance cognition and global function of AD patients, and recent advances in understanding AD pathogenesis has led to the development of numerous compounds that might modify the disease process. 23170058: PURPOSE: Recent studies have indicated that accumulation of amyloid beta(1-42) (Abeta(1-42)), which is associated with the progression of Alzheimer disease, may also be responsible for retinal ganglion cell death in glaucoma. 23376032: Neurologic conditions including stroke, Alzheimer disease, Parkinson disease, and Huntington disease are leading causes of death and long-term disability in the United States, and efforts to develop novel therapeutics for these conditions have historically had poor success in translating from bench to bedside. 23397250: Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and Multiple sclerosis (MS) involve activation of glial cells and release of inflammatory mediators leading to death of neurons. 23399672: Alzheimer's disease (AD) is the most common cause of dementia, and its pathological hallmarks are senile plaques and neurofibrillary tangles in the brain, which eventually induce neuronal death. 23424127: Alzheimer's disease (AD) is one of the leading causes of death for older people in US with rapidly increasing incidence. 23507120: AD is the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age 65 years or older. 23507421: Potential gains in life expectancy from reducing heart disease, cancer, Alzheimer's disease, kidney disease or HIV/AIDS as major causes of death in the USA. 23624206: Alzheimer's disease (AD) is a neurodegenerative disorder that leads to neuron death and synapse loss in the hippocampus and cortex, with consequent cognitive disability and dementia. 23650720: The basis of AD is neurodegenerative process that leads to death of neurons in the cerebral cortex. 23653484: RESULTS: AD and pneumonia were causes of significant excess mortality and the most common underlying causes of death in the AD patient group (23.53 and 17.65%, respectively). 23742787: Alzheimer's disease is the sixth leading cause of death in the United States and the fifth leading cause for people aged 65 years and over (1). 23984328: Alzheimer's disease is the most common form of dementia and is the only top 10 cause of death in the United States that lacks disease-altering treatments. 24201446: We have also focused on their involvement in neurodegenerative diseases including Parkinson's and Alzheimer's diseases, discussing the contribution of this type of glial cell toward mechanisms that can lead to neuronal death, which was previously attributed exclusively to neurons. 24471710: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of beta-amyloid peptides and neurofibrilllary tangles in brain, resulting in neuronal death and loss of cognitive abilities. 24689364: Alzheimer's disease (AD) is the most common form of dementia and the sixth leading cause of death in the United States. 24818261: In 2010, official death certificates recorded 83,494 deaths from AD, making AD the sixth leading cause of death in the United States and the fifth leading cause of death in Americans aged 65 years or older. 24838579: Alzheimer's disease (AD) is a neurodegenerative condition that leads to neuronal death and memory dysfunction. 24846640: Alzheimer's disease (AD) is the most common type of dementia (accounting for 60% to 80%) and is the fifth leading cause of death for those people who are 65 or older. 24850589: Alzheimer's disease (AD) is one of the most frequent causes of death and disability worldwide and has a significant clinical and socioeconomic impact. 24878198: Alzheimer's disease is the most common neurodegenerative disease and is one of the main causes of death in developed countries. 24922524: This study was designed to uncover the cellular and biochemical mechanisms underlying the neuroprotective effects of tacrine-3-caffeic acid (T3CA), a novel promising multifunctional anti-Alzheimer's dimer, against OS-induced neuronal death. 25075874: Alzheimer's disease, the seventh leading cause of death in 2006, became the sixth leading cause in 2007, and Diabetes mellitus, the sixth leading cause in 2006, dropped to the seventh leading cause in 2007. 25220527: Alzheimer's disease (AD) is the most common form of dementia characterized by deterioration of memory and other cognitive domains which leads to death in 3-9years after diagnosis. In addition to mutations in APP, PSEN1 and PSEN2 genes, that cause early onset autosomal dominant AD, several genetic risk factors for late onset AD are now known. 25250042: AD is the sixth leading cause of death, and one of the leading causes of dementia amongst the aged population in the USA. 25405415: Alzheimer?s disease (AD) is the only cause of death among the top 10 diseases that cannot be prevented, cured, or slowed with the current treatments available. 25408208: RESULTS: The National Death Index identified 175 subjects who died with AD listed as an underlying (n = 116) or contributing (n = 59) cause of death during 11.6-year average mortality surveillance. 25472798: Alzheimer's disease is one of the most common causes of death worldwide, with poor treatment options. 25609918: Alzheimer's disease, the most common type of dementia, is a progressive brain disease that destroys cognitive function and eventually leads to death. 25833944: The expression and subcellular localization of Set-beta are altered in Alzheimer disease, cleavage of Set-beta leads to neuronal death after stroke, and the full-length Set-beta regulates retinal ganglion cell (RGC) and hippocampal neuron axon growth and regeneration in a subcellular localization-dependent manner. 25857971: Beta-amyloid (Abeta) peptide, the hallmark of Alzheimer's disease, invokes oxidative damage to neurons and eventually leads to neuronal death. 25954942: Vitamin D and neurocognitive disorder due to Alzheimer's disease: A review of the literature. AD is the sixth leading cause of death in the United States and the only 1 among the top 10 that cannot be prevented, cured, or even slowed. 2597884: The distinction between Alzheimer's dementia and depressive illness, based on their natural history and causes of death, was reinforced. 25984581: In 2013, official death certificates recorded 84,767 deaths from AD, making AD the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age 65 years. 25989911: Alzheimer's disease (AD) is the most common type of dementia that leads to increasing death and mental disability among humans. 26022359: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by severe cognitive impairment that ultimately leads to death. 26265552: The number of patients with AD will grow rapidly each year and AD is the fifth leading cause of death for those aged 65 and older. 26435705: BACKGROUND: Alzheimer's disease (AD) is the sixth leading cause of death and the most costly disease in the US. 26470401: AD is the sixth leading cause of death in the United States and the only 1 among the top 10 that cannot be prevented, cured, or even slowed. Vitamin D and neurocognitive disorder due to Alzheimer's disease: A review of the literature. 26510980: Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the fourth leading cause of death in the United States and most common cause of adult-onset dementia. 26517378: A variety of stressors, including beta-amyloid (Abeta) in the case of AD, can force neurons to leave quiescence and to initiate an ectopic DNA replication process, leading to neuronal death rather than division. 26690394: Alzheimer's disease (AD) is a debilitating progressive neurodegenerative disorder that ultimately leads to the patient's death. 2680026: Alzheimer's disease is the fourth most common cause of death in the United States, and is the leading cause of functional disability in the elderly. 2682166: Alzheimer's disease, once a rarely applied medical diagnosis, is now considered to be the fourth or fifth leading cause of death in the United States. 26983930: Alzheimer's disease (AD) is the fourth leading cause of death in Puerto Rico. 27127760: In Western societies, Alzheimer's disease (AD) is the most common form of dementia and the sixth leading cause of death. 27182464: As a result, Alzheimer's disease (AD), the 5th leading cause of death for people aged 65 and older, is likely to increase in these groups. 27190276: Alzheimer's disease (AD) is a leading cause of death and disability among older adults. 27235708: AD is now considered to be the third major cause of death in developed countries, after cardiovascular disease and cancer. 27570871: In 2013, official death certificates recorded 84,767 deaths from Alzheimer's disease, making it the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age >= 65 years. 27758699: BACKGROUND: In 2016, the statistical reports stated that Alzheimer is not just memory loss but it kills and has become the 6th leading cause of death. 27776890: AD is the sixth leading cause of death in the United States and is the only cause of death among the top ten that cannot currently be treated or cured (Alzheimer's Association, 2011; Selkoe, 1996). 27942104: BACKGROUND: Cognitive disorders and dementia are common problems, and Alzheimer's disease is one of the major leading causes of death worldwide. 28043897: Alzheimer's disease (AD) is a severe, chronic and progressive neurodegenerative disease associated with memory and cognition impairment ultimately leading to death. 28246336: Alzheimer's disease (AD) is one of the fastest-growing causes of death and disability in persons 65 years of age or older, affecting more than 5 million Americans alone. 28396328: METHODS: We obtained data on all community-dwelling adults with a recent diagnosis of Alzheimer disease in Finland (2005-2011) from the Medication use and Alzheimer disease (MEDALZ) cohort, which incorporates national registry data on prescriptions, reimbursement, hospital discharges and causes of death. 28417590: Alzheimer's disease (AD) is leading cause of death among older characterized by neurofibrillary tangles, oxidative stress, progressive neuronal deficits, and increased levels of amyloid-beta (Abeta) peptides. 28426958: Alzheimer's disease (AD) is the sixth leading cause of death in the United States and the most common cause of dementia in the elderly. 28442216: Alzheimer's disease (AD) is the most common form of dementia and the 6th leading cause of death in the US. 28490901: Breast cancer and Alzheimer's disease (AD) are major causes of death in older women. Amyloidosis, the aggregation of amyloid proteins to form amyloid bodies, plays a central role in the pathogenesis of AD and other human neuropathies by forming intracellular fibrillary proteins. 28542120: Alzheimer's disease (Alzheimer's), an ultimately fatal form of dementia, is the sixth leading cause of death in the United States, accounting for 3.6% of all deaths in 2014 (1,2). 28624131: Alzheimer disease (AD) is an irreversible, progressive brain disorder that causes slow loss of memory and thinking skills, normally leading to death in 3-9 y. 28634681: Currently, AD is one of the leading causes of death in developed countries and the only one of the top ten diseases without a means to prevent, cure, or significantly slow down its progression. 28825647: Alzheimer's disease (AD) is currently ranked as the sixth leading cause of death in the United States and recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people. 28889269: Alzheimer's disease (AD) is the most common form of adult neurode-generation and is characterised by progressive loss of cognitive function leading to death. 29024348: Alzheimer's disease (AD) is the sixth leading cause of death in the USA today; therefore, it is imperative that public health initiatives and clinical strategies are developed to prevent and effectively treat AD. 29060753: Alzheimer's Disease (AD) is one of the leading causes of death and dementia worldwide. 29061973: Alzheimer's disease (AD) is one of the leading causes of death for people over 65 years. 29164499: Alzheimer's disease, thought to be the most common underlying pathology for elders' cognitive dysfunction (Willis and Hakim 2013), is already the sixth leading cause of death in the United States (Alzheimer's Association 2016). 29270150: Alzheimer's disease is the most common neurodegenerative form of dementia that steadily worsens and eventually leads to death. 29336270: Characterized by the formation of beta-amyloid plaques, Alzheimer's disease (AD) is currently one of the leading causes of death across the world. 29372919: In Alzheimer's disease, it is believed that amyloid-beta proteins may be responsible for pore and defect formation within cellular membranes, leading to a breakdown of cellular homeostasis causing eventual neuronal death. 29446066: Those who died of AD were selected based on underlying cause of death. 29538632: Background: Alzheimer's disease is a progressive disease that degrades cognitive functioning and ultimately results in death. 29549645: Among different neurological disorders, Alzheimer's disease (AD) is recognized as the sixth leading cause of death globally. 29677545: Beta-amyloid (Abeta) peptide, the hallmark of Alzheimer's disease (AD), invokes a cascade of oxidative damage to neurons and eventually leads to neuronal death. 29714994: Alzheimer disease (AD) occurs in 8.8% of older US adults and is the sixth leading cause of death among older adults. 29749899: Alzheimer's disease is one of the leading causes of death worldwide and currently does not have any cure. 29772289: According to the Alzheimer Association Report (2017), Alzheimer's disease (AD) is the 6th primary cause of death in the USA, which affects nearly 5.5 million people. 29862455: Alzheimer's disease (AD) is the sixth leading cause of death in the United States where it is estimated that one in three seniors dies with AD or another dementia. 29932100: Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease, distinctively characterized by senile plaques, neurofibrillary tangles, and synaptic loss, finally resulting in neuronal death. 30039745: With rapid aging of world population, Alzheimer's disease is becoming a leading cause of death after cardiovascular disease and cancer. 30106219: AIMS: Alzheimer's disease (AD) is one of the leading causes of death in elderly people. 30108425: Prolonged AD leads to moderate-to-severe AD, which is one of the leading causes of death. 30110946: Alzheimer's disease (AD) is a neurodegenerative disorder mostly influencing the elderly, and causes death due to dementia. 30171866: Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common cause of dementia and the 6th leading cause of death. 30236015: Alzheimer disease (AD) is a progressive neurodegenerative disorder that affects approximately 5 million people in the United States and is the sixth leading cause of death in the country. 30243157: Alzheimer, the fourth leading cause of death embodies a key responsible event including formation of beta-amyloid protein clustering to amyloid plaque on blood vessels. 30328325: PURPOSE: Alzheimer's disease (AD) is the sixth most common cause of death in the United States. 30371351: SIGNIFICANCE: AD is one of the leading causes of death in America and continues to affect a growing population. 30486438: Alzheimer's disease (AD) is a progressive neurodegenerative disease that represents a major cause of death in many countries. 30532546: Nowadays, due to the increase in the number of aging population groups, there is also a growth of aging diseases such as Alzheimer's disease (AD), which is a progressive brain disorder that eventually results in death. 30545070: Brain ischemia is the second naturally occurring neuropathology, such as Alzheimer's disease, which causes the death of neurons in the CA1 region of the hippocampus. 30560544: Despite major academic and industry efforts, Alzheimer's disease (AD) remains the only leading cause of death for which no disease-modifying treatment is available. 30565076: Alzheimer's disease (AD) is the sixth leading cause of death globally and the main reason for dementia in elderly people. 30707915: The pathogenesis of Alzheimer's disease (AD) is involved in the aggregation of misfolded amyloid beta (Abeta), which upregulates the activity of acetylcholinesterase (AChE), increases the production of reactive oxygen species (ROS), enhances neuroinflammation, and eventually leads to neuronal death. 30740125: Alzheimer disease (AD) is the fourth major cause of death in the elderly following cancer, heart disease and cerebrovascular disease. In this study, we combined expression quantitative trait locus (eQTL) studies with the GWAS, to comprehensively define the genes that cause Alzheimer disease. 30747418: In the aging world population, Alzheimer's disease accounts for more than 70% of all cases of dementia and is the sixth leading cause of death. 30881282: Alzheimer's disease (AD) and cancer are among the leading causes of human death around the world. 30922415: OBJECTIVE: Alzheimer's disease (AD) is the sixth leading cause of death, with an average survival estimated between 5 and 10 years after diagnosis. 31068785: Alzheimer's disease (AD) has been categorized by the Centers for Disease Control and Prevention (CDC) as the 6th leading cause of death in the United States. 31201463: Alzheimer's Disease (AD) is the sixth-leading cause of death in industrialized countries. 31211444: AD is one of the leading causes of death in the United States. 31262433: In recent years, autophagy dysfunction has gained considerable attention in AD and other neurodegenerative diseases because it has been linked to the accumulation of misfolded proteins that ultimately causes neuronal death in many of these disorders. 31354494: AD is a leading cause of death worldwide and is progressive in nature with symptoms worsening over time. 31379558: Alzheimer's disease (AD) afflicts an estimated 20 million people worldwide and is the fourth-leading cause of death in the developed world. 31422384: Alzheimer's disease (AD) is a progressive neurodegenerative disease that ranks as the fourth most common cause of death in developed countries. 31430752: AD is the sixth leading cause of death in the USA, affecting an estimated 5 million Americans. 31524171: Most ADRDs are characterized by progressive neurodegeneration, and Alzheimer's disease (AD) is the sixth leading cause of death in the United States. 31540705: Alzheimer's and Parkinson's diseases are one of the world's leading causes of death. 31592230: In 2018, AD was the fifth leading cause of death in Americans with 65 years of age or older, but the progress of AD drug research is very limited. 31689949: Increasing evidence has demonstrated that amyloid-beta peptide (Abeta), the hallmark of Alzheimer's disease (AD), evokes oxidative and inflammatory cascades, which ultimately lead to the death of neurons. 31704512: There are several processes which can cause AD, including mitochondrial dysfunction-mediated oxidative stress (OS), intracellular buildup of hyper-phosphorylated tau as neurofibrillary tangles (NFTs) and excessive buildup of extracellular amyloid beta (Abeta) plaques, and/or genetic as well as the environmental factors. Alzheimer's disease (AD) is a progressive, chronic and severe neurodegenerative disorder linked with cognitive and memory impairment that eventually lead to death. 31837630: Alzheimer's Disease (AD) is one of the leading causes of death in developed countries. 31848379: Assessing the therapeutic potential of Graptopetalum paraguayense on Alzheimer's disease using patient iPSC-derived neurons.Alzheimer's disease (AD) is the most common type of dementia and also one of the leading causes of death worldwide. 31862920: Alzheimer disease and other dementias have become the 7th cause of death worldwide. 31866858: In developed countries, AD is now acknowledged as the third leading cause of death, following cardiovascular disease and cancer. 31871211: Alzheimer's disease: A clinical perspective and future nonhuman primate research opportunities.Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the sixth leading cause of death and the most common cause of dementia worldwide. 31989900: Recent trends in management of Alzheimer's disease: Current therapeutic options and drug repurposing approaches.Alzheimer's disease is one of the most progressive forms of dementia ultimately leading to death in aged populations. 32097673: Magnetic targeted delivery of the SPIONs-labeled mesenchymal stem cells derived from human Wharton's jelly in Alzheimer's rat models.Alzheimer's disease (AD) as a progressive neurodegenerative disorder is one of the leading causes of death globally. 32157811: Official death certificates recorded 122,019 deaths from AD in 2018, the latest year for which data are available, making Alzheimer's the sixth leading cause of death in the United States and the fifth leading cause of death among Americans age 65 and older. 32241275: Differential co-expression analysis reveals early stage transcriptomic decoupling in alzheimer's disease.BACKGROUND: Alzheimer's disease (AD) is one of the leading causes of death in the US and there is no validated drugs to stop, slow or prevent AD. 32265696: AD was ranked as the 5 th leading cause of global deaths in 2016 by the World Health Organization (WHO). 32327491: Antiepileptic drug use and mortality among community-dwelling persons with Alzheimer disease.OBJECTIVE: To evaluate the risk of death in relation to incident antiepileptic drug (AED) use compared with nonuse in people with Alzheimer disease (AD) through the assessment in terms of duration of use, specific drugs, and main causes of death. 32337953: miR-143-3p inhibition promotes neuronal survival in an Alzheimer's disease cell model by targeting neuregulin-1.INTRODUCTION: Alzheimer's disease (AD) is still the fifth leading cause of death and most common dementia worldwide. 32341952: More than 45 million people worldwide have Alzheimer's disease (AD), a deterioration of memory and other cognitive domains that leads to death within 3 to 9 years after diagnosis. 32481301: Acupuncture therapy for Alzheimer's disease: A protocol for an overview of systematic reviews.BACKGROUND: Alzheimer's disease (AD) is the fifth-leading cause of death in people more than 65 years old. 32486897: AD is currently ranked as the sixth leading cause of death, but some sources put it as third, following heart disease and cancer. 32515311: PTML Modeling for Alzheimer's Disease: Design and Prediction of Virtual Multi-Target Inhibitors of GSK3B, HDAC1, and HDAC6.BACKGROUND: Alzheimer's disease is characterized by a progressive pattern of cognitive and functional impairment, which ultimately leads to death. 32531244: The Physiology, Pathology, and Potential Therapeutic Applications of the TREM2 Signaling Pathway.Alzheimer's disease, obesity-related metabolic syndrome, and cancer are the leading causes of death and among the most costly medical conditions in the Western world. 32593336: Clinical and biomarker changes of Alzheimer's disease in adults with Down syndrome: a cross-sectional study.BACKGROUND: Alzheimer's disease and its complications are the leading cause of death in adults with Down syndrome. 32600151: Rapid improvement in Alzheimer's disease symptoms following fecal microbiota transplantation: a case report.Alzheimer's disease (AD), the most common form of dementia, is a leading cause of death and a major cause of morbidity in older people. 32628119: Diabetes-Related Topics in an Online Forum for Caregivers of Individuals Living With Alzheimer Disease and Related Dementias: Qualitative Inquiry.BACKGROUND: Diabetes and Alzheimer disease and related dementias (ADRD) are the seventh and sixth leading causes of death in the United States, respectively, and they coexist in many older adults. 32709243: Alzheimer disease (AD) is the most prominent form of dementia and the 5th leading cause of death in individuals over 65. 32807227: Cerebrospinal fluid profile of NPTX2 supports role of Alzheimer's disease-related inhibitory circuit dysfunction in adults with Down syndrome.BACKGROUND: Alzheimer's disease (AD) is the major cause of death in adults with Down syndrome (DS). 3285438: This could be responsible for the occurrence of senile changes (senile plaques and neurofibrillary tangles) which are both characteristic of so-called normal aging of the brain and of Alzheimer's disease and lead to neuronal death. 32894711: Multi-view Separable Pyramid Network for AD Prediction at MCI Stage by 18F-FDG Brain PET Imaging.Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 33011665: Estimates indicate that AD may rank third as a cause of death for older people, after heart disease and cancer. 33047398: RATIONALE: Alzheimer's disease (AD) is a chronic, severe, progressive neurodegenerative disorder associated with cognitive and memory impairment that ultimately causes death. 33126501: Alzheimer's Disease (AD) is a progressive multifactorial age-related neurodegenerative disorder that causes the majority of deaths due to dementia in the elderly. 33138782: BACKGROUND: Alzheimer's disease (AD) is related to higher mortality but it is not entirely evident which causes of death explain this. 33282526: AD is considered the fifth leading cause of death in Americans who are older than 65 years which prioritizes the importance of understanding the etiology of AD in its early stages before the onset of symptoms. 33316174: Diabetes, Alzheimer disease, and heart disease caused the most non-COVID-19 excess deaths. 33434704: Alzheimer's dementia (AD) is the sixth leading cause of death in the U.S., with an estimated $305 billion cost of care in 2020. 33438444: OBJECTIVES: Neurodegenerative diseases (NDs), such as Parkinson's disease and Alzheimer's disease and related dementias, are a leading cause of death and disability in China. 33500732: Alzheimer's disease (AD) is currently ranked as the third leading cause of death for eldly people, just behind heart disease and cancer. 33529936: Alzheimer's Disease (AD) is the most frequent illness and cause of death amongst the age related-neurodegenerative disorders. 33532133: Alzheimer's disease (AD) is one of the most common neurodegenerative diseases and a major cause of death among elderly individuals. 33532699: Background: Alzheimer's disease (AD) is the 6th leading cause of death in the United States and has no cure or progression prevention. 33750334: BACKGROUND: Alzheimer's disease (AD) is one of the leading causes of death world-wide, but little is known on the role of comorbidities on mortality among people with AD. 33756057: Official death certificates recorded 121,499 deaths from AD in 2019, the latest year for which data are available, making Alzheimer's the sixth-leading cause of death in the United States and the fifth-leading cause of death among Americans age 65 and older. 33802718: Specifically, 3.2 million deaths are reported yearly due to heart disease, cancer, Alzheimer's disease, diabetes, and COVID-19. 33839469: The paper recognizes the value and need to fight the image of AD as social death in research, the medical system, and popular understanding, but proposes a family Memory-Relationship self to conceptually capture the trauma many families feel as AD increasingly impairs the loved one with AD and leads to their death (unless they die of something else first). 33916001: Recent studies suggested that gut microbiota can influence AD progression; however, potential mechanisms linking the gut microbiota with AD pathogenesis remain obscure. Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, is a major cause of death and disability among the older population. 34021875: Alzheimer's disease (AD) is the fourth leading cause of death in the United States and the most common cause of adult-onset dementia. 34030620: Alzheimer's disease (AD) is the only leading cause of death for which no disease-modifying therapy is currently available. 34098466: Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease, characterized by irreversible cognitive impairment, memory loss and behavioral disturbances, ultimately leading to death. 34208980: Alzheimer's disease (AD) and other dementias are now the seventh leading cause of death in the world and are projected to affect 115.4 million people by 2050. 34219726: BACKGROUND: Hispanic older adults are a high-risk population for Alzheimer's disease and related dementias (ADRD) but are less likely than non-Hispanic White older adults to have ADRD documented as a cause of death on a death certificate. 34228042: Importance: Alzheimer disease (AD) is the leading cause of death in individuals with Down syndrome (DS). 34229061: Alzheimer's disease (AD) is a severe irreversible neurodegenerative disease that has great sufferings on patients and eventually leads to death. 34273065: Alzheimer's disease (AD) is now ranked as the third leading cause of death after heart disease and cancer. 34350508: Alzheimer's disease (AD) is a neurodegenerative disease characterized by amyloid plaques and tangles that have become the fifth leading cause of death worldwide. 34353220: BACKGROUND AND PURPOSE: Alzheimer disease (AD) is the most common form of dementia and the sixth leading cause of death in the United States. 34424488: AD is recognized as the sixth leading cause of death in the USA, and its prevalence is predicted to increase exponentially in the coming years. 34522196: Background and purpose: Alzheimer's disease is considered one of the lead causes of elderly death around the world. 34535721: Alzheimer's disease (AD) and other dementias have become the fifth leading cause of death worldwide. 34572985: Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. 34577590: Several risk factors are involved in the progression of AD, modifying neuronal circuits and brain cognition, and eventually leading to neuronal death. 34606321: Compared with White males and females, non-COVID-19 excess deaths per 100 000 persons were 2 to 4 times higher in Black, AI/AN, and Latino males and females, including deaths due to diabetes, heart disease, cerebrovascular disease, and Alzheimer disease. 34646644: Alzheimer's disease (AD) is the most common type of dementia and is among the leading cause of death in the United States. 34687637: Adults with Down syndrome develop the neuropathological hallmarks of Alzheimer's disease and are at very high risk of developing early-onset dementia, which is now the leading cause of death in this population. 34707479: Given that Alzheimer's Disease is the sixth leading cause of adult death in the U.S., elucidating the molecular interactions that characterize Alzheimer's Disease pathogenesis will allow for better treatment options. 34712129: Around 58% of the affected patients live in low and middle-income countries, with estimates of increasing deaths caused by AD in the coming decade. 34751889: Alzheimer's disease (AD) is considered the sixth leading cause of death in elderly patients and is characterized by progressive neuronal degeneration and impairment in memory, language, etc. 34867153: Alzheimer's disease (AD) is a neurodegenerative disease that impacts 45 million people worldwide and is ranked as the 6th top cause of death among all adults by the Centers for Disease Control and Prevention. 34891761: Alzheimer's Disease (AD) is the sixth leading cause of death in the US. 34971144: BACKGROUND: Alzheimer's Disease (AD), a progressive neurodegenerative disease and the second most common cause of death in Australia (ABS 2019), is an increasingly prominent societal issue, exacerbated by an ageing population and the absence of effective disease modifying treatments. 35023084: INTRODUCTION: Alzheimer's disease is one of the irreversible dementias and leads to death. 35109084: BACKGROUND: Alzheimer's disease (AD) is the leading cause of disability and 5th cause of death in people over 65 years of age. 35109462: Alzheimer's disease is the 6th leading cause of death in the United States. 35186657: Alzheimer's disease (AD) is a neurodegenerative disease and the fourth leading cause of death after cardiovascular disease, tumors, and stroke. 35218718: Apart from deaths due to AD, expenditure of treatment and care of AD patients is higher than that of treatment of HIV and cancer diseases combined. 35280344: AD is a progressive neurodegenerative disorder characterized by decline of memory, behavioral impairments that affects a person's ability to function independently ultimately leading to death. 35289055: Alzheimer's disease was officially listed as the sixth-leading cause of death in the United States in 2019 and the seventh-leading cause of death in 2020 and 2021, when COVID-19 entered the ranks of the top ten causes of death. 35431257: Alzheimer's disease (AD) is the only cause of death ranked in the top ten globally without precise early diagnosis or effective means of prevention or treatment. 35458896: Alzheimer's disease is the most common form of dementia and the fifth-leading cause of death among people over the age of 65. 35486224: Alzheimer's disease (AD), currently the single leading cause of death still on the rise, almost always coexists alongside vascular cognitive impairment (VCI). 35556967: Currently, an estimated 6.2 million Americans are living with AD, and it is ranked as the 6 th leading cause of death in the United States. 35599847: It ranks as the sixth leading cause of death in the United States, and the proportion of deaths due to AD has been increasing since 2000, while the proportion of many other leading causes of deaths have decreased or remained constant. 35624938: Alzheimer's disease (AD) is an incurable neurodegenerative disorder and the leading cause of death among older individuals. 35665670: Alzheimer's disease is the sixth leading cause of death in the United States, and the number of patients with the disease is set to hit 20 million by 2050. 35748395: Alzheimer's disease (AD) is a cumulative form of dementia associated with memory loss, cognition impairment, and finally leading to death. 35784755: In recent years, neurological diseases including Alzheimer's disease, Parkinson's disease and stroke are one of the main causes of death in the world. 35836098: Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease, characterized by irreversible cognitive impairment, memory loss, and behavioral disturbances, ultimately resulting in death. 35858523: Alzheimer's disease (AD), as the fourth leading cause of death among the elderly worldwide, has brought enormous challenge to the society. 35887134: As a neurodegenerative disease, Alzheimer's disease (AD) shows a higher incidence during the aging process, mainly revealing the characteristics of a significant decrease in cognition, uncontrolled emotion, and reduced learning and memory capacity, even leading to death. 35961638: Introduction : Alzheimer's disease (AD) dementia is the sixth leading cause of death in the United States. 35968378: Alzheimer's disease (AD) is the sixth leading cause of death worldwide and cannot be effectively cured or prevented; thus, early diagnosis, and intervention are important. 36165518: Alzheimer's disease (AD) has become the fourth leading cause of death in the world. 36197131: AD is the leading type of dementia, accounting for 60% to 80% of cases, and the sixth leading cause of death in the United States. 36268188: Alzheimer's disease (AD) is the most common form of dementia and is ranked as the 6th leading cause of death in the US. 36408377: Background: Alzheimer's disease (AD) is the most common form of dementia, which is among the top five causes of death in the United States. 36475205: Alzheimer's dementia (AD) is the most common major neurocognitive impairment and the fifth leading cause of death in older adults in the United States. 36502321: Later in life, AD leads to death as a result of the degeneration of specific brain areas. 36537919: Alzheimer's disease is the sixth-leading cause of death in the United States, and the number of deaths from all related dementias may be twice as high.[i] Years of investment and research in Alzheimer's disease and related dementias (ADRD) are sowing seeds of hope. 36583187: AD is the fifth leading cause of death among Americans age 65 and older. 36589440: Non-communicable diseases, like diabetes, cardiovascular diseases, cancer, stroke, chronic obstructive pulmonary disease, osteoporosis, arthritis, Alzheimer's disease and other more are a leading cause of death in almost all countries. 36593834: Alzheimer's disease is ranked among the top five causes of death for old people. 36674771: Nowadays, cancers and dementia, such as Alzheimer's disease, are the most fatal causes of death. 36708701: The pivotal characteristics of Alzheimer's disease (AD) are irreversible memory loss and progressive cognitive decline, eventually causing death from brain failure. 36780546: RESULTS: When analyzing death certificates without addressing the reporting of Down syndrome as the underlying cause of death, rates of death due to Alzheimer disease and dementia ranked as the third leading cause of death for both adults with and without Down syndrome. After amending death certificates that reported Down syndrome as the underlying cause of death, Alzheimer disease and dementia were the leading cause of death among those with Down syndrome, occurring 2.7 times more in adults with compared to without Down syndrome. 36841050: Alzheimer's disease (AD) implicates neuronal loss, plaque and neurofibrillary tangle formation, and disturbed neuronal Ca 2+ homeostasis, which leads to severe dementia, memory loss, as well as thinking and behavioral perturbations that could ultimately lead to death. 36842068: BACKGROUND AND OBJECTIVES: Alzheimer's disease or related dementia are a major cause of death in the United States. 36918389: Official death certificates recorded 121,499 deaths from AD in 2019, and Alzheimer's disease was officially listed as the sixth-leading cause of death in the United States. 36940723: Wealth of data has shown that oxidative stress and AD are closely connected that causes the death of neuronal cells by producing reactive oxygen species (ROS). 36961417: The notion that AD causes the death of neurons point towards protection of neuronal morphology and function as important therapeutic strategies. 36993752: Alzheimer's Disease (AD) continues to be a leading cause of death in the US. 36995136: METHODS: publicly accessible data on the prevalence, death and disability-adjusted life years (DALYs) because of AD, and other types of dementia, were retrieved from the global burden of disease 2019 project for all MENA countries from 1990 to 2019. 37038213: BACKGROUND: Alzheimer's disease (AD) is the 5th leading cause of death in people 65 years and older. 37109528: Presently more than 55 million individuals are affected by AD all over the world, and it is a leading cause of death in old age. 37208979: Compared with AD, hazard ratios for \nervous system\ causes of death were significantly elevated in all LBD groups. 37256433: INTRODUCTION: Clinical Alzheimer's disease (AD) begins with mild cognitive impairment (MCI) and progresses to mild, moderate, or severe dementia, constituting a disease continuum that eventually leads to death. 37304012: Alzheimer's Disease (AD) and related dementias are a leading cause of death globally and are predicted to increase in prevalence. 37375767: Alzheimer's disease (AD) is the most common type of dementia and is listed as the sixth-leading cause of death in the United States. 37486697: Alzheimer's disease is the only major cause of death that is still growing. 37507902: Currently, no drug is effective in delaying the cognitive impairment of Alzheimer's disease, which ranks as one of the top 10 causes of death worldwide. 37612307: In 2015, AD is reported the US's sixth cause of death. 37672968: Alzheimer's disease (AD) is the most common dementia type and a leading cause of death and disability in the elderly. 37679478: Alzheimer's Disease (AD) continues to be a leading cause of death in the US. 37693600: Alzheimer's Disease (AD) is the 6th leading cause of death in the US. 37955252: Alzheimer's disease (AD) is a progressive brain disease characterised by progressive memory loss and cognition impairment, ultimately leading to death. 37997077: BACKGROUND: Dementia and Alzheimer's disease are the leading cause of death in England, with prevalence estimated to rise with an ageing population. 38131985: In 2021, Alzheimer's disease resulted in 36 deaths per 100,000 in the U.S. Alzheimer's disease is the sixth most common cause of death in the United States (U.S.), with one in three adults 65 years of age and older dying of the disease each year. 38137554: Conditions such as Alzheimer's disease (AD), Parkinson's disease (PD), and dementia are becoming more prevalent and are now the fourth leading cause of death, following heart disease, cancer, and stroke. 38213663: AD (for which there is no exact cause and cure known so far) is the sixth leading cause of deaths in the United States. 38326859: Alzheimer's disease (AD) is the sixth leading cause of death in the USA. 38371416: A recent report from the Office of National Statistics showed that AD is the leading cause of death in 2022. 38381402: We know that many neurological age-related diseases, such as Alzheimer's disease, stroke, dementia, and Parkinson's disease, are the main cause of death in the last decades of life. 38414336: INTRODUCTION: There is no cure for Alzheimer's disease, which is the sixth leading cause of death in the U.S.A.. 38429957: RESULTS: During the study period, 751,493 deaths (1.7%, 233,271 males and 518,222 females) occurred in the EU-27 because of AD. 38612514: Interestingly, as AD progresses, less Abeta42 is detectable in the plasma, a phenomenon thought to result from Abeta becoming more aggregated in the brain and less Abeta42 and Abeta40 being transported from the brain to the plasma via the CSF. Alzheimer's disease (AD) is the fifth leading cause of death among adults aged 65 and older, yet the onset and progression of the disease is poorly understood. 38640743: Although Alzheimer's Disease is a leading cause of death in Vietnam and other post-conflict, low- and middle-income countries, aside from studies of veterans in western populations, research on war-related violence and deprivation as risk factors for cognitive disorders remains sparse. 3876409: Such a DNA repair defect could cause an abnormal accumulation of spontaneously occurring DNA damage in Parkinson's disease and Alzheimer's disease neurons in vivo, resulting in their premature death. 7485229: AD is the fourth leading cause of death in elderly persons 65 years or older in Western industrialized societies. 7921490: Alzheimer's disease is the fourth major cause of death in the developed world and is a major social and health care issue. 7997077: After heart disease, cancer and stroke, Alzheimer's disease (AD) is the fourth major cause of death in the developed countries. 8195568: AD is the fourth leading cause of death for adults, taking more than 100,000 lives annually. 8195569: Alzheimer's disease (AD) is the fourth leading cause of death of older persons. 8610107: In rat hippocampal culture, betaA exposure activates tau protein kinase I/glycogen synthase kinase 3beta (TPKI/GSK-3beta), which phosphorylates tau protein into Alzheimer disease-like forms, resulting in neuronal death. 8752460: Other forms of dementias like Alzheimer disease (AD) and vascular dementias are on the rise and the leading cause of death is cerebro- and cardiovascular diseases. 9154214: Since its first description by Aloys Alzheimer about 90 years ago, this neurodegenerative condition has advanced to become the fourth most common cause of death in the elderly, and is found in more than half of the very elderly demented. 9165306: The major hurdle in understanding Alzheimer's disease (AD) is a lack of knowledge about the etiology and pathogenesis of selective neuron death. 9333421: AD is the fourth commonest cause of death in humans, after heart attack, cancer and stroke. 9413702: Alzheimer's disease (AD) is a common neurodegenerative disorder and a leading cause of death among the elderly. 9460797: There was no significant association detected between a diagnosis of presenile Alzheimer's disease and dementia as a parental cause of death (p = 0.25), nor for vascular dementia (p = 0.67). 9520072: Alzheimer's disease (AD) is the most common neurodegenerative disorder characterized by progressive dementia that ultimately leads to death. 9647903: We examined exposure to magnetic fields, assessed as duration of work in exposed jobs and through an index of cumulative exposure based on magnetic field measurements, in relation to mortality from Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, considering both underlying and all mentioned causes of death. 12955221: PURPOSE: Alzheimer disease (AD) causes cortical degeneration with subsequent degenerative changes of the white matter. 14675724: The ensuing homeostatic responses to myelin breakdown further increase intracortical toxicity and results in the relentless progression and non-random anatomical distribution of AD lesions that eventually cause neuronal dysfunction and degeneration. 15140940: Alzheimer's disease (AD), the most common neurodegenerative disorder, results in progressive degeneration of synapses and aberrant sprouting of axon terminals. 15234342: Alzheimer's disease is a neurological disorder resulting in the degeneration and death of brain neurons controlling memory, cognition and behavior. 15285803: BACKGROUND: Neuroinflammation plays a prominent role in the progression of Alzheimer's disease and may be responsible for degeneration in vulnerable regions such as the hippocampus. 15817373: Recent studies shed new light on a potential cascade of events by which neurological diseases such as Alzheimer's lead to axonal degeneration. 16096820: BACKGROUND: Alzheimer's disease (AD) leads to a degeneration of the nucleus basalis of Meynert and thus to decreased cholinergic tonus in the brain. 1614354: Considerable evidence suggests that in Alzheimer's disease, olfactory bulb damage may be a primary factor, causing degeneration and neurofibrillary tangles primarily in neurons connected with this brain area. 16389306: Rare inherited forms of AD provide insight into the molecular pathways leading to degeneration and have made possible the development of transgenic animal models. 16533591: Progenitor cells in the adult human brain subependymal layer are capable of producing new neurons and glial cells that may be useful as a source of cells for endogenous cell replacement for regions of the brain that undergo degeneration due to a neurodegenerative disease such as Huntington's disease, Parkinson's disease or Alzheimer's disease. 17393059: CAA is present in most cases of AD, and it is characterized by the deposition of beta-amyloid (Abeta) in brain vessels, inducing the degeneration of vascular smooth muscle cells and endothelial cells. 20634578: The addition of Abeta(1-42) reduced the amount of synaptophysin in cultured cortical neurons in a model of AD-induced synapse degeneration. 20817045: beta-amyloid has been implicated in the pathogenesis of AD, and its accumulation may lead to degeneration of neuronal or non-neuronal cells. 20965261: Such changes are associated with traditional imaging metrics of degeneration and may provide a unique biomarker of the tissue loss that occurs as a result of AD. 21214538: Similarly, the toxic accumulation of Abeta peptides underlying Alzheimer's disease (AD) triggers synaptic degeneration, circuit remodeling, and abnormal synchronization within the same networks. 21241801: These findings suggest that, in neurons affected by AD, Abeta is toxic, impairs mitochondrial movements, reduces mitochondrial length, and causes synaptic degeneration. 22329649: In this review, we provide an overview of some of the most recent evidence for metabolic dysregulation in Alzheimer's disease, Huntington's disease, and Parkinson's disease, and discuss several potential mechanisms that may underlie the potential relationships between metabolic dysfunction and etiology of nervous system degeneration. 24635394: However, a multi-target approach using combinations of (micro)nutrients might have beneficial effects on cognitive function in neurodegenerative brain disorders like AD leading to synaptic degeneration. 25129614: Despite growing recognition of the importance of white matter abnormalities in the pathogenesis of AD, the causes of white matter degeneration are still unknown. 25477959: Alzheimer's disease is a neurodegenerative disorder characterized by the accumulation of beta amyloid plaques (Abeta) which can induce neurite degeneration and progressive dementia. 26973531: In Alzheimer's disease (AD), which is generally characterized by memory dysfunction, connections amongst the cells in the brain are attenuated or lost leading to degeneration of neural networks. 27466341: UNLABELLED: Alzheimer's disease (AD) is characterized by the progressive accumulation of amyloid beta (Abeta) and microtubule associate protein tau, leading to the selective degeneration of neurons in the neocortex, limbic system, and nucleus basalis, among others. 29155703: Alzheimer's disease (AD) is a debilitating neurodegenerative disease in which accumulation of toxic amyloid-beta42 (Abeta42) peptides leads to synaptic degeneration, inflammation, neuronal death, and learning deficits. 29587294: Topographic differences between subicular degeneration caused by ALS and Alzheimer disease (AD) had also not been characterized. 29782616: Results: A step-by-step workflow was developed and used to take patients' Digital Imaging and Computing in Medicine magnetic resonance brain images through a process resulting in illustrative 3D-printed brain and hippocampus models that clearly demonstrate the progressive degenerative changes caused by Alzheimer's disease. 30930730: Administration of the immunotoxin 192IgG-saporin to rats, an animal model of AD, leads to degeneration of cholinergic neurons in the medial septal area. 31356828: Even though traditionally Alzheimer's disease has been associated to Abeta deposits and hyperphosphorylated Tau intracellular tangles, several studies show that neuroinflammation may be the initial cause that triggers degeneration. 31415594: BACKGROUND: Alzheimer's Disease (AD) can cause degeneration in the retina and optic nerve either directly, as a result of amyloid beta deposits, or secondarily, as a result of the degradation of the visual cortex. 3732820: Alzheimer's disease presently is the commonest cause in the developed world, causing a cortical-subcortical degeneration of ascending cholinergic neurons and large pyramidal cells in the cerebral cortex. 7016437: Even though the laboratory animals develop tangles resembling those seen in patients with Alzheimer's Disease, no evidence has been published to show that the tangles seen in Alzheimer's Disease are induced by the elevated brain aluminum content. The patients with Alzheimer's Disease develop characteristic neurofibrillary tangles which lead to the degeneration of the affected neurons. 8318230: Thus, phosphorylation of Ser396 may destabilize MTs in AD, resulting in the degeneration of affected cells. 15375590: Since ApoE4 imparts risk for both hyperlipidemia and AD, it seemed worthwhile to investigate the possible role of ApoE in the pathogenesis of AD and VaD. 15883314: The diagnosis of vascular dementia is difficult in epidemiologic studies because poststroke dementia can be due to Alzheimer disease (AD) and evidence of vascular disease can be found in the MRI of dementia cases without clinical strokes. The dementia was attributable to only vascular factors in 56 cases (probable VaD); VaD coexisted with AD in 61 cases, although the VaD component was the leading cause of dementia (probable VaD with AD); AD was the leading cause of dementia in 61 cases (possible VaD and probable AD); and in 29 cases, it was not clear that either AD or VaD was the primary diagnosis (possible AD and possible VaD). 19896503: The latter findings are consistent with the concept that AD is a dietary-fat induced phenotype of vascular dementia, reflecting the extraordinary entrapment of peripherally derived lipoproteins endogenously enriched in Abeta. 22739039: DEVELOPMENT: The criteria for the diagnosis of vascular cognitive impairment have evolved, but available criteria were designed basically for differentiating between vascular dementia and dementia due to Alzheimer disease, and for research purposes. 23862185: BACKGROUND: Vascular dementia represents the second most common type of dementia after that caused by Alzheimer's disease. 26157520: Epidemiological studies have found associations between HHcy and Alzheimer's disease (AD) progression that eventually leads to vascular dementia (VaD). 28839167: The ultra-sensitive IMR assay was applied to detect the plasma tau protein levels of subjects with prevalent neurodegenerative diseases, such as Alzheimer's disease (AD), mild cognitive impairment (MCI) due to AD, Parkinson's disease (PD), frontotemporal dementia (FTD) and vascular dementia (VD). 30696930: Dementia was further categorised into Alzheimer's disease (AD), vascular dementia (VaD), and dementia caused by other diseases (ODs). 35986673: BACKGROUND: Vascular dementia (VaD) is the most common type of dementia secondary to Alzheimer's disease. 38226362: Despite its importance, research into VCID has lagged as compared to cognitive impairment due to Alzheimer's disease. 12410910: Only 13% of a group of patients receiving the AD therapy donepezil had AD as the primary diagnosis, and AD is rarely included as a primary or secondary DRG diagnosis when the condition precipitating admission to the hospital is caused by AD. In addition, AD is often not mentioned on death certificates, although it may be the proximate cause of death. 12707840: DLB is clinically under-diagnosed and frequently misclassified as systemic delirium or dementia due to Alzheimer's disease or cerebrovascular disease. 15683939: This definition is well adapted to Alzheimer's disease but results in delayed diagnosis or misclassification of dementias such as frontotemporal dementia or dementia with Lewy bodies in which memory deficits are minor or late. 17048151: However, Abeta/amyloid deposition is likely necessary but not sufficient to cause AD, and other putative downstream pathologies, including the aggregation of phospho-tau in neurofibrillary tangles, synaptic and neuronal loss, and glial and inflammatory responses, are likely equally important to AD pathogenesis. Alzheimer's disease (AD) is the most commonly diagnosed etiology of dementia and may be caused by the progressive accumulation and deposition of neurotoxic Abeta/amyloid plaques and aggregates in brain with aging-the amyloid hypothesis of AD. 20511105: RESULTS: Overall, 24.1% (425/1764) patients had a diagnosis of dementia, most frequently secondary to Alzheimer's disease (260/425, 61.2%). 21514249: The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. 21514250: The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. 21747305: Alzheimer disease (AD) accounts for most dementia diagnoses. 22573143: MCI patients were re-classified according to the conversion status upon follow-up: 25 individuals retained the diagnostic status of MCI and were considered as stable cases (MCI-MCI); conversely, in nine cases the diagnosis of dementia due to AD was ascertained. 23011220: In conclusion, a measure of story recall may increase the confidence in making a diagnosis of MCI due to AD in clinical settings. The identification of memory measures that are associated with Abeta is of clinical relevance as this may enhance the confidence in making a diagnosis of MCI due to AD in clinical settings. 23070466: Supporting evidence for using biomarkers in the diagnosis of MCI due to AD. The results of this study provide evidence in favour of the use of biomarkers for the diagnosis of MCI due to AD, in line with recently published research criteria. The aim of this study is to support the use of biomarkers in the diagnosis of mild cognitive impairment (MCI) due to Alzheimer's disease (AD) according to the revised NIA-AA diagnostic criteria. 23114667: CONCLUSIONS: These new criteria are immediately helpful to the practicing clinician, providing more accurate and specific guidelines for the diagnosis of AD dementia and MCI due to AD. REVIEW SUMMARY: Four articles in the journal Alzheimer's & Dementia in 2011 describe new criteria for AD dementia and mild cognitive impairment (MCI) due to the AD pathophysiological process (MCI due to AD) and the underlying rationale for them. 23531500: In Alzheimer's disease (AD), fatal neuronal cell loss occurs long before relevant evidence can lead to a reliable diagnosis. 24392252: Practical diagnosis and management of dementia due to Alzheimer's disease in the primary care setting: an evidence-based approach. 24678299: This piece aims to stimulate discussion by identifying the ethical challenges involved in the use of biomarkers to make a diagnosis of mild cognitive impairment due to AD and disclose it to patients. 25150733: Seventy-nine percent of responders felt \very/extremely\ comfortable delivering a diagnosis of MCI due to AD when both amyloid and neuronal injury biomarkers were abnormal (P < .02 versus any individual biomarker). 25201782: Hippocampal volume is a promising biomarker to enhance the accuracy of the diagnosis of dementia due to Alzheimer's disease (AD). 25605659: The observation that similar diagnostic sensitivity was obtained in two separate study populations, allied to the scalability and usability of the test in community memory clinics, supports future application of the 4MT in the diagnosis of pre-dementia due to AD. 26424328: BACKGROUND: It may be assumed that increased public awareness of dementia due to Alzheimer's disease (AD) together with the availability of efficacious treatment will result in diagnostic evaluation at earlier stages of cognitive decline and diagnosis of dementia due to AD at earlier stages. 26478889: Use of these biomarkers for the detection of early and preclinical AD has become of central importance following publication of two international expert working group's revised criteria for the diagnosis of AD dementia, mild cognitive impairment (MCI) due to AD, prodromal AD and preclinical AD. 26502818: We suggest that amygdala function should be incorporated into the cognitive screening tool for the diagnosis of mild cognitive impairment due to AD. 26567733: Recommended guidelines for the diagnosis of dementia due to Alzheimer's Disease (AD) were revised in recent years, including Positron Emission Tomography (PET) as an in-vivo diagnostic imaging technique for the diagnosis of neurodegeneration. 27372368: METHOD: We mailed questions to all active patients with diagnoses of MCI or dementia due to AD of a rural memory clinic and compare features of the responders versus the non-responders. 28522977: The diagnosis of MNCD-AD was made according to DSM-5 criteria for possible MNCD-AD. 28733959: Here we present a streamlined questionnaire-enriched, biomarker-enriched approach that is more cost-effective than the current diagnosis of exclusion and is designed to increase clinical confidence for a diagnosis of dementia due to AD. 28787712: METHODS: Physicians identified patients seeking a diagnosis for mild cognitive impairment or dementia, possibly due to Alzheimer disease (AD), and recorded a working diagnosis and a management plan. 28891447: RESULTS: Molecular imaging marker of amyloid pathology, and volumetric markers of regional and whole brain atrophy support the diagnosis of AD dementia and MCI due to AD, and contribute to confidence in the differential diagnosis of AD and non-AD related dementias in specialized care. 29051531: Towards this end, we characterized the bacterial taxonomic composition of fecal samples from participants with and without a diagnosis of dementia due to AD. 29164600: However, the National Institute on Aging and Alzheimer's Association (NIA-AA) revised the diagnostic criteria for Alzheimer's disease and confidence in the diagnosis of mild cognitive impairment (MCI) due to Alzheimer's disease may be increased when using some amyloid biomarkers tests like 18F-florbetaben. 29164602: However, the National Institute on Aging and Alzheimer's Association (NIA-AA) revised the diagnostic criteria for Alzheimer's disease and the confidence in the diagnosis of mild cognitive impairment (MCI) due to Alzheimer's disease may be increased when using some amyloid biomarkers tests like 18F-flutemetamol. 29164603: However, the National Institute on Aging and Alzheimer's Association (NIA-AA) revised the diagnostic criteria for Alzheimer's disease and confidence in the diagnosis of mild cognitive impairment (MCI) due to Alzheimer's disease may be increased when using amyloid biomarkers tests like 18F-florbetapir. 29213740: A review of the evidence on cognitive, functional and behavioral assessment for the diagnosis of dementia due to Alzheimer's disease (AD) is presented with revision and broadening of the recommendations on the use of tests and batteries in Brazil for the diagnosis of dementia due to AD. 29318973: After a median follow-up of 36 months (range 7-74), the final diagnosis was AD MCI or dementia for 9 (24%) patients, and unlikely due to AD for 28 (76%) patients. 29365053: The primary outcome was progression from normal cognition to the onset of clinical symptoms of mild cognitive impairment due to Alzheimer's disease at 5 years post-baseline. The goal of this study was to determine which measures, obtained when individuals were cognitively normal, predict on an individual basis, the onset of clinical symptoms associated with a diagnosis of mild cognitive impairment due to Alzheimer's disease. 29512075: The diagnosis of dementia probably due to Alzheimer's disease is still primarily a clinical one. 29582053: Eligibility required a diagnosis of mild to moderate dementia due to AD and individuals aged 55 to 80 years. 29704037: While clinical outcome studies supporting the diagnosis of MCI due to AD showed varying accuracies (ranging from 58 to 100%) and varying areas under the receiver-operator characteristic curves (0.66 to 0.97), no respective data were identified for MCI due to FTLD or for MCI due to DLB. 29729732: However, the modern diagnostic strategies of AD present several disadvantages: the low accuracy and specificity resulting in some false-negative diagnoses, and the poor sensitivity leading to a delayed treatment. 30010131: Diagnosis of Mild Cognitive Impairment Due to Alzheimer's Disease with Transcranial Magnetic Stimulation. 30399602: Final diagnosis in most patients was Dementia due to probable Alzheimers disease, followed by Frontotemporal dementia. 30560245: We set out to investigate the insights general practitioners (GPs) have into the early signs and symptoms of Alzheimer's disease (AD), factors that may be responsible for the late diagnosis, as well as their recommendations for early diagnosis of AD. 30756114: The primary objective is to assess the ability of the Alzheimer's Prevention Initiative Cognitive Composite Test Score and Repeatable Battery for the Assessment of Neuropsychological Status to predict clinically meaningful outcomes such as diagnosis of mild cognitive impairment or dementia due to Alzheimer's disease, and change in Clinical Dementia Rating - Global Score. 30814473: METHODS: We recruited 32 subjects with a diagnosis of probable AD dementia (ADD, n = 20) and mild cognitive impairment due to AD (MCI-AD, n = 12) according to the NIA-AA 2011 criteria. 30829855: As a consequence, the diagnosis of AD can be delayed, often occurring too late for meaningful intervention. 30900850: Disclosing the diagnosis of cognitive impairment or dementia due to Alzheimer's disease (AD) and Related Dementias (ADRD) can be one of the most challenging aspects of dementia care for clinicians. 31211217: Primary outcomes include time to event, with event defined as diagnosis of mild cognitive impairment due to AD and/or dementia due to AD, and the Alzheimer's Prevention Initiative preclinical composite cognitive test battery. 31439020: Over 70% of the physicians considered that a diagnosis of prodromal AD/MCI due to AD had an added value over the MCI diagnosis. 31488095: A diagnosis of MCI due to Alzheimer's disease was given and a co-morbidity with a silent arachnoid cyst was assumed. 11142178: Alzheimer's disease (AD), the leading cause of disability in people older than 75 years of age, has direct and indirect medical costs estimated at $100 billion per year. 11345519: These results agree with the suggestion that the well-documented impairment in brain-energy metabolism in AD may be a direct cause of the clinical disability. 12226541: This paper discusses the hypothesis that the cerebrometabolic deficiency in Alzheimer's disease(AD) is the proximate cause of the clinical disability. 14611864: Without medical progress, dementing diseases such as Alzheimer's disease will become one of the main causes of disability. 14738700: Alzheimer's disease (AD) is associated with neuropsychologic and neuropsychiatric dysfunction and is a leading cause of disability among the elderly. 15554415: Stroke and a wide spectrum of neuropsychiatric illnesses such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, traumatic head injury, and schizophrenia all lead to severe disability. 16997144: Alzheimer's disease (AD) is the most common form of senile dementia and the fourth highest cause of disability and death in the elderly. 17132969: Alzheimer disease is the most common form of dementia in Western countries and the leading cause of disability in the over-65 population. 17226739: AD is a major cause of disability and mortality, and its impact on health care costs, including direct and indirect medical and social service costs, is estimated to be greater than $100 billion per year. 17334267: Most studies have primarily focused on disability due to Alzheimer disease (AD), and less is known about profiles of functional impairment in other dementia syndromes. 1781964: Alzheimer disease is a common neurodegenerative disorder consisting of memory impairment and intellectual function that produces not only profound disabilities in the patient, but a significant cost to society as well. 18368375: AD is among the leading causes of disability and death in older people. 19586077: Alzheimer's disease (AD) is a leading cause of disability in the elderly, leading to a high burden on caregivers and costs to society. 20976693: Dementia, Alzheimer's disease in particular, is one of the major causes of disability and decreased quality of life among the elderly and a leading obstacle to successful aging. 21197431: Alzheimer's Disease (AD) is the most frequent form of dementia and represents one of the main causes of disability among older subjects. 21843595: Alzheimer's disease (AD) is a major cause of disability in the elderly. 22178471: Most chronic diseases--such as cancer, cardiovascular disease (CVD), Alzheimer disease, Parkinson disease, arthritis, diabetes and obesity--are becoming leading causes of disability and death all over the world. 22201914: As the aging population increases, the prevalence of AD has increased remarkably worldwide and AD has become one of the leading causes of disability and death among the elderly. 22447723: Alzheimer's disease (AD), one of the major causes of disability and mortality in Western societies, is a progressive age-related neurodegenerative disorder. 22541861: Alzheimer's disease (AD), which is the most common form of dementia, constitutes one of the leading causes of disability and mortality in aging societies. 23538412: Alzheimer disease prevails as a major cause of disability in the elderly population and ranks as the most common form of dementia that affects 1 of 8 individuals older than 65 years of age. 23762322: Among these medications, some might benefit, while others might exacerbate, the pathogenesis of AD. Alzheimer's disease (AD) is rapidly becoming one of the leading causes of disability and mortality in the elderly. 24323427: Neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), prion disease, and other diseases that affect the neuromuscular system, are a leading cause of disability in the aging population. 26188654: Alzheimer's disease (AD) is the most common form of dementia and is a major cause of disability and dependency amongst older people. 26991979: The only disease-specific variable that improved the logistic model was 'disability due to AD'. 'Disability due to AD' was the only disease-related marker for depression in AD, although this marker cannot be considered specific for AD. 27074540: Alzheimer's disease (AD) and Parkinson's disease (PD) are the leading causes of disability associated with neurodegeneration worldwide. 27123241: Alzheimer's disease (AD) is the most common cause of disability in individuals aged >65 years worldwide. 27567824: Alzheimer's disease (AD) is a major cause of disability in the elderly, leading to a considerable burden on caregivers and high costs to society. 27697061: Our review concludes with some suggestions for future studies aimed to advance research into NBS as a potential treatment for the symptoms and disabilities caused by AD and to enable comparison of results across trials. 28861757: AD-like pathology was produced by administering AbetaP (1-40) intracerebroventricular (i.c.v.) in the left lateral ventricle (250 ng/10 MUl, once daily) for 4 weeks. Alzheimer's disease (AD) is one of the leading causes for disability and death affecting millions of people worldwide. 29256351: Likewise, neurodegenerative diseases such as Alzheimer's disease, Parkinson's diseases, multiple sclerosis or glaucoma defined as ocular Alzheimer's disease, are associated with a large public health burden and are among the leading causes of disability. 29260173: These results suggested that fucoidan might exert its protective effects against Abeta-induced toxicity in transgenic AD C. elegans by reducing the accumulation of toxic Abeta and decreasing Abeta-induced production of ROS, thus ameliorating the progression of the AD phenotype. As the aging population is increasing, AD is becoming one of the leading causes of disability and death among the elderly. 29460787: The present study aimed to evaluate the validity and reliability of the visual estimation method, in long-term inpatients with different levels of eating disability caused by Alzheimer's disease. 29466244: Neurological disorders have aroused a significant concern among the health scientists globally, as diseases such as Parkinson's, Alzheimer's and dementia lead to disability and people have to live with them throughout the life. 29575030: Alzheimer's disease (AD) is the most common form of dementia and one of the major causes of disability and dependency in older people. 30336640: Alzheimer's disease (AD) is one of the main causes of disability and dependency among elderly people. 30428832: BACKGROUND: One of the crucial challenges for the future of therapeutic approaches to Alzheimer's disease (AD) is to target the main pathological processes responsible for disability and dependency. 30775973: Among the elderly, AD shortens life expectancy, results in disability, decreases quality of life, and ultimately, leads to institutionalization. 31226738: Alzheimer's disease (AD) is the most common type of dementia and is the leading cause of disability in elderly people worldwide. 31367416: Aim: To clarify the characteristics of appropriate care methods for people with daily life disabilities due to Alzheimer's type dementia. 31413325: Alzheimer's disease and other types of dementia are the top cause for disabilities in later life and various types of experiments have been performed to understand the underlying mechanisms of the disease with the aim of coming up with potential drug targets. 31456679: Alzheimer's disease, and dementia, represent a common cause of disability and one of the most relevant challenges in the health world. 31788340: Alzheimer's disease (AD) is a neurodegenerative disorder and one of the leading causes of disability and mortality in the late life with no curative treatment currently. 10559765: In conclusion, the quality of life for adults with DS can be improved by routine, systematic health care screening to identify treatable diseases that may be missed because of poor communication or confusion due to Alzheimer disease. 10993489: Cerebrovascular pathology, Lewy bodies, or hippocampal sclerosis in combination with neuropathological signs of AD of only limited severity results in a disease that is essentially different from severe, purely degenerative AD. 11450439: The systematization of modern biochemical and structural date related to the action of physiologically active compounds on the nervous system apparatus engaged in the AD-like disorders pathogenesis was performed. 11513911: INTERPRETATION: In-vivo detection of increased [11C](R)-PK11195 binding in Alzheimer-type dementia, including mild and early forms, suggests that microglial activation is an early event in the pathogenesis of the disease. 11532247: All three isoforms are aberrantly expressed in Alzheimer's disease giving rise to elevated levels of nitric oxide apparently involved in the pathogenesis of this disease by various different mechanisms including oxidative stress and activation of intracellular signalling mechanisms. 11585670: Utilizing both cDNA- and genomic-based approaches, these mouse models for Alzheimer's disease have already provided valuable insights into the pathogenesis of the disease and potential therapeutic interventions. 11813874: A central question involving the role of A beta in AD concerns how A beta causes disease and whether it is extracellular A beta deposition and/or intracellular A beta accumulation that initiates the disease process. The discovery of familial AD (FAD) mutations in the genes for the amyloid precursor protein (APP) and presenilins (PSs), all of which increase A beta42 production, support the view that A beta is centrally involved in the pathogenesis of AD. 11816795: Further investigation of alpha-synuclein and its relationship to pathological conditions promoting Lewy body formation in AD, PD, and DLB may yield further insight into pathogenesis of these diseases. 11935076: BACKGROUND: The main stumbling block in the clinical management and in the search for a cure of Alzheimer disease (AD) is that the cause of this disorder has remained uncertain until now. 12459889: In addition to the association between apoE4 and an increased risk of AD, oxidative stress is believed to play a role in the pathogenesis of this disease. 12464614: The abnormal accumulation of beta-amyloid (Abeta) in the brain is an early and invariant feature in Alzheimer's disease (AD) and is believed to play a pivotal role in the etiology and pathogenesis of the disease. 12473185: The controlled activation of PKC-epsilon plays a protective role in the development of cardiac ischemia and Alzheimer's disease, whereas its uncontrolled chronic activation results in severe diseases such as malignant tumors and diabetes. 12587940: Recent research, however, has shown that inflammatory mechanisms are also associated with AD and that they could have a role in contributing to the pathogenesis of this disease. 12629906: Mutations in the amyloid precursor protein gene (APP) and the presenilin genes (PSEN1 en PSEN2) cause early onset Alzheimer's disease. Research in the field of Alzheimer's disease has shown that genetic factors play an important role in the aetiology of the disease. 12845151: The prolongation of life and the rapidly increasing incidence of Alzheimer's disease have brought to the foreground the need for greater understanding of the etiology of the disease and the means to prevent or at least slow down the process. 12884970: Small animal models that manifest many of the characteristic neuropathological and behavioral features of Alzheimer's disease (AD) have been developed and have proven of great value for studying the pathogenesis of this disorder at the molecular, cellular and behavioral levels. 12900170: Although it remains uncertain whether the UPR plays a mechanistic role in prototypical neurodegenerative disorders such as Alzheimer's disease, this is plausible because misfolded proteins are directly implicated in the pathogenesis of these disorders. 14599482: Cholinergic deficits in Alzheimer's disease are accompanied by a number of alterations in other transmitter systems including glutamate, noradrenaline and serotonin, suggesting the involvement also of other neurotransmitter systems in the pathogenesis of the disease. 14720176: Pathological relationships between damage to the deep white matter of the cerebral cortex [as evidenced by myelin loss (ML)], cerebral amyloid angiopathy (CAA) and arteriosclerosis (ART) were investigated in the brains of 137 patients with autopsy-confirmed Alzheimer's disease (AD), in order to better understand the causes of white matter damage in AD, and the contribution of this to the pathogenesis of the disorder. 14758647: The specifics of disorders in the operative memory due to Alzheimer's disease suggest that cholinergic mechanisms determining the sensory processing differ from those involved in decision-making. 15172740: Despite very numerous studies on Alzheimer's disease (AD), especially on amyloid plaques and neurofibrillary tangles, little information has been obtained thus on the causes of the disease. 15219712: Behavioral assessment of genetically-manipulated mouse lines for Alzheimer's disease has become an important index for determining the efficacy of therapeutic interventions and examining disease pathogenesis. 15708428: It is well established that oxidative stress plays a key role in the degenerative neuronal death and progression of Alzheimer's disease (AD), although it is not clear if it is the primary triggering event in the pathogenesis of this disorder. 15723159: The recent elucidation of the inflammatory pathways involved in Alzheimer's disease however, has opened doors for better treatment and prevention by identification of areas of therapeutic intervention that target the cause of the disease rather than the symptoms. 15964666: Aging represents the main risk factor to develop Alzheimer disease (AD) and protein aggregation constitutes a pathological hallmark thought to be involved in the etiology of this disease. 16139258: BACKGROUND: Identification of all susceptibility loci for Alzheimer's disease has been a major goal in resolving the pathogenesis of this disease. 16250840: Genetic and pharmacological manipulation of these Abeta-depositing transgenic mice is providing some intriguing and unexpected insights into the role of innate and adaptive immune mechanisms in the pathogenesis of AD. There is extensive evidence that changes in immune system activation accompany the pathological changes of Alzheimer's disease (AD), but a mechanistic understanding of how the immune system actually participates in disease pathogenesis is still largely lacking. 16396232: During the past 20 years, research on AD has increased the knowledge of the physiopathological mechanisms leading to the disease. 16471078: The overlap between cerebrovascular disease and Alzheimer disease produces a disorder that might be amenable to therapeutic approaches based on either mechanism. 16472207: Most investigators studying the underlying cause of AD have focused on amyloid-beta (Abeta) such that the Amyloid Cascade Hypothesis is the predominant mechanism thought to be responsible for the disease. 16624449: Besides the genetic, biochemical and neuropathological analogies between Down's syndrome (DS) and Alzheimer's disease (AD), there is ample evidence of the involvement of oxidative stress (OS) in the pathogenesis of both disorders. 16752360: These data suggest that ABCA2 may exert population-dependent effects on the genetic risk for sporadic AD and support a role of ABC lipid transporters in the pathogenesis of this disease. 16782202: Lack of an adequate animal model for Alzheimer's disease (AD) has limited an understanding of the pathogenesis of the disease and the development of therapeutic agents targeting key pathophysiological processes. 16914877: For Alzheimer's disease (AD), the classical pathology is now known for quite some time; however, the disease pathogenesis has eluded our understanding for a complete century. 16999991: Autophagic vacuoles also accumulate abnormally in affected neurons of several major neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, where they have been linked to various aspects of disease pathogenesis including neuronal cell death. 17119296: Although the causes of AD remain still unknown, it seems that certain environmental factors may be involved in the etiology and pathogenesis of the disease. 17229880: To determine which hypothesis relates best to Alzheimer disease requires a broader view of disease pathogenesis and is discussed herein. 17245412: The distinct protein aggregates that are found in Alzheimer's, Parkinson's, Huntington's and prion diseases seem to cause these disorders. 17305591: There is considerable evidence showing that oxidative damage is one of the earliest neuronal and pathological changes of Alzheimer disease and many, if not all, of the etiological and pathological causes of the disease are related, directly or indirectly, to free radical production and oxidative damage. 17556794: It is accepted that amyloid beta (A beta) peptides are responsible for the etiopathology of AD, but the precise signaling pathways leading to the disease have not been elucidated. 17557921: Statins are reported to be beneficial in treating a multitude of disorders including dementia due to Alzheimer disease (AD) and vascular dementia (VaD) with varying, yet-to-be determined mechanisms of actions. 17605000: Oxidative stress is one of the earliest events of Alzheimer disease (AD), with implications as an important mediator in the onset, progression and pathogenesis of the disease. 17940659: With respect to Alzheimer's disease, several proteins involved in the etiology of the disease, including tau, neurofilaments, beta-amyloid precursor protein, and synaptosomal proteins are GlcNAcylated in normal brain. 17981707: The neurobiological links between the renin-angiotensin system and Alzheimer's disease have been investigated and become a source of interest in the pathogenesis of the disease. 17986152: Alterations in lipid molecular species in the brain induced by neurodegenerative diseases, such as Alzheimer's disease (AD) could provide fundamental clues to disease pathogenesis. 1814411: In Alzheimer's disease, we found all ganglio-series gangliosides (GM1, GD1a, GD1b, GT1b) to be decreased in regions (temporal and frontal cortex and nucleus basalis of Meynert) involved in pathogenesis of disease. 18245893: The impact of genotype of apoE, a major vitamin K transporter, on ostepporosis as well as Alzheimer disease and atherosclerosis, raises a question whether vitamin K is involved in the pathogenesis of these diseases. 18289026: Alzheimer disease and the role of free radicals in the pathogenesis of the disease. 18302763: Explorations of IL-1's role in chronic neurodegenerative disease have mainly focused on Alzheimer disease (AD), where indirect evidence has implicated it in disease pathogenesis. 18378224: We postulate that a combination of diet, lifestyle, vascular, genetic, and amyloid related factors, which enhance each other's contribution in the onset and course of Alzheimer's disease, will be more likely the cause of the disease instead of one sole mechanism. 18629638: Alzheimer's and Parkinson's diseases or Friedreich ataxia are neurological diseases sharing, as a common denominator, production of abnormal proteins, mitochondrial dysfunction and oxidative stress, which contribute to the pathogenesis of these so called \protein conformational diseases\. 1877089: Molecular dissection of the neuropathology of AD has provided insight into the pathogenesis of this disease and has defined areas where investigation may prove useful in elucidating the cause of this disorder and suggest new treatments. 18855662: Furthermore, several therapeutic strategies for treating AD on the basis of the important role of tau hyperphosphorylation in the pathogenesis of the disease are described. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. 1927686: Metabolic abnormalities of the neocortices in late-stage AD correlate with regional densities of neurofibrillary tangles but not of senile plaques post mortem, suggesting that tangle formation is important in disease pathogenesis. 19288120: Further, Abeta models of AD strongly support the notion that oxidative stress induced by Abeta may be a driving force in AD pathogenesis. Studies conducted on arguably the earliest stage of AD, MCI, may elucidate the mechanism(s) leading to AD pathogenesis by identifying early markers of the disease, and to develop therapeutic strategies to slow or prevent the progression of AD. 19424834: Murine models that mimic the neuropathology of Alzheimer's disease (AD) have the potential to provide insight into the pathogenesis of the disease and lead to new strategies for the therapeutic management of afflicted patients. 19746990: Our results provide further evidence for the capacity of proteomics applications to identify conserved sets of disease-specific proteins in AD, to enhance our understanding of disease pathogenesis, and to deliver new candidates for the development of effective therapies for this, and other, devastating neurodegenerative disorders. 20021415: Here we provide further characterization of a genomic-based, amyloid precursor protein yeast artificial chromosome transgenic mouse model of AD, R1.40, that makes few assumptions regarding disease pathogenesis to study the relationship between brain pathology and altered behavior. 20049724: Surrogate markers for the Alzheimer disease (AD)-associated 42-amino acid form of amyloid-beta (Abeta42) have been sought because they may aid in the diagnosis of AD and for clarification of disease pathogenesis. 20054780: Such a conclusion has implications both for the diagnosis of AD and in studies of disease pathogenesis. 20064547: Alzheimer's disease (AD) and age-related cataract, disorders characterized by protein aggregation causing late-onset disease, both involve oxidative stress. 20157260: The present study was aimed to investigate neuropathological changes in AbetaPP/PS1 transgenic mice (Tg), as a model of Alzheimer's disease, subjected to supplementary iron administration in a critical postnatal period, in order to reveal the interaction of genetic and environmental risk factors in the pathogenesis of the disease. 20308790: Circulating angiogenic cells and Alzheimer's disease: contribution of the bone marrow to the pathogenesis of the disease. 20431570: Among these, strategies targeting the production and clearance of the amyloid-beta peptide - a cardinal feature of Alzheimer's disease that is thought to be important in disease pathogenesis - are the most advanced. 20471965: Transgenic models of AD are a promising tool in understanding the underlying mechanisms and cause of disease. 20497615: Neuropathological assessment using molecular biology and immunohistochemistry, homogeneous definitions, harmonized interlaboratory methods, and assessment standards can identify 54 to 97% of AD cases and can eliminate 62 to 100% of nondemented subjects, but only between 8 and 42% of non-AD dementias, without, however, being able to clarify the etiology of most of these disorders. 20558146: Transgenic models of AD are a promising tool in understanding the underlying mechanisms and cause of disease. 20608291: The atrophy of the brain with Alzheimer's disease is considered to be caused by the amyloid angiopathy of small blood vessels and the degeneration of capillaries and vascular feet. Based on this viewpoint, this review article emphasizes that the morphological changes to small blood vessels in the brain with Alzheimer's disease convey crucial information and clues for solving the underlying mechanism that causes the disease. 20676620: Models of disease or the response of cellular networks to pharmacological compounds can be studied in vitro, allowing one to investigate pathologies, such as cardiac arrhythmias, memory impairment due to Alzheimer's disease, or vision impairment caused by ganglion cell degeneration in the retina. 20840725: The global pathway crosstalk network and the clusters of relevant pathways of AD provide evidence of cooperativity among pathways for potential pathogenesis of the neuron complex disease. 20936705: The wheat germ agglutinin-fractionated proteome of subjects with Alzheimer's disease and mild cognitive impairment hippocampus and inferior parietal lobule: Implications for disease pathogenesis and progression. 21091946: The identification of disease-causing mutations in Alzheimer's disease has contributed greatly to the understanding of the pathogenesis of this disease. The amyloid-beta (Abeta) peptide has come into focus and is believed to be central to the pathogenesis of Alzheimer's disease. 21150306: These diseases, including Morbus Alzheimer, Parkinson disease and Transmissible Spongiform Encephalopathies (TSEs)--also termed prion disorders--afflict a substantial proportion of the human population and as such the etiology and pathogenesis of these diseases has been the focus of mounting research. 21439035: Although the idea that vascular defects are present in AD and may be important in disease pathogenesis was suggested over 25 years ago, little work has focused on an active role for cerebrovascular mechanisms in the pathogenesis of AD. 2149746: These results suggest that Alzheimer's disease may be an heterogeneous disorder and that a modification on the catalytic activity of hexokinase may play a role in the pathogenesis of the disease in at least a subgroup of patients. 2184091: Recent linkage findings for psychiatric disorders, in particular schizophrenia, manic-depression, and Alzheimer disease, have raised a number of important conceptual issues regarding the genetic etiology of these diseases, as well as the appropriate interpretation of linkage results in studying complex diseases. 21902668: The origins of the sporadic cases of AD are still not known but there is evidence for a role of epigenetics in the etiology of the disease. 22079091: Furthermore, endocytic abnormalities have been identified in cases of Alzheimer's disease (AD), however, the relevance of these changes to the aetiology of the disease remains unclear. 22178988: Our data point to common deficits in the insulin-signaling pathway in both neurodegenerative diseases and support the idea that AD may cause disorders outside the higher CNS. 22251135: In Alzheimer's disease, for example, astrocytes may contribute to the etiology of this disorder. 22374313: Alzheimer's disease (AD) is the most common form of dementia among older people and the pathogenesis of this disease is associated with oxidative stress. 22458501: EXPERT OPINION: The use of transgenic mouse models that recapitulate various aspects of AD has expanded our knowledge and understanding of disease pathogenesis immensely. 22784036: Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. 22795785: These data suggest that although the characteristic features of AD appear later in life, hypoxemia in the prenatal stage may contribute to the pathogenesis of the disease, supporting the notion that environmental factors can trigger or aggravate AD. 22805236: These findings suggest that bepridil is a plausible therapeutic candidate in AD or stroke owing to its multifunctional role in key cellular events that are relevant for the pathogenesis of these diseases. 22815194: Alzheimer's disease (AD) poses a huge challenge for society and health care worldwide as molecular pathogenesis of the disease is poorly understood and curative treatment does not exist. 22922141: The research conducted on animal models of Alzheimer's disease (AD) has provided valuable information about the pathogenesis of this disease and associated behavioral and cognitive deficits as well as the disease-associated anatomical and histopathological lesions of the brain. [Selected mice models based on APP, MAPT and presenilin gene mutations in research on the pathogenesis of Alzheimer's disease]. 23036020: However, therapeutic approaches in neurological diseases such as AD, including those for BM-MSCs, are increasingly centered on the potential for prophylactic therapy in pro-dromal states where the underlying cause of the disease is apparent but functional deficits are not. 23104637: The molecular basis of Alzheimer's disease has not been clearly established, but disruption of brain metal ion homeostasis, particularly copper and zinc, might be closely involved in the pathogenesis of this disease and its characteristic beta-amyloid neuropathological features. 23395747: This review focuses on the role of Zn(II) and Cu(II) in AD, and revisits the amyloid cascade hypothesis demonstrating the possible roles of Zn(II) and Cu(II) in the disease pathogenesis. 23546882: Amyloid beta-peptide (Abeta) accumulating in the brain of Alzheimer disease (AD) patients is believed to be the main pathophysiologcal cause of the disease. 23604855: Extensive studies of AD have yet to result in a generally accepted hypothesis on the pathogenesis of the disorder. 23695007: According to the amyloid hypothesis of Alzheimer's disease (AD), the amyloid beta (Abeta) peptide, as the primary neurotoxic species, plays a key role in the pathogenesis of the disease. 23834172: The elucidation of the intriguing relationship between oxidative stress and Alzheimer's disease is crucial to understand the pathogenesis of the disease as also to design a suitable drug trial with antioxidants against this condition. 23847532: We suggest that Abeta*56 has a critical role during the earliest phase of AD and might serve as a molecular trigger of the disease. 23850509: Perturbed cerebral glucose metabolism, an invariant pathophysiological feature of AD, may be a critical contributor to the pathogenesis of this disease. 24032632: Studies of oxidative damage during the progression of Alzheimer's disease (AD) suggest its central role in disease pathogenesis. 24059309: According to recent studies, there are molecular similarities in the inflammatory pathways involved in both AD and T2DM, which opens a new avenue for researchers with different perspectives to target the cause of these diseases rather than their obvious symptoms. 24059311: Although a number of risk factors have been postulated that may trigger the development of AD, the root cause of this disease is still a matter of debate. 24059319: In this review, we provide evidence for the link between T2D and AD, highlighting the critical role of insulin in the pathogenesis of these diseases, and we provide information on the genes that might be involved in the interplay between these two disorders. 24124693: Extensive research into the genetic etiology of AD has yielded knowledge of some genetic factors that are causative and other genetic factors that increase risk for disease. 24190781: Over the past 3 decades, advances in the understanding of the biology of AD have led to a somewhat unified hypothesis of disease pathogenesis that emphasizes the precipitating role of beta amyloid protein. 24198785: A change in the normal tau protein phosphorylation is also characteristic of AD, which contributes to the pathogenesis of the disease and is useful in early diagnosis. 24204258: Once thought to be unique to these diseases, this mechanism is now recognized as a ubiquitous means of information transfer in biological systems, including other protein misfolding disorders such as those causing Alzheimer's and Parkinson's diseases. 24486820: Three points of interest lie in considering how Alzheimer, and more significantly Perusini, struggled to throw light on the cause of this devastating disease. 24737939: Because there are only a few therapeutic strategies against Alzheimer's disease, we need to understand the pathogenesis of this disease. 24778618: The fact that alterations in SUMO/deSUMOylation equilibrium occur from the early phases of AD suggests that global posttranslational modifications may play an important role in the mechanisms underlying disease pathogenesis, thus providing potential targets for pharmacological interventions. 24852227: The amyloid beta (Abeta) hypothesis posits that cerebral beta-amyloidosis is a critical early event in AD pathogenesis. We review the genetics, epidemiology and pathology of sporadic AD and give an updated account of what is currently known about the molecular pathogenesis of the disease. 24951455: Alzheimer's disease risk genes and mechanisms of disease pathogenesis. 25080056: The development of a cure for Alzheimer's disease (AD) has been impeded by an inability to pinpoint the root cause of this disorder. 25120477: Several lines of research are focused on understanding AD pathophysiology, and although the etiology of the disease remains a matter of intense debate, increased brain levels of amyloid-beta (Abeta) appear to be a critical event in triggering a wide range of molecular alterations leading to AD. 25225492: Diseases once considered constrained to a limited range of organ systems, e.g., central neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington' disease (HD), the role of multiple central and peripheral organ systems in the etiology of such diseases is now widely accepted. 25516763: Investigations on environmental factors implicated in AD are scarce and the etiology of the disease remains up to now obscure. 2554169: Young provides an excellent discussion of the alterations in excitatory amino acid transmitter systems that accompany Alzheimer's disease, and the interesting possibility that excitotoxicity may participate in disease pathogenesis. 25597552: An investigation of the efficiency of the mini-Kingston standardized cognitive assessment-revised in classifying patients according to DSM-5 major and mild neurocognitive disorders due to possible Alzheimer's disease. BACKGROUND: The aim of this study was to examine the efficiency of the mini-Kingston standardized cognitive assessment-revised (mini-KSCAr) in classifying patients according to DSM-5 major and mild neurocognitive disorders (NCD) due to possible Alzheimer's disease (AD). CONCLUSIONS: The mini-KSCAr is an efficient instrument for the diagnosis of DSM-5 major and mild NCD due to possible AD in a specialized psychogeriatric setting, and its utility is greater than that of the MMSE and the CDT. Medical history, psychiatric and physical status, basic and instrumental activities of daily living, as well as scores on the Cambridge cognitive examination-revised (CAMCOG-R), and the clinical dementia rating (CDR) scale were used to establish DSM-5 diagnoses of major or mild neurocognitive disorders (NCD) due to possible AD or no cognitive decline. 25680928: Neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) are characterized by neuronal impairment that leads to disease-specific changes in the neuronal proteins. 25792373: Despite a causative link between diabetes and AD, general molecular mechanisms underlying pathogenesis of these disorders are still far from being understood. 25847999: These findings suggest that Edaravone holds a promise as a therapeutic agent for AD by targeting multiple key pathways of the disease pathogenesis. 25954942: Vitamin D and neurocognitive disorder due to Alzheimer's disease: A review of the literature. AD is the sixth leading cause of death in the United States and the only 1 among the top 10 that cannot be prevented, cured, or even slowed. 26236550: The review, therefore, emphasizes the importance of AD related risk factors, especially those with metabolic implications, identified from various epidemiological studies, in providing clues to the pathogenesis of this complex disorder. 26396519: In our review, the specific disease is dementia caused by Alzheimer's disease. 26398935: Animal models of familial juvenile onset of Alzheimer's disease (AD) often fail to produce diverse pathological features of the disease by modification of single gene mutations that are responsible for the disease. 26401704: New therapeutic strategies in Alzheimer's disease (AD) are focused on targeting amyloid-beta (Abeta) to modify the underlying cause of the disease rather than just the symptoms. 26470401: AD is the sixth leading cause of death in the United States and the only 1 among the top 10 that cannot be prevented, cured, or even slowed. Vitamin D and neurocognitive disorder due to Alzheimer's disease: A review of the literature. 26499250: Chinese older adults (aged 60 to 90 years) with mild neurocognitive disorder due to Alzheimer's disease (DSM-5 criteria) would be randomized into a 4-week intervention of either tDCS-working memory (DCS-WM), tDCS-control cognitive training (DCS-CC), and sham tDCS-working memory (WM-CD) groups. Would transcranial direct current stimulation (tDCS) enhance the effects of working memory training in older adults with mild neurocognitive disorder due to Alzheimer's disease: study protocol for a randomized controlled trial. 26567746: Neuroinflammation in Alzheimer's disease has been identified as major contributor to disease pathogenesis. 26639971: Although the neuropathological characteristics of AD have been known for decades, the molecular mechanisms causing the disease are still under investigation. 26733416: The level of RPS23RG1 mRNA is significantly lower in the brains of AD compared to non-AD patients, suggesting its potential role in the pathogenesis of the disease. 26741695: METHODS: 36 adults with NCD due to Alzheimer's disease (NCD-AD), 31 adults with NCD due to vascular disease (NCD-vascular) and 137 healthy controls were recruited. 26756385: Alzheimer disease (AD) is the most frequent cause of major neurocognitive disorders with a huge economical and medical burden. 26801191: A reduction in glucose transporters at the blood-brain barrier that occurs before the onset of the main pathophysiological changes and symptoms of Alzheimer's disease is a potential causative effect in the vascular hypothesis of the disease. 2690095: Clinical research in Alzheimer's disease (AD) is complicated by inadequate understanding of the etiology and pathogenesis of the disorder, lack of good animal models to predict potentially useful compounds, and methodological issues such as the need for new diagnostic tools and validated assessment criteria. 26907663: Response to the Letter from Lu et al, \Utility of Montreal Cognitive Assessment (Hong Kong Version) in the Diagnosis of Mild Neurocognitive Disorders (NCD): NCD Due to Alzheimer Disease (NCD-AD) and NCD Due to Vascular Disease (NCD-Vascular)\. 27058526: Alzheimer's disease (AD) is the major causative disease of dementia and is characterized pathologically by the accumulation of senile plaques (SPs) and neurofibrillary tangles (NFTs) in the brain. Although genetic studies show that beta-amyloid protein (Abeta), the major component of SPs, is the key factor underlying AD pathogenesis, it remains unclear why advanced age often leads to AD. 27100611: While histological changes in microglia have long been recognized as a pathological feature of Alzheimer's disease (AD), recent genetic association studies have also strongly implicated microglia in the etiology of the disease. 27414695: Dementias are disorders that affect memory and intellectual functioning, and are caused primarily by Alzheimer's disease and vascular disorders (multi-infarct dementia). 27498879: Dementia with Lewy bodies shares clinical and pathological features with both Parkinson's disease and Alzheimer's disease so it is therefore likely that it also has similar pathogenic mechanisms leading to disease. 27514990: Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases, yet current therapeutic treatments are inadequate due to a complex disease pathogenesis. 27628303: Understanding how epigenetic dysregulation in the brainstem contributes to AD susceptibility could be of pivotal importance for understanding the etiology of the disease and for the development of novel diagnostic and therapeutic strategies. 27943641: With the gradual aging of the world's population, leading to increased prevalence of AD, and the substantial cost of care for those afflicted, identifying the genetic causes of disease represents a critical effort in identifying therapeutic targets. 28228716: Our results suggest that BMP9 may be a promising candidate for treating AD by targeting multiple key pathways in the disease pathogenesis. 28294067: Preventive and therapeutic approaches to AD in the context of an infectious etiology of the disease are also discussed. 2836376: The voluminous data on Alzheimer's disease raise intriguing possibilities about the key event in the pathogenesis of the disease, but further investigation is necessary to identify the event conclusively. 28364127: A flanker test was conducted in 31 adults with NCD due to vascular disease (NCD-vascular), 36 patients with NCD due to Alzheimer's disease (NCD-AD), and 137 healthy controls. 28516241: It is now widely known that inflammation plays an important role in the development of AD, a role that is not only a response to the surrounding pathological environment, but rather seems to be strongly implicated in the aetiology of the disease as indicated by the genetic studies. 28527207: OBJECTIVE: We aimed to investigate the IPS with two types of measurements in the patients with NCD due to vascular disease (NCD-vascular) and NCD due to Alzheimer's disease (NCD-AD), and examine the associations between IPS measures and morphometric features. 28680398: Notably, loss-of-function mutations of either DAP12 or TREM2 result in a disorder known as Nasu-Hakola disease (NHD); and mutations of these genes have been associated with the risk for Alzheimer's disease (AD), suggesting that TREM2 and DAP12 may regulate common signaling pathways in the disease pathogenesis. 28739984: Clinical trials for AD are now moving toward these earlier stages of the disease, targeting MCI due to AD and preclinical AD. 28829364: While there is no cure for AD, pharmacological approaches to alleviate symptoms and target underlying causes of the disease have been developed, albeit with limited success. 28947385: Although the continuous investigations about AD have been made in recent decades, the pathogenesis of this disease is still not definitely confirmed. 29109429: Disturbances in calcium homeostasis have been observed in various cellular and animal models of AD and are proposed to underlie the pathogenesis of the disease. 29151989: Key messages: Human/mouse chimeric models using iPSCs to study AD offer much promise in better replicating AD pathology and can be further exploited to elucidate disease pathogenesis with regards to the neuroinflammation hypothesis of AD. 29206067: In AD, oligomeric Abeta42 species is widely thought to be a major contributor to the disease pathogenesis. 29228201: The evolution of Alzheimer's disease tauopathy in cognitively unimpaired individuals needs to be examined to better understand disease pathogenesis. 29492246: Alzheimer's disease (AD) is the most common cause of major neurocognitive disorders worldwide. 29551631: Although an accumulation of brain amyloid-beta (Abeta) peptide and hyperphosphorylated tau protein have been implicated in the pathogenesis of AD, the etiology of the disease remains unclear. Mitochondrial dysfunction has been identified as an early event in AD pathogenesis and is reflected by reduced metabolism, disruption of Ca2+ homeostasis, and increased levels of reactive oxygen species, lipid peroxidation, and apoptosis. 29552692: Hyperhomocysteinemia is a trigger for many diseases, such as atherosclerosis, congestive heart failure, age-related macular degeneration, Alzheimer's disease and hearing loss. 29630139: The dominant theory of the?AD development is amyloid cascade?hypothesis, but at the same time, important?in the etiology of this disease is?the overphosphorylation of tau protein.? 29660940: The research community is yet to decipher why the ApoE4 variant pre-disposes to AD, and how aging causes the disease. 29689726: METHODS: We included 62 patients with mild or major NCDs due to pure AD (with positive CSF biomarker assays), and 174 patients (from the GRECogVASC cohort) with pure VCI. 29745345: Till date, there is no cure for AD, but the pathogenesis of the disease could be delayed by the use of natural antioxidants. 29856605: Amyloid plaque formation constitutes one of the main pathological hallmarks of Alzheimer's disease (AD) and is suggested to be a critical factor driving disease pathogenesis. 30033062: TREM2 is a transmembrane receptor expressed in cells of the myeloid lineage, and its association with Alzheimer's disease supports the involvement of immune and inflammatory pathways in the cause of the disease, rather than as a consequence of the disease. 30040725: Although considerable progress has been made to elucidate the pathogenesis of AD, the specific causes of the disease remain highly unknown. 30136680: Alzheimer's disease (AD) is the most common form of dementia in the older population, however, the precise cause of the disease is unknown. 30315452: Lack of a satisfactory animal model for Alzheimer's disease (AD) has limited the reach progress of the pathogenesis of the disease and of therapeutic agents aiming to important pathophysiological points. Animal Model of Aluminum-Induced Alzheimer's Disease. In this chapter, we analyzed the research status of animal model of aluminum-induced Alzheimer's disease. 30340518: Despite considerable progress in the understanding of the pathophysiology of AD, the precise molecular mechanisms that cause the disease remain elusive. 30415068: Being the most common type of dementia, AD is studied extensively; however, the data concerning changes in neurogenesis in the pathogenesis of this disease are inconsistent. 30445661: Despite its prevalence, only five therapies are currently approved for AD, all dealing with the symptoms rather than the underlying causes of the disease. 30465785: As a new starting point for studying AD, genetic and genomic investigations consistently strive to discover causative variants that are related to disease pathophysiology. 30521994: The drug discovery to treat AD consists to develop compounds able to act in multiple molecular targets involved in the pathogenesis of the disease and the repositioning of old drugs for new application. The aim of the present study was to investigate whether ebselen (1-10 mg/kg), a multifunctional selenoorganic compound, ameliorates memory impairment, hippocampal oxidative stress, apoptosis and cell proliferation in a mouse model of sporadic AD induced by icv STZ (3 mg/kg, 1 MUl/min). In conclusion, the multifunctional selenoorganic compound ebselen was effective to reverse memory impairment, hippocampal oxidative stress and apoptosis in a mouse model of sporadic AD induced by icv STZ. 30609547: Aluminum ions, as a kind of non-essential element, show a negative impact on plants growth and contribute to diseases caused by nervous breakdown like Alzheimer's disease and Parkinson's disease. 30632506: Therefore, investigating the mechanism of APP mutation on Alzheimer's disease may help understanding of disease pathogenesis. Mutations of beta-amyloid precursor protein alter the consequence of Alzheimer's disease pathogenesis. Approximately 25 mutations in beta-amyloid precursor protein (APP) are pathogenic and cause autosomal dominant Alzheimer's disease. 30741678: Air pollution is a risk factor for the development of AD and as the number of Americans with AD continues to grow without a cure, we need to focus on preventable, early causes of this fatal disease and intervene appropriately. 30760863: It seems reasonable to hypothesize that the amyloid cascade is intimately involved in AD, in parallel with disease pathogenesis, but that removal of toxic Abeta is insufficient for an effective disease modification. 30819626: LINKAGE TO OTHER MAJOR THEORIES: Our hypothesis may link previous theories to establish a bidirectional relationship between sleep disorders and AD, which may finally form a new schematic mechanism to understand the disease pathogenesis and disease progression. 30877738: Because of its severity, AD has been the subject of extensive studies that address the pathogenesis of the disease. 30932886: Furthermore, the fact that osteoporosis and Alzheimer's disease are two common age-related disorders raises the possibility that these two organ systems are interconnected in terms of disease pathogenesis. 31030513: The enzyme is overexpressed in several types of cancer and Alzheimer's disease, and its genetic defect causes different incurable disorders. 31122236: This suggest that the threapy should not base on a single cause of Alzheimer's disease but rather a number of different pathways that lead to the disease. 31332445: The failure of recent clinical trials in Alzheimer's disease has highlighted the need for the development of a more complete understanding of the pathogenesis of the disorder and also a belief that therapies may only work if given very early in the disease process before overt symptoms occur. 31403949: These findings suggest that EDA possesses clinical and pathological benefits for AD with CCH in the present mouse model and has a potential as a therapeutic agent for AD with CCH via targeting multiple key pathways of the disease pathogenesis. The hallmarks of AD including amyloid-beta (Abeta)/phosphorylated tau (pTau) and pathology-related events such as neural oxidative stress and neuroinflammation play critical roles in pathogenesis of AD with CCH. 31577960: In the last few years the views about the drivers of AD have been changing and nowadays it is believed that neuroinflammation takes center stage in disease pathogenesis. 31771153: Hypoxia is a common feature of neurodegenerative diseases, including Alzheimer's disease that may be responsible for disease pathogenesis and progression. 32065096: OBJECTIVE: Thus, revealing the interplay between AD and major depression may provide novel insights into the pathogenesis of these diseases. 32292421: This process is well documented in Alzheimer's disease (AD), where it may participate in the etiology of the disease. 32390857: The data suggest that a 40-Hz light flicker can ameliorate AD-associated circadian rhythm disorders, presenting a new type of therapeutic treatment for rhythm disorders caused by AD. 32592177: The discovery that neuron-specific sodium pump activity is impaired in AD and other neurodegenerative diseases such as Parkinson's disease has suggested a role for the sodium pump in the pathogenesis of these diseases. 32625049: The expression of miR-29 family is significantly reduced in AD, suggesting a part for the family members in pathogenesis of the disease. 32719612: Despite a large improvement in understanding the pathogenesis of AD, the etiology of this disorder remains still unclear, and no current treatment is able to prevent, slow, or stop its progression. 32727580: Phosphorylated Abeta peptides in human Down syndrome brain and different Alzheimer's-like mouse models.The deposition of neurotoxic amyloid-beta (Abeta) peptides in extracellular plaques in the brain parenchyma is one of the most prominent neuropathological features of Alzheimer's disease (AD), and considered to be closely related to the pathogenesis of this disease. 32955528: Unfortunately, both effective diagnosis and treatment for AD remain elusive, probably owing to the complicated and uncertain etiology of the disease. 32958234: Following this view, part of the recent scientific literature has generated a new reading frame for AD pathophysiology, based on the application of the prion paradigm to the amyloid cascade hypothesis in an attempt to definitely explain the key events causing the disease and inducing its occurrence under different clinical phenotypes. 33035604: While senile plaques and neurofibrillary tangles have been proposed as the principal histopathologic hallmarks of AD, the exact etiology of this disease is still far from being clearly understood. 33078674: Results demonstrated that both AD and control participants generated more self-statements in the odour condition than in the odor-free condition, especially psychological self-statements. 33178313: Acorus tatarinowii (AT) is widely used in the treatment of Alzheimer disease, epilepsy, depression, and stroke, which leads to disorders of consciousness disease. 33228179: Aging is the major factor contributing to AD; however, the initial cause that triggers the disease is yet unknown. 33384577: Using the APPswe/PS1dE9 (APP/PS1) mouse model of Alzheimer's disease, we utilized the Morris water maze spatial learning paradigm to systematically evaluate mild behavioral deficits that occur during the early stages of disease pathogenesis. 33642365: In this review, we briefly examine fragile X syndrome, amyotrophic lateral sclerosis, Alzheimer's disease, and spinal muscular atrophy, with a focus on disease pathogenesis with regard to local mRNA translation and axon transport, suggesting possible treatment directions. 33673244: Thus, Al 3+ should be considered as an important factor, alongside the known characteristic hallmarks of AD, in the development and aetiology of the disease. 34161823: While the detailed mechanism of the pathogenesis of AD is still unknown, evidence suggests that mitochondrial dysfunction likely plays a fundamental role in the pathogenesis of this disease. 34200581: Although the sporadic form of Alzheimer's disease (AD) is the prevalent form, the cellular events underlying the disease pathogenesis have not been fully characterized. 34481234: In the classical model for the etiology of AD, amyloid-beta (Abeta)-an APP derivative and hyperphosphorylated tau form aggregates in the brain that underlie the pathogenesis of the disease. 34589757: Although tauopathies, such as Alzheimer's disease and Frontotemporal dementia, are common amongst the ageing population, current effective treatment options are scarce, primarily due to the incomplete understanding of disease pathogenesis. 34657885: BACKGROUND: Mild cognitive impairment (MCI) is a heterogeneous condition and MCI patients are at increased risk of progression to dementia due to Alzheimer's disease (AD). 34765631: Neurodegenerative disorders, such as Parkinson's and Alzheimer's disease, are claimed to be of major concern causing a significant disease burden worldwide. 34842276: Our results support a common molecular basis for initiation of the pathological processes leading to both early and late onset forms of Alzheimer's disease and illustrate the utility of zebrafish and of knock-in, single EOfAD mutation models for understanding the causes of this disease. 35346005: The two important hallmarks of AD are the appearance of plaques and tangles of amyloid beta (Abeta) and tau proteins, respectively, in the brain based on the etiology of the disease including cholinergic impairment, metal dyshomeostasis, oxidative stress, and degradation of neurotransmitters. 35555555: Although it remains unclear what primarily triggers and drives the progression of AD, different lines of investigation point out to a central role of oligomeric Abeta conformations for the disease pathogenesis. 35710783: The most accepted hypothesis in Alzheimer's disease (AD) is the amyloid cascade which establishes that Abeta accumulation may induce the disease development. This accumulation may occur years before the clinical symptoms but it has not been elucidated if this accumulation is the cause or the consequence of AD. 35805958: Role of Impaired Mitochondrial Dynamics Processes in the Pathogenesis of Alzheimer's Disease. This review highlights aspects of altered mitochondrial dynamics in AD that may contribute to the etiology of this debilitating condition. 35832342: Several reports have shown that it has promising potential in the prevention and treatment of AD due to its significant antioxidative, anti-inflammatory, and antiapoptotic properties along with several other mechanisms that target the altered signaling pathways due to the disease pathogenesis. 35965800: Conclusions: Using a deep CNN and iterated RF architecture, we showed that brain image stratification is a promising means for evaluating AD, and examining the underlying etiology of the disease, by applying computer and medical images to achieve the early auxiliary diagnosis of AD. 35986296: CONCLUSIONS: The reciprocal effects of amyloid deposition and systemic infectious burden may lead to a vicious cycle fueling Alzheimer's disease pathogenesis. The infectious theory linked various infectious agents with the development of AD, raising the possibility that they serve as etiological causes of the disease. 36073854: Innumerable changes have been linked to the pathology of AD; however, there remains much discord regarding which might be the initial cause of the disease. 36324230: Alzheimer's disease and related dementias: From risk factors to disease pathogenesis. 36399267: For the last decade, human models of AD using induced pluripotent stem cells (iPSCs) have emerged as a powerful way to understand disease pathogenesis in relevant human cell types. 36469008: Our hypothesis may establish a linkage between the cerebellum and AD, thereby potentially providing new perspectives on the pathogenesis of the disease. 36552984: Herein, we provide a comprehensive review on Alzheimer's disease pathophysiology to provide a better understanding of disease pathogenesis hypotheses and decipher the role of genetic and epigenetic factors in disease development and progression. 36671568: Although growing evidence demonstrates that AD is a significant comorbidity of T2D, and there is a ~1.4-2-fold increase in the risk of developing AD among T2D patients, the involvement of possible common triggers in the pathogenesis of these two diseases remains largely unknown. 37158125: Emerging evidence suggests that abnormalities in ER/mitochondrial brain functions and dysregulation of Ca 2+ homeostasis are neuropathological hallmarks of neurological disorders like Alzheimer's disease, but little evidence is available to demonstrate their relationship to disease pathogenesis and therapeutic approaches. 37163849: Alzheimer's disease (AD) is emerging as a serious problem with the rapid aging of the population, but due to the unclear cause of the disease and the absence of therapy, appropriate preventive measures are the next best thing. 37366656: In the elderly, a debilitating condition known as dementia, which is a major health concern, is caused by Alzheimer's disease (AD). 37395272: Clinically diverse neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis, exhibit unique and disease-specific biochemical protein signatures and abnormal protein depositions that often correlate with disease pathogenesis. 37452088: While our understanding of the molecular biology of Alzheimer's disease (AD) has grown, the etiology of the disease, especially the involvement of peripheral infection, remains a challenge. 37476485: The output showed no difference between the patterns of AD-like disorder induction. 37580797: Understanding this biology will ensure that people who have Down syndrome access the most appropriate Alzheimer's disease therapeutics and moreover will provide unique insight into disease pathogenesis more broadly. 37631373: The etiology and pathogenesis of Alzheimer's disease are multifactorial, so one of the treatment strategies is the development of the drugs that affect several targets associated with the pathogenesis of the disease. 37654709: Extracted fingertip interaction digital biomarkers were used to assess participants' SEP disorders, ultimately enabling intelligent diagnosis of MCI due to AD. Conclusion: Patients with MCI due to AD may have SEP disorders, and this new method based on dynamic evaluation of SEP will provide a novel human-computer interaction and intelligent early warning method for home and community screening of MCI due to AD. 37848007: The purpose of our study is to explore the genetic linkage between AD and MS through bioinformatic analysis, providing new insights into the shared signatures and possible pathogenesis of two diseases. 37855293: Although studies on the discovery of amyloid beta (Abeta) and tau (the essential elements of plaques and tangles in AD) have shed light on the molecular pathological processes of AD, the exact cause of the condition is still largely unknown. 37875373: CONCLUSIONS: These findings suggest that sodium benzoate may exert its influence on important pathways associated with AD, thus contributing to the improvement in the pathogenesis of the disease. 38064104: Even though a century has passed since the discovery of AD, the exact cause of the disease still remains unknown. Since dysregulation of this kinase affects all the major characteristic features of the disease, such as tau phosphorylation, amyloid formation, memory, and synaptic function, it is thought to be a major player in the pathogenesis of AD. 38300883: BACKGROUND: Despite the number of people living with Alzheimer disease (AD), awareness of the early stages of this condition, including mild cognitive impairment due to AD-which poses management challenges-continues to be low. 38357597: Additionally, the concept of entropy was used to detect the disorder of proteasome system, it was discovered that entropy is down-regulated continually with AD progression against system chaos caused by AD. 38473858: Alzheimer's disease is a neurodegenerative condition characterized by a gradual onset and progressive deterioration, making it the primary cause of dementia, although the exact cause of the disease remains elusive. 38623383: The molecular links between DS and AD shed insights into the underlying causes of both diseases and highlight potential therapeutic targets. 7582040: The genes identified by studying inherited forms of Alzheimer's disease are now being used to understand the initiating steps in the pathogenesis of the disease. 7583683: Cerebrospinal fluid (CSF) biochemical markers for Alzheimer's disease (AD) would be of great value, both to improve clinical diagnostic accuracy and to increase our knowledge of the pathogenesis of the disorder. 7653697: CONCLUSIONS: Paraventricular CRH neurons in Alzheimer's disease and depression are hyperactivated, and this hyperactivation may contribute to the etiology of these disorders. 7877576: There's no cure yet for Alzheimer's, but researchers are narrowing in on possible causes of the disease and identifying patients who may be predisposed to developing it. 7967720: Senile plaques (SP) are the most characteristic neuropathologic lesions of Alzheimer's disease (AD) and studies of plaque cortical distribution, density, and morphology may lead to new information about the origin and pathogenesis of this disease. 8090716: As an example, a homoplasmic, Caucasian, tRNA(Gln) mutation at nucleotide pair (np) 4336 has been observed in 5% of Alzheimer disease and Parkinson disease patients and may contribute to the multifactorial etiology of these diseases. 8239278: Studies of autosomal-dominant forms of AD have established the central role of APP in the pathogenesis of the disease. 8446172: Structural alterations of APP are implicated in the pathogenesis of Alzheimer's disease, but it is not known how they cause the disease. 8528377: This case confirms that AD may result in prominent white matter disease caused by incomplete infarction or demyelination. 8861021: Abnormalities of the endosomal-lysosomal system in Alzheimer's disease: relationship to disease pathogenesis. 8881379: This review reports the different genetic factors that have been identified either as risk factor for Alzheimer's disease (AD) or directly causing the disease. The second part describes the mutations responsible for early-onset autosomal dominant AD found in three different genes. 9520006: Among subjects diagnosed during life as having DAT or incipient DAT, only 7% were found to have a neuropathologic disorder other than AD causing their dementia. 9546791: Alzheimer's disease (AD) is characterized by the accumulation of cerebral plaques composed of 40- and 42-amino acid beta-amyloid (Abeta) peptides, and autosomal dominant forms of AD appear to cause disease by promoting brain Abeta accumulation. 9749615: Recently, alpha-synuclein was shown to be a structural component of the filaments in Lewy bodies (LBs) of Parkinson's disease (PD), dementia with LBs (DLB) as well as the LB variant of Alzheimer's disease, and this suggests that alpha-synuclein could play a mechanistic role in the pathogenesis of these disorders. 9990552: Four different genes have now been associated with AD and are providing insights into the pathogenesis of the disease. 32134942: There is a limited evaluation of an independent linguistic battery for early diagnosis of Mild Cognitive Impairment due to Alzheimer's disease (MCI-AD). 32956392: Evaluation of choroidal thickness in prodromal Alzheimer's disease defined by amyloid PET.OBJECTIVE: To assess and compare the involvement of choroidal thickness (CT) in patients with mild cognitive impairment (MCI) and dementia due to Alzheimer's disease (AD) defined by amyloid PET and healthy controls (HC). 34029274: The purpose of this investigation was to determine the capacity for new rapid image and number naming tests and other measures of visual pathway structure and function to distinguish individuals with MCI due to AD from those with normal aging and cognition. 35523023: In this work, we report the preliminary evaluation of a self-driven AD multi-class discrimination approach based on a commercial EEG acquisition system using sixteen channels. 36318372: Reports on a significant positive correlation between consumption of carotenoid-rich food and prevention of Alzheimer's disease (AD) led to the investigation of carotenoids for the treatment and prevention of AD. 36372804: Positron emission tomography (PET) offers a great opportunity to visualize AD from diverse perspectives by using radiolabeled agents involved in various pathophysiological processes; PET imaging technique helps to explore the pathomechanisms of AD comprehensively and find out the most appropriate biomarker in each AD phase, leading to a better evaluation of the disease. 37603693: Evaluation of the NIH Toolbox Odor Identification Test across normal cognition, amnestic mild cognitive impairment, and dementia due to Alzheimer's disease. 37654709: Extracted fingertip interaction digital biomarkers were used to assess participants' SEP disorders, ultimately enabling intelligent diagnosis of MCI due to AD. Conclusion: Patients with MCI due to AD may have SEP disorders, and this new method based on dynamic evaluation of SEP will provide a novel human-computer interaction and intelligent early warning method for home and community screening of MCI due to AD. 37900942: Although we did not perform extensive histopathological evaluations or measured microtubule stability, our findings show that MSAs can rescue the consequences of AD-like conditions but otherwise be harmful if administered at a prodromal stage of the disease. 38251056: Contingent Negative Variation in the Evaluation of Neurocognitive Disorders Due to Possible Alzheimer's Disease. 32123490: MCLENA-1: A Phase II Clinical Trial for the Assessment of Safety, Tolerability, and Efficacy of Lenalidomide in Patients with Mild Cognitive Impairment Due to Alzheimer's Disease. 33355065: RESULTS: At latest assessment (mean 2 years) 61 patients had probable MCI with Lewy bodies, 26 possible MCI with Lewy bodies and 57 MCI due to Alzheimer's disease. 33731557: Experimental pain studies using psychophysics can further our understanding of the pain experience in AD, which may lead to improved assessment and management of pain in people living with AD. 35813951: To comprehensively understand the context and distribution of pathways that contribute to AD, we performed text-mining to generate an exhaustive, systematic assessment of the breadth and diversity of biological pathways within a corpus of 206,324 dementia publication abstracts. 37213535: Validation of the European Cross-Cultural Neuropsychological Test Battery (CNTB) for the assessment of mild cognitive impairment due to Alzheimer's disease and Parkinson's disease. 37355905: Diagnostic Performance of an Eye-Tracking Assisted Visual Inference Language Test in the Assessment of Cognitive Decline due to Alzheimer's Disease. 37502020: INTRODUCTION: Although many cognitive measures have been developed to assess cognitive decline due to Alzheimer's disease (AD), there is little consensus on optimal measures, leading to varied assessments across research cohorts and clinical trials making it difficult to pool cognitive measures across studies. 37838690: Clinical assessment and biomarkers, together with ML techniques, could prove pivotal in improving diagnostic tools for MCI due to AD. 38230722: Future longitudinal studies of population aging, incorporating biomarker assessment to confirm AD diagnoses, are needed to better characterize the course of MCI due to AD and AD dementia. 38356475: The HOPE4MCI study: A randomized double-blind assessment of AGB101 for the treatment of MCI due to AD. INTRODUCTION: In addition to the accumulation of amyloid plaques and neurofibrillary tangles, the presence of excess neural activity is a pathological hallmark of Alzheimer's disease (AD) and a prognostic indicator for progression of AD pathology and clinical/cognitive worsening in mild cognitive impairment due to Alzheimer's disease (MCI due to AD). 11640946: The novel localization of such a transcriptional activating protein to selectively vulnerable neurons in Alzheimer disease provides compelling evidence for mitotic re-entry as part of the pathogenesis of neuronal dysfunction and death in Alzheimer disease. 12451676: Alzheimer's disease(AD) is the most common form of neurodegenerative diseases that causes intellectual dysfunction. 14675724: The ensuing homeostatic responses to myelin breakdown further increase intracortical toxicity and results in the relentless progression and non-random anatomical distribution of AD lesions that eventually cause neuronal dysfunction and degeneration. 14970312: The pathogenesis of AD is tightly linked to Abeta deposition and oxidative stress, but it remains unclear as to how these factors result in neuronal dysfunction and death. 15249195: The calcium hypothesis of Alzheimer's disease (AD) invokes the disruption of calcium signaling as the underlying cause of neuronal dysfunction and ultimately apoptosis. 15950763: Mutations of presenilin 1 (PS1) gene are the causative gene for early onset familial AD (FAD) due to the overproduction and deposition of pathogenic Abeta1-42 peptides. The pathogenesis of Alzheimer's disease (AD) is now thought to be tightly linked to Abeta deposition and oxidative stress, but it is still unknown how these factors result in neuronal dysfunction and cell death. 16998901: Accumulation of the beta-amyloid peptide (Abeta) in the brain is a major pathological hallmark of Alzheimer's disease (AD), leading to synaptic dysfunction, neuronal death, and memory impairment. 17413025: Then, we will review preliminary findings applying imaging-guided microarray to AD and normal aging, in an attempt to isolate molecular profiles that dissociate the two main causes of age-related hippocampal dysfunction. 17416103: Early caution about the role of tau as a significant factor in neurodegenerative disease, especially Alzheimer's disease, has been superseded by acceptance of its key involvement in pathways which led to cell dysfunction and death. 17908035: These data suggest there is a shift in cholinotrophic molecular events in MCI and early AD which may lead to cell dysfunction and eventual cell death over the course of the disease. 18201950: I propose that inflammation and cellular stress associated with aging are key events in the development of AD through the induction of glial dysfunction. 18480253: Retromer deficiency observed in Alzheimer's disease causes hippocampal dysfunction, neurodegeneration, and Abeta accumulation. 19332976: The causes of cognitive dysfunction range from the devastating effects of Alzheimer's disease (AD) to treatable causes of dysfunction and the normal mild forgetfulness described by many older individuals. 19350381: Evidence suggests that amyloid-beta (Abeta) protein is a key factor in the pathogenesis of Alzheimer's disease (AD) and it has been recently proposed that mitochondria are involved in the biochemical pathway by which Abeta can lead to neuronal dysfunction. 19551456: While progressive accumulation of oligomeric amyloid-beta protein (Abeta) has been identified as one of the central toxic events in AD leading to synaptic dysfunction, accumulation of alpha-synuclein (alpha-syn) resulting in the formation of oligomers has been linked to PD. Most of the studies in AD have been focused on investigating the role of Abeta and Tau; however, recent studies suggest that alpha-syn might also play a role in the pathogenesis of AD. 19614678: OBJECTIVE: In Alzheimer's disease, toxic soluble and insoluble forms of amyloid beta (Abeta) cause synaptic dysfunction and neuronal loss. 19774105: Functional impairments in ETS components have been reported in several central nervous system (CNS) diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD); however, it remains largely unknown how the suppression of individual ETS complex function could lead to specific dysfunction in different cell types, resulting in distinct disease phenotypes. 19839939: These will reveal how key players in the pathogenesis of Alzheimer's disease and frontotemporal dementia, such as the peptide Abeta (amyloid beta) and the protein tau, cause neuronal dysfunction and eventually, neuronal demise. 19860724: This datum may be of high relevance for a better understanding of Alzheimer's Disease (AD) since molecular, cellular, and animal model studies have revealed that the formation of amyloid beta (Abeta) and other derivatives of the APP are key pathogenic factors in AD, causing mitochondrial dysfunction, free radical generation, oxidative damage, and inflammation. 20445057: While Abeta deposition is the most prominent feature of AD, oligomeric forms of Abeta have been implicated as the toxic species inducing the neuronal dysfunction. 20816785: There is strong evidence that intracellular calcium dysregulation plays an important pathological role in Alzheimer's disease, and specifically that beta amyloid may induce increases in intracellular calcium and lead to neuronal cell dysfunction and death. 21219931: Amyloid plaques composed of the 42 amino acid form of amyloid-beta peptide (Abeta42) are a pathological hallmark of Alzheimer's disease (AD), but soluble and intraneuronal Abeta42 are the more proximal causes of synaptic dysfunction and neurotoxicity. 21237171: Mounting evidence points to the soluble oligomers of amyloid beta (Abeta) peptide as important neurotoxic species in Alzheimer's disease, causing synaptic dysfunction and neuronal injury, and finally leading to neuronal death. 21429865: Amyloid-beta accumulation in the brain is thought to be one of the earliest events in Alzheimer's disease, possibly leading to synaptic dysfunction, neurodegeneration and cognitive/functional decline. 21799246: In this article, we evaluate the hypothesis according to which tau deposition in the anterior subhippocampal region during the earliest stages of the most common form of AD, with predominant MTL dysfunction, will lead to dysfunction of neural networks implicated in context-free memory. 22101739: Alzheimer disease (AD) is characterized by chronic neuroinflammation, which may lead to dysfunction in neuronal circuits. 22726800: Amyloid-beta 1-42 accumulation is the major pathogenetic event in Alzheimer's disease (AD), believed to be responsible for synaptic dysfunction and neuronal cell death. 22753410: Swedish Alzheimer mutation induces mitochondrial dysfunction mediated by HSP60 mislocalization of amyloid precursor protein (APP) and beta-amyloid. 22879025: The vascular hypothesis of Alzheimer's disease (AD) considers cerebral hypoperfusion as a primary trigger for neuronal dysfunction. 23011810: The pathology of AD is strongly associated with accumulated misfolding proteins that results in neuronal dysfunction within the brain. 23799536: In Alzheimer's disease, soluble amyloid-beta causes synaptic dysfunction and neuronal loss. 23979025: In Alzheimer's disease (AD), amyloid-beta (Abeta) deposits in the cerebrovasculature can result in neurovascular dysfunction and/or cerebral amyloid angiopathy. 24024140: These data are consistent with a two-hit hypothesis of AD: oxidative stress leads to lipid peroxidation that, in turn, causes oxidative dysfunction of key energy-related complexes in mitochondria, triggering neurodegeneration. 24251395: OBJECTIVE: Preclinical and post-mortem studies suggest that Alzheimer disease (AD) causes cerebrovascular dysfunction, and therefore may enhance susceptibility to cerebrovascular disease (CVD). 24251604: With AD, the loss of connectivity should first induce dysfunction in those representational networks with the weakest connectivity. 24715417: Based on lots of medical reports, ER stress in postmortem brains from Alzheimer's disease (AD) patients, animals, and vitro models have indicated that ER dysfunction might work as an important part in causing AD. 24918635: Deposition of amyloid-beta (Abeta) 1-42, the major component of senile plaques characteristic of Alzheimer disease, affects brain microvascular integrity and causes blood-brain barrier dysfunction, increased angiogenesis, and pericyte degeneration. 24954589: Analysis of the literature suggests that the main factors of AD and PD pathogenesis (oxidative stress, structural disorders and aggregation of proteins, mitochondrial dysfunction, energy deficiency) that initiate a cascade of events resulting finally in the dysfunction of neuronal networks are mediated by the disbalance of Zn2+ and Cu2+. Disbalance of zinc (Zn2+) and copper (Cu2+) ions in the central nervous system is involved in the pathogenesis of numerous neurodegenerative disorders such as multisystem atrophy, amyotrophic lateral sclerosis, Creutzfeldt-Jakob disease, Wilson-Konovalov disease, Alzheimer's disease, and Parkinson's disease. 25230232: Alzheimer's disease (AD) is a progressive neurodegenerative disorder, characterized by deposition of amyloid beta, neurofibrillary tangles, astrogliosis and microgliosis, leading to neuronal dysfunction and loss in the brain. 25359615: Abeta oligomers (AbetaOs), the typical cause of AD, lead to mitochondrial dysfunction and neuronal loss. 25552414: A reduction of this enzyme causes neurodegeneration and aggravates the AD features of the 3xTgAD mouse, inducing neuronal dysfunction, cell death and impairing memory and synaptic plasticity. 25710536: Subtle disruptions of APP signaling functions may be major contributors to AD-causing neuronal dysfunction. 25753421: The fact that AD-induced cellular dysfunctions can be avoided by UPS activity at mitochondria has potentially far-reaching pathophysiological implications. 25821477: Alzheimer's disease (AD) causes progressive hippocampus dysfunctions leading to the impairment of learning and memory ability and low level of uptake rate of glucose in hippocampus. 26118731: Amongst these, degenerative diseases involving hippocampus like Alzheimer's disease (AD) and temporal lobe epilepsy (TLE) are ranked higher as it is vulnerable to excitotoxicity induced neuronal dysfunction and death resulting in cognitive impairment. 26275910: In a mouse model of AD, C5a-peptide vaccines reduce microglia activation and thus neuroinflammation, which is supposed to lead to reduced neuronal dysfunction and AD symptomatic decline. 26484912: The major symptom of AD is progressive dementia that eventually results in dysfunction of daily life. 26487830: Alzheimer's disease is a progressive neurodegenerative disorder, characterized by deposition of amyloid beta, neurofibrillary tangles, astrogliosis and microgliosis, leading to neuronal dysfunction and loss in the brain. 26529297: Alzheimer's disease (AD) is a progressive neurodegenerative disorder, characterized by deposition of amyloid plaques and neurofibrillary tangles, as well as microglial and astroglial activation, and, finally, leading to neuronal dysfunction and death. 27199641: We review current work suggesting that neuronal differentiation is defective in Alzheimer's disease, leading to dysfunction of the dentate gyrus. 27430312: BACKGROUND: Amyloid-beta (Abeta) accumulation is a hallmark of Alzheimer's disease (AD) that can lead to neuronal dysfunction and apoptosis. 27748454: This study confirms earlier reports on an association between increased brain iron-burden and risk for neurocognitive dysfunction due to AD, and indicates that disease-progression is conferred by spatial colocalization of brain iron deposits with Abeta-plaques. 27897204: In the mitochondria-mediated vicious cycle of Alzheimer's disease (AD), intracellular amyloid beta (Abeta) induces mitochondrial dysfunction and reactive oxygen species, which further accelerate Abeta accumulation. 27910888: In Alzheimer's disease, the microtubule cytoskeleton is compromised, leading to neuronal dysfunction and eventually cell death. 28003750: Group I: normal control group treated with water; Group II: disease control treated with AlCl3 to induce the mimicking AD for 4 successive weeks (SW); Group III: normal control group treated with baicalein (5 mg/kg) for 2 SW followed by combination of baicalein and AlCl3 for 4 SW; Group IV: normal control group treated with baicalein (10 mg/kg) for 2 SW followed by combination of baicalein and AlCl3 for 4 SW; Group V: normal control group treated with rivastigmine (0.3 mg/kg) for 2 SW followed by combination of rivastigmine and AlCl3 for 4 SW. Baicalein improves behavioral dysfunction induced by Alzheimer's disease in rats. 28081713: BACKGROUND: Deposition of aggregated amyloid beta (A?) protein is hallmark of Alzheimer's disease, leading to dysfunction and apoptosis of neurons. 28208063: Data suggest that the contribution of WML to the dysfunction of the cholinergic system in MCI due to AD depends on WML distribution. 28869759: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a progressive deposition of amyloid beta (Abeta) and dysregulation of neurotrophic signaling, causing synaptic dysfunction, loss of memory, and cell death. 28988799: Dysfunction of autophagy and endosomal-lysosomal pathways: Roles in pathogenesis of Down syndrome and Alzheimer's Disease. The same genetic factors that cause or increase AD risk are also direct causes of endosomal-lysosomal dysfunction, underscoring the essential partnership between this dysfunction and APP metabolites in AD pathogenesis. 29116174: In early stages of Alzheimer's disease (AD), neuronal hyperexcitability leads to network dysfunction observed in cortical regions such as the hippocampus. 29156571: Studies for Improving a Rat Model of Alzheimer's Disease: Icv Administration of Well-Characterized beta-Amyloid 1-42 Oligomers Induce Dysfunction in Spatial Memory. 29274876: Moreover, LC neurodegeneration is not only a consequence of AD, but also drives clinical and pathological manifestations of AD, such as microglial dysregulation, sleep disturbance, cognitive decline, and neurovascular dysfunction. 29388925: The amyloid-beta peptide (Abeta), derived from amyloid precursor protein, is one driver of AD, but how it leads to neuronal dysfunction is not established. 29776894: Amyloid plaques with neurofibrillary tangles are a neuropathological hallmark of AD that produces synaptic dysfunction and culminates later in neuronal loss. 30031108: In Alzheimer's disease (AD), beta-amyloid (Abeta) protein toxicity increases the formation of reactive oxygen species (ROS) and intracellular calcium levels, resulting in neuronal dysfunction, neurodegenerative disorders, and cell death. 30108498: Background: The deposition of beta-sheet rich amyloid in senile plaques is a pathological hallmark of Alzheimer's disease (AD), which is thought to cause neuronal dysfunction. 30166454: Emerging studies implicate Tau as an essential mediator of neuronal atrophy and cognitive impairment in Alzheimer's disease (AD), yet the factors that precipitate Tau dysfunction in AD are poorly understood. 30244163: Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. 30474638: Alzheimer's disease (AD) is a progressive neurodegenerative condition in which aggregated tau and amyloid proteins accumulate in the brain causing neuronal dysfunction which eventually leads to cognitive decline. 7699466: METHODS: Twelve patients with higher cortical dysfunction due to Alzheimer's disease and 18 age-matched controls were examined. 12009502: Amyloid-beta protein (Abeta) is implicated in the pathogenesis of Alzheimer's disease because of its neurotoxicity and the ability to trigger local inflammation. 12646202: beta-Amyloid peptide (A beta), a major component of senile plaques, the formation of which is characteristic of Alzheimer's disease (AD), is believed to induce inflammation of the brain mediated by microglia, leading to neuronal cell loss. 15811602: The major pathological consequence of Alzheimer disease (AD) is accumulation of beta-amyloid (Abeta) peptide fibrillar plaque in the brain and subsequent inflammatory reaction associated with the surrounding cells due to the presence of these aggregates. 17027528: Although the precise molecular and cellular relationship between AD and inflammation remains unclear, interleukins and cytokines might induce activation of signaling pathways leading to futher inflammation and neuronal injury. Epidemiologic data as well as clinical trial evidence suggest that nonsteroidal anti-inflammatory drug (NSAID) use may decrease the incidence of AD, further supporting a role for inflammation in AD pathogenesis. 20205641: Morbidities of aging and Alzheimer's disease (AD) have been related to defective functions of both T cells and macrophages leading to brain amyloidosis and inflammation. 21278785: Furthermore, the dose of evodiamine significantly decreased the expression of IL-1beta, IL-6, TNF-alpha, and COX-2 that were involved in the inflammation due to Alzheimer's disease. 24424131: It plays an important role in rheumatoid arthritis, organ transplant rejection, Alzheimer's disease and also causes inflammation. 26827642: CSF YKL-40, a biomarker of glial inflammation, is associated with a cerebral structural signature distinct from that related to p-tau neurodegeneration at the earliest stages of cognitive decline due to AD. 29883947: In diseases of the central nervous system such as stroke, Alzheimer's disease, and Parkinson's disease, they often cause inflammation or phagocytosis; however, some studies have found that despite the current controversy over M1, M2 polarization could be beneficial. 30282364: The dominant model for Alzheimer's disease (AD) is the amyloid cascade hypothesis, in which the accumulation of excess amyloid-beta (Abeta) leads to inflammation, excess glutamate and intracellular calcium, oxidative stress, tau hyperphosphorylation and tangle formation, neuronal loss, and ultimately dementia. 30314800: In AD, chronic activation of this pathway leads to sustained inflammation and neurodegeneration. 31374883: Biomarkers of inflammation tended to be higher in the MX than in either the AD or VCID, suggesting dual pathology leads to increased inflammation, which could explain accelerated cognitive decline in that group. 32215721: Knock-on effect of periodontitis to the pathogenesis of Alzheimer's disease?BACKGROUND: Alzheimer's disease has chronic inflammatory components, which can be enhanced by systemic immune activation resulting in inflammation or vice versa. 33313759: Conversely, specific systemic inflammatory regulators may be downstream effects of Alzheimer's disease or consequences of common factors causing both inflammation and Alzheimer's disease. 33963669: While screening for natural product scaffolds as potential anti Alzheimer's disease (AD), oxymatrine (OMT) was found to relieve symptoms of AD through diminishing death of neuronal cells caused by microglia induced inflammation. 34503373: We concluded that the FGF23/alpha-Klotho axis can regulate the AD-induced cell inflammation through the Wnt/beta-catenin pathway. Blocking the Wnt/beta-catenin pathway increased inflammatory cytokine production in AD-PBMCs and annulled the effects of the FGF23/alpha-Klotho axis on AD-induced cell inflammation. 34620254: However, it is still ambiguous whether this observed inflammation is cause or consequence of AD pathogenesis. 35166975: This paper aims to highlight the down-stream pathophysiology of noise-induced mental disorders, including hearing loss, annoyance, anxiety, depression, memory loss, and Alzheimer's disease, describing the underlying mechanisms of induction of inflammation and oxidative stress. 36048350: Disturbance of these microRNAs is associated with mitochondrial dysfunction, oxidative damage, inflammation, apolipoprotein E4 (APOE4) pathogenic process, synaptic loss, and cognitive deficits induced by AD. 37571319: Neuropsychiatric disorders including Alzheimer's disease (AD) may cause gut inflammation and dysbiosis. 38382009: BACKGROUND AND OBJECTIVES: Fine particulate matter (PM 2.5 ) exposure has been found to be associated with Alzheimer disease (AD) and is hypothesized to cause inflammation and oxidative stress in the brain, contributing to neuropathology. 17362834: FINDINGS: Abnormal scans had a mean sensitivity of 77.7% for detecting clinical probable DLB, with specificity of 90.4% for excluding non-DLB dementia, which was predominantly due to Alzheimer's disease. 22118943: Our results suggest a contribution of established AD and PD genes to the genetic etiology of DLB and PDD though to a limited extent. The contribution of both sequence and copy number variants (CNVs) in known AD and PD genes to the genetic etiology of DLB and PDD however is currently unclear. 26405688: Receiver operator characteristic (ROC) curves assessed the ability of LBCRS to differentiate: (a) DLB from Alzheimer's disease (AD); (b) DLB from all dementia, and (c) Mild cognitive impairment (MCI) due to DLB from MCI due to AD. 30083812: PCA is a clinico-radiological syndrome that is often caused by Alzheimer's disease and other neurodegenerative diseases as Lewy body dementia and corticobasal degeneration. 32236399: Of the remaining subjects, 24 were classified as normal cognition and were asymptomatic, 6 were classified as subjective cognitive decline, and 3 were amyloid-positive (one with pre-clinical AD, one with pre-clinical Lewy-Body Dementia, and one with mild cognitive impairment due to AD). 32480310: We aimed to investigate the ratio between alpha and theta band power (alpha/theta ratio), as a synoptic index of quantitative EEG (qEEG) slowing-down, in a peculiar group of patients with mild cognitive impairment (MCI) due to an early-stage Lewy body disease (MCI-LBD), as compared to de novo PD patients without cognitive impairment (PD-MOT), to patients with MCI due to Alzheimer's disease (MCI-AD), and to healthy controls (HC). 32636325: To determine whether electroencephalography (EEG) differentiates the prodromal phase of DLB from other causes of mild cognitive impairment (MCI) and whether EEG is predictive for time to conversion from MCI to DLB, we compared EEGs and clinical follow-up of patients with MCI due to DLB with MCI due to Alzheimer's disease (MCI-AD). 33793069: METHODS: The LBD-MOD was completed in a single-site study in 342 participants: 53 controls, 78 AD, and 110 DLB; 79 mild cognitive impairment due to AD (MCI-AD); and 22 MCI-DLB. 34328531: PURPOSE: The purpose of this study is to develop and validate a 3D deep learning model that predicts the final clinical diagnosis of Alzheimer's disease (AD), dementia with Lewy bodies (DLB), mild cognitive impairment due to Alzheimer's disease (MCI-AD), and cognitively normal (CN) using fluorine 18 fluorodeoxyglucose PET (18F-FDG PET) and compare model's performance to that of multiple expert nuclear medicine physicians' readers. 8676755: Immunologic features of Alzheimer disease and Parkinson disease suggest the involvement of similar phenomena in Lewy body diseases pathogenesis. 10410180: With the onset of memory loss secondary to Alzheimer disease, she became increasingly anxious and compulsive as a result of a failure to remember. 11795357: Alzheimer's disease (AD) is an irreversible, progressive brain disorder that occurs gradually and results in memory loss, behavior and personality changes, and a decline in cognitive abilities. 18288928: Alzheimer's Disease (AD) is caused by the deposition of insoluble and toxic amyloid peptides (Abeta) in the brain leading to memory loss and other associated neurodegenerative symptoms. 19104051: Although defects in Notch have been implicated in memory loss because of Alzheimer's disease, downstream signaling linking Notch to memory have not been determined. 21154880: Alzheimer's disease (AD) is an age-related neurodegenerative disorder of the central nervous system resulting in memory loss and dementia. 22044024: Alzheimer's disease (AD) is a devastating disorder that leads to memory loss and dementia. 22266017: Alzheimer's disease (AD) is a progressive neurodegenerative disease that affects a staggering percentage of the aging population and causes memory loss and cognitive decline. 24304575: Memory loss could be caused by Alzheimer's disease (AD) and vascular dementia (VaD). 24365147: Alzheimer's is a neurodegenerative disorder resulting in memory loss and decline in cognitive abilities. 24667360: Alzheimer's disease (AD), the most common form of dementia, is characterized by the loss of normal functions of brain cells and neuronal death, ultimately leading to memory loss. Dipeptidyl peptidase-4 inhibition by Pterocarpus marsupium and Eugenia jambolana ameliorates streptozotocin induced Alzheimer's disease. Therefore, PM and EJ extracts contain cognitive enhancers as well as neuroprotective agents against STZ induced AD. Therefore, in the present study, the neuroprotective roles of PM and EJ for ameliorating the streptozotocin (STZ) induced AD have been tested in rat model. 25281744: Alzheimer disease (AD) is a progressive neurodegenerative disease leading to memory loss. Abeta is generated by the proteolytic processing of the amyloid precursor protein (APP), and alterations to this processing can result in Alzheimer disease. 25752209: Alzheimer's disease (AD) is a progressive neurodegenerative disorder leading to memory loss and other functional impairments. 25919992: Alzheimer's disease (AD) is a progressive disorder of the brain that leads to memory loss, dementia, and death. 26200391: In Alzheimer's disease (AD), activated microglia invade and surround beta-amyloid plaques, possibly contributing to the aggregation of amyloid beta (Abeta), which affect the survival of neurons and lead to memory loss. 26220908: Alzheimer's disease (AD) is a neurodegenerative disorder in which the death of brain cells causes memory loss and cognitive decline, i.e., dementia. 26292618: BACKGROUND: Mild cognitive impairment (MCI) is a clinical transitional stage between normal aging and Alzheimer disease, which leads to memory loss and a reduction in cognitive function. 26325402: Alzheimer's disease (AD), a big cause of memory loss, is a progressive neurodegenerative disorder. 26358038: Alzheimer's disease (AD) is a complicated neurodegenerative disease which causes memory loss and dementia. 27414248: Alzheimer's disease (AD) is a neurodegenerative disorder in which the death of brain cells leads to memory loss and cognitive decline. 28098452: Alzheimer's disease (AD) is the most common form of dementia, in which the death of brain cells causes memory loss and cognitive decline. 28111296: Alzheimer's disease (AD) is a well-known cause of memory loss and dementia in elderly people all across the world. 28522119: Furthermore, using optogenetics to stimulate neurons can rescue learning and memory loss caused by AD. 28677497: BACKGROUND: Alzheimer's disease is a severe neurodegenerative brain disorder, showing severe beta-amyloid depositions in the brain (plaques) and in vessels (cerebral amyloid angiopathy, CAA), tau pathology, neurodegeneration (and loss of acetylcholine), inflammation with reactive astrocytes and microglia and cerebrovascular damage, all resulting in memory loss. 29445429: Alzheimer's disease (AD) is a progressive, and often fatal, brain disease that causes neurodegeneration, resulting in memory loss as well as other cognitive and behavioral problems. 29530541: Alzheimer's disease (AD) is a progressive neurological disorder in which the death of brain cells causes memory loss and cognitive decline. 29622019: BACKGROUND: Alzheimer's disease (AD), one of the major causes of dementia, is an overwhelming neurodegenerative disease that particularly affects the brain, leading to memory loss and impairment of language and judgment capacity. 29707568: Alzheimer's disease is characterized by the abnormal accumulation of extracellular amyloid-beta plaques and intraneuronal neurofibrillary tangles in brain regions and manifests as a type of dementia in aged individuals that results in memory loss, multiple cognitive abnormalities, and intellectual disabilities that interfere with quality of life. 8146663: In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation. Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels. 10809400: CONCLUSIONS: These findings which are in line with previous results in Alzheimer's disease (Stadelmann et al., 1998) and Parkinson's disease (Banati et al., 1999) suggest that mechanisms distinct from classical apoptosis play a central role in the pathogenesis of PD and related neurodegenerative diseases. 15262733: CONCLUSION: The lack of familial aggregation of PD and AD does not support the hypothesis of major shared genetic contributions to the etiology of the 2 most common neurodegenerative disorders. 15533611: Many possible risk factors for Alzheimer's disease (AD) have been investigated, with only a very few showing positive associations and none defining the etiology of the neurodegenerative disease. 15935398: We determined the concentrations of free homocysteine (HC) and total HC in the cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD) or Parkinson's disease (PD) in order to elucidate whether HC is related to the pathogenesis of these neurodegenerative diseases. 19997871: Alzheimer's disease (AD) is a prevalent dementia-causing neurodegenerative disease. 21045163: Alzheimer disease (AD) is the most common causes of neurodegenerative disorder in the elderly individuals. 21172065: BACKGROUND: Alzheimer's disease (AD) is one of the most frequent cause of neurodegenerative disorder in the elderly. 21834057: The main component of the amyloid plaques found in the brains of those with Alzheimer's disease (AD) is a polymerized form of the beta-amyloid peptide (Abeta) and is considered to play a central role in the pathogenesis of this neurodegenerative disorder. 24687814: Frontotemporal dementia (FTD) is a clinically and pathologically heterogeneous neurodegenerative disease that can result from either frontotemporal lobar degeneration (FTLD) or Alzheimer's disease (AD) pathology. 25079797: More importantly, 205 dysregulated genes in AD blood have been linked to neurological disease, including AD/dementia and Parkinson's disease, and 43 are known to be the causative genes of 42 inherited mental retardation and neurodegenerative diseases. 26402766: Although monocytes and macrophages could serve as new therapeutic targets for treatment of Alzheimer's disease (AD) and aging of the human innate immune system, its role in the pathogenesis of neurodegenerative disorders such as AD are only poorly understood. 26528186: Neurodegenerative diseases such as Alzheimer's disease, Creutzfeldt-Jakob disease (CJD), Parkinson's disease, Huntington's disease, frontotemporal dementia (FTD), and amyotrophic lateral sclerosis (ALS) result from the loss of a specific subsets of neurons, which is closely associated with accumulation and deposition of specific protein aggregates. 27280392: BACKGROUND: Parkinson's disease (PD) is depicted as the most prevailed neurodegenerative disease being secondary to the alzheimer's disease. 27586004: Alzheimer's disease (AD) is a chronic neurodegenerative disease while the ectopic P-granules autophagy protein 5 homolog (EPG5 gene) is highly expressed in human brain and may implicate in the pathogenesis of neurodegenerative disorders. 28251365: Alzheimer's disease (AD) is a difficult puzzle to solve, in part because the etiology of this devastating neurodegenerative disorder remains murky. 28839167: The ultra-sensitive IMR assay was applied to detect the plasma tau protein levels of subjects with prevalent neurodegenerative diseases, such as Alzheimer's disease (AD), mild cognitive impairment (MCI) due to AD, Parkinson's disease (PD), frontotemporal dementia (FTD) and vascular dementia (VD). 29632940: Alzheimer's disease (AD) is the most common cause of neurodegenerative disorder in elderly people, and has become a social problem in aging societies globally. 29687731: Age-related dementias are now a major mortality factor among most human populations in the world, with Alzheimer's disease (AD) being the leading dementia-causing neurodegenerative disease. 30845903: BACKGROUND: Prodromal Neurodegenerative Disease (ND) due to tauopathies such as Alzheimer's Disease (AD) and Synucleinopathies (SN) such as Parkinson's Disease (PD) and Dementia with Lewy Bodies (DLB) present subtly. 31876280: In this review, based on the latest experimental data on structure-function properties of chemically modified amyloid-beta isoforms, the concept of the origin and the mechanism of action of amyloid-beta with isomerized Asp7 residue, as a molecular agent of Alzheimer's disease pathogenesis, is presented. Advances in the research of molecular factors involved in the onset and progression of Alzheimer's disease, have led to the creation of several pathogenesis concepts of the most common neurodegenerative disease in the world, and amyloid, cholinergic, and neuroinflammatory hypotheses became leading. 32507685: Inhibition of STAT3 phosphorylation attenuates impairments in learning and memory in 5XFAD mice, an animal model of Alzheimer's disease.The pathophysiological roles of astrocytes in the reactive state are thought to have important significance in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). 32908122: The objective of this review is to discuss the possible molecular mechanisms that contribute to the pathogenesis of neurological diseases in which CHIP has a pivotal role, such as stroke, intracerebral hemorrhage, Alzheimer's disease, Parkinson's disease, and polyglutamine diseases; furthermore, CHIP mutations could also cause neurodegenerative diseases. 33114455: Potential Drug Candidates to Treat TRPC6 Channel Deficiencies in the Pathophysiology of Alzheimer's Disease and Brain Ischemia.Alzheimer's disease and cerebral ischemia are among the many causative neurodegenerative diseases that lead to disabilities in the middle-aged and elderly population. 34072862: After a brief summary of the molecular and cell biology of AD and HD this review covers what is known about the role of these three groups of kinases in the brain and in the pathogenesis of the two neurodegenerative disorders. Alzheimer's disease (AD) is a mostly sporadic brain disorder characterized by cognitive decline resulting from selective neurodegeneration in the hippocampus and cerebral cortex whereas Huntington's disease (HD) is a monogenic inherited disorder characterized by motor abnormalities and psychiatric disturbances resulting from selective neurodegeneration in the striatum. 35434157: Background: Alzheimer's disease (AD) is the main cause of the neurodegenerative disorder, which is not detected unless the cognitive deficits are manifested. 35719134: In the field of neurodegenerative diseases, an example of a digital biomarker-based technology is instrumental activities of daily living (iADL) digital medical application, a predictive biomarker of conversion from mild cognitive impairment (MCI) due to Alzheimer's disease (AD) to dementia due to AD in individuals aged 55 + . 36579548: Immunosenescence and Aging: Neuroinflammation Is a Prominent Feature of Alzheimer's Disease and Is a Likely Contributor to Neurodegenerative Disease Pathogenesis. 37927338: Controversies surrounding the validity of the toxic proteinopathy theory of Alzheimer's disease have led the scientific community to seek alternative theories in the pathogenesis of neurodegenerative disorders (ND). 38243562: AD is the most common cause of neurodegenerative disorder in the elderly. 12707087: Unexplained sudden amnesia, postencephalitic Parkinson disease, subacute sclerosing panencephalitis, and Alzheimer disease: does viral synergy produce neurofibrillary tangles? 1307688: These patterns closely match the hierarchical topographic distribution of NFT and SP observed in AD, suggesting a commonality in the pathologic processes that lead to NFT and SP in both aging and AD. 15265277: The microvasculature plays a crucial role in maintaining brain homeostasis and deterioration of its integrity may have deleterious effects on brain function in AD, possibly leading to neurofibrillary degeneration, plaque formation, and cell loss. 1614354: Considerable evidence suggests that in Alzheimer's disease, olfactory bulb damage may be a primary factor, causing degeneration and neurofibrillary tangles primarily in neurons connected with this brain area. 17055667: Here I hypothesize that it is chronic infection of human neurons in Alzheimer's disease that produces neurofibrillary tangles by a pathway similar to the chronic SSPE infection tangle pathway. 20188796: GRB-associated binding protein 2 (GAB2) may function as a risk factor of Alzheimer disease (AD) by affecting hyperphosphorylation of tau, causing neurofibrillary tangles. 20679486: Accumulation of tau into neurofibrillary tangles is a pathological consequence of Alzheimer's disease and other tauopathies. 21507528: As with prior studies, our data indicate that the development of neocortical neurofibrillary tangles is the key pathological event that is not observed in pAD cases: Braak stages III or IV pathology are hence not truly a substrate for \intermediate likelihood\ that cognitive impairment is due to Alzheimer's disease (AD). 21630160: Once both of these hits are activated, AD can develop and produce senile plaques and neurofibrillary tangles throughout brain tissue. 21813771: We have previously shown that expression of nonmutated human truncated tau (151-391, 4R), derived from sporadic Alzheimer's disease, induced neurofibrillary degeneration accompanied by microglial and astroglial activation in the brain of transgenic rats. 25963683: Herpes simplex virus-1 has been proposed as potential cause of AD because of its ability to form beta amyloid(Abeta) and neurofibrillary tangles due to tau hyperphosphorylation and action of beta & gamma secretase on amyloid precursor protein(APP) together with genetic association with apolipoprotein-E4(ApoE-E4), which points out to latent Herpes Simplex virus-1 as an agent causing AD. 26289409: Alzheimer's disease (AD) is a polygenic and multifactorial disease with a complex inheritance caused by the formation of amyloid plaques and neurofibrillary tangles in the brain. Increasing evidence indicates that many genes including interleukin-6 (IL-6) and alpha 2-macroglobulin (A2M) may contribute to the pathogenesis of AD. 27814651: Alzheimer disease (AD) and Parkinson disease (PD) brains have reduced respiratory capacity and impaired mitobiogenesis, which could result in beta-amyloid plaques and neurofibrillary tangles. 30412490: In AD, neurofibrillary tangles (NFTs) appear first in entorhinal cortex, implying that aging processes in entorhinal neurons promote NFT pathogenesis. 8988457: In Alzheimer's disease, susceptible neurons produce neurofibrillary tangles and neuropil threads, while in Parkinson's disease, they develop Lewy bodies and Lewy neurites. 9617789: In AD, susceptible neurons produce neurofibrillary tangles (NFTs) and neuropil threads (NTs), while in PD, they develop Lewy bodies (LBs) and Lewy neurites (LNs). 10809400: CONCLUSIONS: These findings which are in line with previous results in Alzheimer's disease (Stadelmann et al., 1998) and Parkinson's disease (Banati et al., 1999) suggest that mechanisms distinct from classical apoptosis play a central role in the pathogenesis of PD and related neurodegenerative diseases. 14722078: The genetic defects underlying several monogenic familial forms of AD and PD have recently been identified, however, the causes of other AD and PD cases, particularly sporadic cases, remain unclear. 20634620: Camptocormia can be due to central nervous system diseases, such as Parkinson's disease, dystonia, multisystem atrophy, or Alzheimer's disease, due to peripheral nervous system diseases, such as primary myopathy, secondary myopathy, motor neuron disease, myasthenia, or chronic inflammatory demyelinating polyneuropathy, due to side effects of drug treatment, due to disc herniation, arthritis or spinal trauma, or due to paraneoplasia. 23303475: The activity of metabotropic glutamate receptors (mGluRs) is known to be altered as the consequence of neurodegenerative diseases such as Alzheimer, Parkinson, and Huntington disease. 26209472: In Alzheimer's disease, beta-amyloid peptide-containing plaques and intraneuronal neurofibrillary tangles composed of hyperphosphorylated microtubule-associated protein tau are the two main neuropathological lesions, while Parkinson's disease is defined by the presence of Lewy Bodies that are intraneuronal proteinaceous cytoplasmic inclusions. alpha-Synuclein has been identified as a major protein component of Lewy Bodies and heavily implicated in the pathogenesis of Parkinson's disease. 26528186: Neurodegenerative diseases such as Alzheimer's disease, Creutzfeldt-Jakob disease (CJD), Parkinson's disease, Huntington's disease, frontotemporal dementia (FTD), and amyotrophic lateral sclerosis (ALS) result from the loss of a specific subsets of neurons, which is closely associated with accumulation and deposition of specific protein aggregates. 27166223: Impaired protein degradation has been discussed as a cause or consequence of various neurodegenerative diseases, such as Alzheimer's, Parkinson's and Huntington's disease. 27280392: BACKGROUND: Parkinson's disease (PD) is depicted as the most prevailed neurodegenerative disease being secondary to the alzheimer's disease. 27699087: Evidence from rodent and cell models show a number of neurotrophic and neuroprotective effects of guanosine preventing deleterious consequences of seizures, spinal cord injury, pain, mood disorders and aging-related diseases, such as ischemia, Parkinson's and Alzheimer's diseases. 28839167: The ultra-sensitive IMR assay was applied to detect the plasma tau protein levels of subjects with prevalent neurodegenerative diseases, such as Alzheimer's disease (AD), mild cognitive impairment (MCI) due to AD, Parkinson's disease (PD), frontotemporal dementia (FTD) and vascular dementia (VD). 28974380: INTRODUCTION: We used a functional MRI paradigm involving conventional vs. unconventional views of objects to assess bottom-up vs. top-down visual processing in Parkinson's disease (PD) with normal cognition, PD with mild cognitive impairment (MCI), and MCI due to Alzheimer's disease (AD) as compared to healthy controls. 32634809: We compared the serial position effects (SPE) between patients with mild cognitive impairment (MCI) due to Parkinson's disease (PD), i.e., PD-MCI, and patients with MCI due to Alzheimer's disease (AD-MCI), and evaluated the influence of SPE and frontostriatal deficits on verbal memory recall. 36717892: We summarize the impact of COVID-19 infection on symptom severity, disease progression, and mortality rate of PD and AD, and discuss whether COVID-19 infection could trigger PD and AD. 8033937: Lastly, degenerative cerebral diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, progressive supranuclear palsy and corticobasal degeneration result in more or less severe eye movement disturbances. 1307688: These patterns closely match the hierarchical topographic distribution of NFT and SP observed in AD, suggesting a commonality in the pathologic processes that lead to NFT and SP in both aging and AD. 14645482: These results demonstrate that, once plaques are cleared, neuronal morphology is self-correcting and that passive antibody treatment has the potential to reverse neuronal damage caused by Alzheimer's disease and, hence, directly impact cognitive decline. 16437529: BACKGROUND: Alzheimer's disease (AD) may result in senile plaques being formed outside the brain as accumulation of beta-amyloid (Ass). 16863248: The identification and characterization of possible environmental factors that may influence amyloid deposition in vivo are important to unveil the underlying etiology of AD. According to the amyloid cascade hypothesis, diffuse plaques are initial and visual deposits in the early event of AD, leading to amyloid plaques. 18254079: BACKGROUND: Alzheimer's disease (AD) may be caused by the formation of extracellular senile plaques comprised of beta-amyloid (Ass). 20384814: Using the Tg2576 transgenic mouse model of AD, this study characterized a promotive effect of neuronal hypoactivity associated with functional deprivation on amyloid plaque pathogenesis in the olfactory pathway. 21630160: Once both of these hits are activated, AD can develop and produce senile plaques and neurofibrillary tangles throughout brain tissue. 22592705: BACKGROUND: Alzheimer's dementia (AD) may be caused by the formation of extracellular senile plaques comprised of beta-amyloid (Abeta). 22924088: The spread of amyloid plaques to the striatum has been reported to be a sensitive and specific indicator of dementia due to Alzheimer's disease (AD). 23478304: The transgenic TgCRND8 mouse is widely used as an animal model of Alzheimer's disease (AD) and exhibits an early onset of senile plaque pathogenesis in the brain. 24563468: BACKGROUND: Alzheimer's dementia (AD) may be caused by the formation of extracellular senile plaques comprised of beta-amyloid (Abeta). 25031402: In sporadic Alzheimer's disease (AD), impaired Abeta removal contributes to elevated extracellular Abeta levels that drive amyloid plaque pathogenesis. 26289409: Alzheimer's disease (AD) is a polygenic and multifactorial disease with a complex inheritance caused by the formation of amyloid plaques and neurofibrillary tangles in the brain. Increasing evidence indicates that many genes including interleukin-6 (IL-6) and alpha 2-macroglobulin (A2M) may contribute to the pathogenesis of AD. 27814651: Alzheimer disease (AD) and Parkinson disease (PD) brains have reduced respiratory capacity and impaired mitobiogenesis, which could result in beta-amyloid plaques and neurofibrillary tangles. 29134465: Recent findings With the advent of 18F-labeled tracers that bind amyloid plaques, amyloid PET is now clinically available for the detection of amyloid pathology and to aid in a biomarker-supported diagnosis of AD or mild cognitive impairment (MCI) due to AD. 29266373: BACE1, a key protein involved in Alzheimer's progression, initiates Abeta42 generation that induce senile plaques in brain. 29611473: Alzheimer's disease (AD) is a complex, neurodegenerative pathology showing, among others, high cholinergic and neurotransmitter deficits, oxidative stress, inflammation, A?-aggregation resulting in senile plaques formation, and hyperphosphorylation of tau-protein leading to neurofibrillary tangles. 32996088: Some of the neurotoxic metals such as lead, aluminum, mercury, manganese, cadmium, and arsenic as well as some pesticides and metal-based nanoparticles have been involved in AD and PD due to their ability to produce senile/amyloid plaques and NFTs which are the main feature of these neuronal dysfunctions. 34906975: DISCUSSION: Plasma Abeta42/Abeta40 is a robust measure for detecting amyloid plaques and can be utilized to aid in the diagnosis of AD, identify those at risk for future dementia due to AD, and improve the diversity of populations enrolled in AD research and clinical trials. 35887070: Furthermore, the crucial role of ANT-1 and VDAC impairment in the onset/progression of AD opens a window for new therapeutic strategies aimed at preserving/improving mitochondrial function, which is suspected to be the driving force leading to plaque and tangle deposition in AD. 36138973: One of the factors, which might play a key role in senile plaques and tau fibrils generation due to Alzheimer's disease, is inflammaging, i.e., systemic chronic low-grade age-related inflammation. 38356475: The HOPE4MCI study: A randomized double-blind assessment of AGB101 for the treatment of MCI due to AD. INTRODUCTION: In addition to the accumulation of amyloid plaques and neurofibrillary tangles, the presence of excess neural activity is a pathological hallmark of Alzheimer's disease (AD) and a prognostic indicator for progression of AD pathology and clinical/cognitive worsening in mild cognitive impairment due to Alzheimer's disease (MCI due to AD). 6803359: Although several studies of Alzheimer's disease suggest that the frequency of neuritic plaques in the cerebral cortex is correlated with the severity of dementia and with reduction in presynaptic cholinergic markers in the cortex, the relationship between cholinergic cortical innervation and the pathogenesis of plaques is unknown. 7884819: S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques. 8892356: We propose that the amyloid deposits in senile plaques of Alzheimer's Disease (AD) result from ancient mechanisms in wound-healing and inflammatory processes that preceded the evolution of the inducible combinatorial immune responses characteristic of jawed vertebrates. 10096843: AD is the leading cause of senile dementia and although the pathogenesis of this disorder is not known, various hypotheses have been developed based on experimental data accumulated since the initial description of this disease by Alois Alzheimer about 90 years ago. 10740829: Alzheimer disease, the leading cause of senile dementia, is characterised by the degeneration of select neuronal populations. 10867221: Alzheimer's disease (AD) and cerebrovascular dementia (CVD) are two major causes of senile dementia in elderly individuals. 12134567: Homocysteine has emerged as an independent risk factor for stroke, and recent studies suggest that vascular disease affecting the brain and Alzheimer's disease may result together in senile dementia. 12625839: BACKGROUND: Lewy body disease is, after Alzheimer's disease, the second most common cause of senile degenerative dementia with progressive cognitive deterioration, fluctuation of cognitive and motoric functions and psychotic symptoms. 14501255: Alzheimer's disease (AD) is the most common cause of senile dementia, for which there is presently no disease-based treatment. 15371644: Alzheimer's disease (AD) is the leading cause of senile dementia, and is a complex disorder. 16788045: Alzheimer's disease (AD) is a common neurodegenerative disorder that causes senile dementia. 18855671: Alzheimer's disease (AD), the leading cause of senile dementia, has become a considerable social and economical problem. 1889888: Since 73% of dementias are at least partly caused by Alzheimer's disease in the area examined and because the short test used discriminates demented from healthy octagenarians as well as tests involving extensive examinations, the findings of this study suggest with a high probability that the [Al] of drinking water is not an essential factor in the pathogenesis of senile dementia. 1895528: Alzheimer's disease is one of the main causes of senile dementia. 19195795: Body iron stores that increase with age could be pivotal to AD pathogenesis and progression. This communication explores the temporal link between the age-associated increase in body iron stores and the age-related incidence of Alzheimer's disease (AD), the most prevalent cause of senile dementia. 19619524: Alzheimer's disease is the major cause of senile dementia with the hallmark of beta-amyloid deposition in neurons. 19737808: AD, characterized microscopically by deposition of amyloid plaques and formation of neurofibrillary tangles in the brain, has become the most common cause of senile dementia. 20101721: Alzheimer's disease is the most common cause of senile dementia in the United States and Europe. 20369844: Alzheimer's disease is a progressive, neurodegenerative disorder that is the leading cause of senile dementia, afflicting millions of individuals worldwide. 20462385: Alzheimer disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for senile dementia. 20552234: Alzheimer's disease (AD), the most prominent cause of senile dementia, is clinically characterized by the extracellular deposition of beta-amyloid (Abeta) and the intracellular neurofibrillary tangles. 21349442: Alzheimer's disease is a neurodegenerative disease that is imposing an increasing burden on society, and is the leading cause of senile dementia worldwide. 23062696: Alzheimer's disease (AD) is the leading cause of senile dementia. 23173066: The pathogenic aggregation of the amyloid beta-peptide (Abeta) is considered a hallmark of the progression of Alzheimer's disease, the leading cause of senile dementia in the elderly and one of the principal causes of death in the United States. 23566654: The pathological hallmark of Alzheimer's disease (AD), the leading cause of senile dementia, involves region-specific neuronal death and an accumulation of neuronal and extracellular lesions termed neurofibrillary tangles and senile plaques, respectively. 24006337: Alzheimer's disease (AD) is a progressive neurodegenerative disease and the leading cause of senile dementia in the United States. 24523906: Alzheimer's disease (AD) is the leading cause of senile dementia in today's society. 24975171: Cu dyshomeostasis has also been concerned in neurodegenerative disorders such as Alzheimer, Amyotrophic lateral sclerosis (ALS) or Menkes disease and is directly related to neurodegenerative syndrome that usually produces senile dementia. 25446741: Alzheimer disease is the most common neurodegenerative disorder and cause of senile dementia. 25476252: Alzheimer's disease is the major cause of senile dementia, flewing out 10% of 65 years old and 50% of 85 years old global population. 26131055: Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of senile dementia all over the world. 26351775: BACKGROUND: Alzheimer's disease (AD) is the most common cause of senile dementia. 26606591: BACKGROUND: Amyloid-beta (Abeta) peptides are a family of proteins that are considered to be a principal aspect of Alzheimer's disease (AD), the most common cause of senile dementia affecting elderly individuals. 26849355: Alzheimer's disease (AD) is the most common cause of senile dementia. Sphingolipids are widely known to have roles in the pathogenesis of inflammatory diseases, where the precise roles for sphingolipids in inflammation-associated pathogenesis of AD are not well understood. 27865835: Super-activation of cholinesterases (acetylcholinesterase and butyrylcholinesterase) are linked to various neurological problems most precisely Alzheimer's disease (AD), which leads to senile dementia. 29220126: Alzheimer's disease (AD) is a neurodegenerative disease and the most common cause of senile dementia. 29260452: Currently, AD is the leading cause of senile dementia worldwide. 29411261: Alzheimer's disease (AD), a progressive neurodegenerative disease of the central nervous system, is the most common cause of senile dementia. 7175555: The temporal lobe cortex and hippocampus were the areas most severely affected by the increased neurofibrillary tangle formation in senile dementia due to Alzheimer's disease. 7778188: The pathological presentation of Alzheimer's disease, the leading cause of senile dementia, involves regionalized neuronal death and an accumulation of intracellular and extracellular filamentous protein aggregates that form lesions termed neurofibrillary tangles and senile plaques, respectively. 9568532: Alzheimer's disease, the most common cause of senile dementia, is characterized by intracellular formation of neurofibrillary tangles, extracellular deposits of beta amyloid as well as cerebrovascular amyloid accumulation and a profound loss of cholinergic neurons within the nucleus basalis Meynert with alterations in cortical neurotransmitter receptor densities. 11084917: Myoclonus is defined as shock-like, brief involuntary abnormal movements in muscle jerking caused by external stimuli; and it arises from progressive myoclonus epilepsy, post-anoxic encephalopathy and Alzheimer's disease, causing disabling symptoms. 11447834: The clinical symptoms of all forms of Alzheimer's disease (AD) result from a slowly progressive neurodegeneration that is associated with the excessive deposition of beta-amyloid (A beta) in plaques and in the cerebrovasculature, and the formation of intraneuronal neurofibrillary tangles, which are composed primarily of abnormally hyperphosphorylated tau protein. 17645242: As the average disease duration in sporadic methionine/valine type 1 CJD is less than 6 months, it seems legitimate to speculate that the initial symptoms resulted from Alzheimer and alpha-synuclein related pathologies. 17719211: Given that neurodegenerative burden and compensatory mechanisms might exist before accepted clinical symptoms of AD are noticeable, the current prospective study aimed to investigate the functioning of brain regions in the visuospatial networks responsible for preclinical symptoms in AD using event-related functional magnetic resonance imaging (fMRI). 21318511: Aberrant processing of APP was incorporated into the Amyloid Hypothesis, which supposes that the clinical symptoms, neuropathology, and ultimate fatality of Alzheimer's result from the actions of Abeta. 22619696: Except for some kind of cancers, no effective and/or definitive therapeutic treatment aimed to reduce or to retard the clinic and pathologic symptoms induced by AD and PD is presently available. 23665480: Memantine and ketamine block N-methyl-D-aspartate (NMDA) receptors with similar affinity and kinetics, yet their behavioral consequences differ: e.g., memantine is used to alleviate symptoms of Alzheimer's disease, whereas ketamine reproduces symptoms of schizophrenia. 25501055: In the past decade, amyloid deposition has been shown to begin many years before the clinical symptoms of dementia in mild cognitive impairment (MCI) due to Alzheimer disease (AD). 26332220: Interventions for Neuropsychiatric Symptoms in Neurocognitive Impairment Due to Alzheimer's Disease: A Review of the Literature. 27697061: Our review concludes with some suggestions for future studies aimed to advance research into NBS as a potential treatment for the symptoms and disabilities caused by AD and to enable comparison of results across trials. 27870597: However, there was insufficient evidence to support a benefit of dyadic exercise intervention on cognitive performance and on behavioral and neuropsychiatric symptoms in participants with dementia due to AD. 28138509: METHODS: Associations among clinical symptoms, gray-matter volume, regional tau, and A? deposition assessed by positron emission tomography with [11C]pyridinyl-butadienyl-benzothiazole 3 (PBB3) and [11C]Pittsburgh compound-B (PiB), were evaluated in 17 AD, 9 mild cognitive impairment due to AD, and 28 PiB(-)-cognitive healthy controls (HCs). 29286086: The pathogenesis of Alzheimer's disease (AD) has still not been fully elucidated, however it is thought that the build up of amyloid plaque at least partially causes the symptoms of AD. 29365053: The primary outcome was progression from normal cognition to the onset of clinical symptoms of mild cognitive impairment due to Alzheimer's disease at 5 years post-baseline. The goal of this study was to determine which measures, obtained when individuals were cognitively normal, predict on an individual basis, the onset of clinical symptoms associated with a diagnosis of mild cognitive impairment due to Alzheimer's disease. 29955659: Introduction: Autosomal-dominant Alzheimer's disease (ADAD) represents a crucial population for identifying prevention strategies that might modify disease course for cognitively unimpaired individuals at high imminent risk for developing symptoms due to Alzheimer's disease (AD), that is, who have \preclinical\ AD. 30282371: The French Minister of Health published a decree on May 29th of 2018 removing the drugs used to fight against symptoms due to Alzheimer's disease (donepezil, rivastigmine, galantamine, memantine) from the list of available reimbursed drugs. 30788058: BACKGROUND/OBJECTIVES: Alzheimer's disease is a neurodegenerative disease that induces symptoms such as a decrease in motor function and cognitive impairment. 32461027: We propose that the degeneration of the prefrontal cortex in AD produces symptoms of apathy. 32840196: We have previously demonstrated that the presence of two or more of these symptoms differentiates MCI-LB from MCI due to Alzheimer's disease (MCI-AD) with a likelihood ratio >4. 32849173: Subsequent analyses involved splitting the course of the disease into diagnostic categories: cognitively unimpaired subjects (CU), mild cognitively impaired subjects (MCI), and subjects with dementia (AD-dementia), where all symptoms were due to AD. 33188391: Future longitudinal studies are needed to further investigate whether mixed ADNC/LATE-NC may be protective against agitation and frontal symptoms in dementia caused by Alzheimer's disease or LATE pathology. 33461093: Brain autopsy confirmed changes typical of Alzheimer's disease without evidence of active inflammation or sequelae of AE, establishing Alzheimer's disease as the likely cause of resurgent symptoms in this patient. 33792886: BACKGROUND: Alzheimer's disease (AD) causes symptoms such as dementia, memory loss, disorientation, and even aggressiveness, and is more common in women than in men. 34249072: NCS was determined by the presence of AD symptoms and neuropsychiatric (NP) symptoms caused by anti-AD (AAD) drugs (D) as a biomarker. 35710783: The most accepted hypothesis in Alzheimer's disease (AD) is the amyloid cascade which establishes that Abeta accumulation may induce the disease development. This accumulation may occur years before the clinical symptoms but it has not been elucidated if this accumulation is the cause or the consequence of AD. 36396271: Recent biomarker and neuroimaging research has revealed how the pathophysiology of AD may lead to symptoms, and as the pathophysiology of AD gains clarity, more potential treatments are emerging that aim to modify the disease and relieve its burden. 36894582: Our results indicate that AD affects specific EEG-RSNs and deteriorated network activity causes symptoms. 36912421: We investigated the cumulative frequency of symptoms in a longitudinal cohort of MCI-LB compared with MCI due to Alzheimer disease (MCI-AD) and analysed the ability of a previously described 10-point symptom scale to differentiate MCI-LB and MCI-AD, in an independent cohort. 38086100: In vivo studies using transgenic mouse models and AD-induced symptoms have shown promising results, with SeNPs treatment leading to cognitive improvements and reduced amyloid plaque burden in the hippocampus. 38363815: Despite negligible or tiny Abeta pathology, patients 1 and 2 were diagnosed with AD as the cause of symptoms. Despite widespread Abeta pathology, patient 3 was not diagnosed with AD as the cause of symptoms. 8146663: In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation. Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels. 11574902: The syndrome of dementia is most commonly caused by Alzheimer's disease (AD), an age-related neurodegenerative process that primarily affects the cortex. 12137606: BACKGROUND: Dementia is an age-associated syndrome most commonly due to Alzheimer's disease (AD) and/or cerebrovascular disease. 1590915: This case, together with other reports, points to the existence of neurologically defined subgroups of AD with unusual clinical deficits that are correlated with the regional and laminar distribution of NP and NFT, and further supports the hypothesis that the symptomatology presented by AD patients results from the loss of specific neuronal populations leading to a syndrome of global cortical disconnection. 16300967: Semantic dementia (SD) and Alzheimer's disease (AD) are both disorders in which early pathology affects the temporal lobe yet they produce distinct syndromes of declarative memory impairment-loss of established semantic knowledge with relatively preserved episodic memory in the former and the converse in the latter. 17898010: AD is a much commoner cause of focal cortical syndromes than previously recognised, particularly in PCA, PNFA and CBS, but rarely causes SD or bvFTD. 20098809: Posterior cortical atrophy (PCA) is a neurodegenerative syndrome, usually due to Alzheimer's disease. 22766737: The first two relate to clinico-pathological studies which established that Alzheimer's disease (AD) is a relatively common cause of focal cortical syndromes, notably progressive aphasia (largely nonfluent), progressive apraxia, and posterior cortical atrophy with complex visual symptoms. 23300102: In CBS due to FTLD, atrophy extended into the prefrontal cortex, striatum, and brainstem, whereas in CBS due to AD, atrophy extended into the temporoparietal cortex and precuneus. 24291869: In CBS due to frontotemporal lobar degeneration (FTLD), atrophy extended into prefrontal cortex, striatum, and brainstem, whereas in CBS due to Alzheimer's disease (AD), atrophy extended into temporoparietal cortex and precuneus.No functional imaging study in pathology-proven CBD or CBS with known histopathology has been published today. 24994944: BACKGROUND: \Posterior shift\ of the neuropathological changes of Alzheimer's disease (AD) produces a syndrome (posterior cortical atrophy) (PCA) dominated by high-level visual deficits. 26200048: Cortical correlates of affective syndrome in dementia due to Alzheimer's disease. 26377458: UNLABELLED: Posterior cortical atrophy (PCA) is a rare focal neurodegenerative syndrome characterized by progressive visuoperceptual and visuospatial deficits, most often due to atypical Alzheimer's disease (AD). 26483753: Different neurodegenerative disorders, such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), lead to dementia syndromes. 29695292: BACKGROUND: Mild cognitive impairment (MCI) is a heterogeneous syndrome resulting from Alzheimer's disease (AD) as well as to non-AD and non-neurodegenerative conditions. 30083812: PCA is a clinico-radiological syndrome that is often caused by Alzheimer's disease and other neurodegenerative diseases as Lewy body dementia and corticobasal degeneration. 30799336: Mixed Alzheimer's and Lewy-related Pathology Can Cause Corticobasal Syndrome with Visual Hallucinations. 30799371: Authors' Reply: Mixed Alzheimer's and Lewy-related Pathology Can Cause Corticobasal Syndrome with Visual Hallucinations. 30997705: Despite its low prevalence, PCA should be considered a syndrome caused by Alzheimer's disease, dementia with Lewy bodies, or other dementias. 31264318: One had been diagnosed with subjective cognitive impairment, 13 with mild cognitive impairment with or without depression, and 17 with dementia syndrome due to Alzheimer's and/or cerebrovascular disease. 32810333: Some aged community dogs acquire a degenerative syndrome termed Canine Cognitive Dysfunction (CCD) that resembles human dementia due to Alzheimer's Disease (AD), with comparable cognitive and behavioural deficits. 32925054: The ROI with the maximal hypometabolism was the dominant middle temporal gyrus in the language variant of AD (mean z score -2.28), middle occipital gyrus in PCA (-3.24), middle temporal gyrus in frontal AD (-2.70), and angular gyrus in corticobasal syndrome due to AD (-2.31). 33206389: OBJECTIVE: To investigate if individual brain [ 18 F]fluorodeoxyglucose-positron emission tomography (FDG-PET) patterns could distinguish CBS due to Alzheimer's disease (AD) from other pathologies based on [ 11 C]Pittsburgh Compound-B (PIB)-PET. 35670835: For the differentiation of Alzheimer's disease from other etiologies of dementia syndromes, established biological markers could be helpful to confirm a distinctive neuropathology. 38261145: PURPOSE OF THE STUDY: Posterior cortical atrophy is a clinico-radiographical syndrome that presents with higher-order visual dysfunction and is most commonly due to Alzheimer's disease. 6835874: Alzheimer's disease is one of a number of conditions that can cause the syndrome of dementia. 9363830: Dementia is one of the most common organic mental syndromes, usually caused by Alzheimer's disease (AD) or vascular dementia (VD) or both. 9434673: Alzheimer's disease (AD) is by far the most common cause of the Type 1 syndrome. 9652488: Early alexia and higher visual impairments characterize Posterior cortical atrophy (PCA), a progressive dementing syndrome most often caused by Alzheimer disease. 11191636: To further address this issue, reflex hypertension evoked by acute sino-aortic deafferentation was chosen as a model. 11230315: Thus, sympathectomy restores the natriuretic response to a high salt intake and prevents the development of salt-sensitive hypertension induced by sensory denervation. 11668076: Role of renin-angiotensin-aldosterone system in salt-sensitive hypertension induced by sensory denervation. 15569407: CONCLUSIONS: Regardless of increased vascular MnSOD levels, salt sensitive hypertension induced by sensory degeneration is associated with increased vascular superoxide production. AIM: To test the hypothesis that production of superoxide in mesenteric resistance arteries is increased and contributes to the development of hypertension induced by sensory denervation plus high salt intake. 15929825: CONCLUSION: Valsartan or Plendil could prevent the development of salt-sensitive hypertension induced by sensory denervation and the overloading of intracellular [Ca(2+)](i), which indicated that salt-sensitive hypertension induced by sensory nerve degeneration might be related to renin-angiotensin-aldosterone system (RAAS) and the over loading intracellular [Ca(2+)](i), and might be more closely to RAAS. 15994858: ET(A) receptor blockade prevents renal dysfunction in salt-sensitive hypertension induced by sensory denervation. Therefore, the blockade of the ET(A) receptor ameliorates the impairment of renal excretory function and prevents the elevation in blood pressure in salt-sensitive hypertension induced by degeneration of sensory nerves, indicating that the activation of the ET(A) receptor impairs renal function and contributes to the development of a salt-induced increase in blood pressure in this model. 28363984: C1 neurons have low activity under normoxia, but their activation is important to BP stability during hypoxia or anesthesia and contributes greatly to the hypertension caused by baroreceptor deafferentation. 3346049: These data indicate that 1) lesion of the nucleus ambiguus facilitates hypertension produced by sinoaortic deafferentation unless lesioning follows deafferentation; and 2) stimulation of the nucleus ambiguus produces a pressor effect that is independent of the bradycardic response. 3718427: It is concluded that sino-aortic baroreceptor deafferentation produces a significant chronic hypertension, probably supported by elevated plasma catecholamine concentrations and enhanced synthesis and release of adrenaline from adrenal medulla. 3812768: There is considerable controversy as to whether removal of baroreceptor input by sinoaortic deafferentation leads to a sustained hypertension in quadripeds. 6507647: The role of the sympathetic nervous system in acute ABD-induced hypertension was evaluated by examining the ability of adrenalectomy, adrenal demedullation, guanethidine or combined adrenal demedullation, and guanethidine pretreatment to prevent, and total autonomic blockade to reverse, ABD-induced hypertension. Only combined adrenal demedullation and guanethidine pretreatment prevented ABD-induced hypertension, and autonomic blockade normalized MAP in ABD rats. Experiments were performed to test the hypothesis that acute hypertension caused by aortic baroreceptor deafferentation (ABD) is the result of sympathetic vasoconstriction. It is concluded that acute ABD-induced hypertension results from vasoconstriction caused by neurally released and/or circulating catecholamines. 6654453: The role of sympathetic and other pressor systems in the development of fulminant hypertension induced by baroreceptor deafferentation is still unclear. 7235028: Salt and water balance, fluid compartment volumes, and arterial pressure were measured before and for 5 days after the induction of hypertension by ABD. 7390610: It was concluded that ABD produces a mild, chronic hypertension in rats without marked pressure lability. 799555: Conversely, bilateral electrolytic lesions or deafferentation of the NTS led to acute hypertension. 9774358: Salt-sensitive hypertension induced by sensory denervation: introduction of a new model. 9931155: We conclude that blockade of the angiotensin type 1 receptor with losartan but not antagonism of the alpha1-adrenoreceptor with prazosin prevents the development of salt-sensitive hypertension induced by sensory denervation. 1297881: [Role of serotonin and its receptors in the pathogenesis of arterial hypertension]. 13964283: [Effect of 5-hydroxytrptamine and nicotine on hypertension induced by 5-hydroxytryptamine, nicotine, tryptamine and acetaldehyde]. 1924500: DOCA treatment alters serotonin metabolism in the central nervous system and it has been proposed that changes in 5-HT metabolism may be important in the genesis of DOCA-induced hypertension. 2285649: Current investigation suggests that serotonin has a pivotal role in the genesis of preeclamptic hypertension. 2414630: Intrinsic release of serotonin from brain was also studied during periods of induced hypertension and hypotension. 2988838: The role of serotonin (5HT) in the pathogenesis of ACTH-induced hypertension in sheep has been examined. 31809283: We found information regarding the role of the brain-gut--bone marrow axis, the brain-gut--kidney axis, the high-salt diet, short-chain fatty acids (SCFAs), neurotransitters, such as serotonin, dopamine and norepinephrine, nitric oxide, endothelin and steroids in modulating gut microbiota and in contributing to the pathogenesis of hypertension. 3419540: A disturbance of GABA-5-HT interactions between GABA and 5-HT in brainstem sites may also contribute to the pathogenesis of hypertension induced by DOCA/NaCl. Central serotonergic alterations in deoxycorticosterone acetate/NaCl (DOCA/NaCl)-induced hypertension. Treatment with DOCA/NaCl produced changes in the metabolism of 5-HT that may be important in the genesis of hypertension, but are not required for the maintenance of elevated arterial pressure. 3532061: [Role of serotonin in the pathogenesis of arterial hypertension]. 3578397: Pharmacologic and methodologic advances over the last decade have resulted in a body of information implicating serotonin as a mediator in the genesis of preeclamptic hypertension. While it is generally accepted that preeclampsia is a disease of the microvasculature characterized by an imbalance between prostacyclin and thromboxane and that the evidence for enhanced responsiveness to some vasopressors is present weeks before clinical disease, the specific cause of the hypertension characterizing the syndrome is unknown. 4612472: [Role of serotonin in the etiology of hypertension of blood vessels of lesser circulation and bronchial spasm (literature review)]. 4755123: [Significance of serotonin and the sympathico-adrenal system in the pathogenesis of the hypertensive disease]. 7902993: Injection of 5-hydroxytryptamine resulted in hypertension, tachycardia and hyperthermia but hypotension, bradycardia and hypothermia were seen with methysergide. 8482325: Feeding a vitamin B6-deficient diet to rats causes a moderate hypertension. The results suggest that decreased synthesis of 5-HT in brain regions and the consequent alterations in 5-HT receptors in the vitamin B6-deficient rats may be the underlying cause of the hypertension seen in these animals. 19668339: The quantitative trait analysis identified 21 genes or chromosomal areas with at least one SNP with a p-value < or =10(-6), which can be considered potential \new\ candidate loci to explore in the etiology of sporadic AD. 20455082: To determine whether there is any single-nucleotide polymorphisms in the BACE1 gene promoter region affecting BACE1 expression in AD pathogenesis, in this study, we screened 2.6 kb of the human BACE1 gene promoter region from late-onset AD patients and found that there was no significant association between single-nucleotide polymorphisms and AD cases. 22167654: Genome-wide association studies (GWAS) identified multiple single-nucleotide polymorphisms (SNPs) that are associated with the pathogenesis of Alzheimer's disease (AD). 26095531: A single nucleotide polymorphism in primary-microRNA-146a reduces the expression of mature microRNA-146a in patients with Alzheimer's disease and is associated with the pathogenesis of Alzheimer's disease. 29993426: Besides, the associated SNPs and brain regions found in this study have also been shown AD-related in previously studies, thus verifying the effectiveness and potential of the proposed method in AD pathogenesis study. 30361487: Functional analyses of these SNPs indicate their potential relevance with AD pathogenesis. 33331110: In addition, apolipoprotein E epsilon4 status promotes them to result in the pathogenesis of AD. AIM: Heredity plays an important role in the pathogenesis of Alzheimer's disease (AD) especially for single-nucleotide polymorphism (SNPs) of susceptible genes, which is one of the significant factors in the pathogenesis of AD. 36140686: Brain imaging genetics examines associations between imaging quantitative traits (QTs) and genetic factors such as single nucleotide polymorphisms (SNPs) to provide important insights into the pathogenesis of Alzheimer's disease (AD). 37065064: A follow-up study to elucidate the impact of our identified m6a-SNPs in the experimental study would validate our findings for AD, which would contribute to the etiology of AD. 37409680: DISCUSSION: The model successfully estimated the contribution of AD-risk SNPs that account for AD progression at the individual level. 10554787: There is clear evidence for obstructive sleep apnea as an independent cause of arterial hypertension. Moderate obstructive sleep apnea appears to be the cause of severe hypertension resistant to pharmacological therapy in this patient. 10580300: INTRODUCTION: The role of obstructive sleep apnea syndrome (OSAS) in the etiology of daytime hypertension is still an issue of debate, which is fed by the high prevalence of the syndrome in hypertensive patients. 10588602: Chronic OSA also leads to sustained decreases in LV systolic performance that could be caused by the development of systemic hypertension and/or transient increases in LV afterload during episodes of airway obstruction. 11725173: CONCLUSIONS: The extraordinarily high prevalence of OSA in these patients supports its potential role in the pathogenesis of drug-resistant hypertension, and justifies the undertaking of a randomized controlled trial to corroborate this hypothesis. 11785071: In its summary, the authors conclude that OSA contributes to the genesis of HTN and advise physicians not to ignore the contribution of frequently comorbid non-OSA factors, such as obesity, to the genesis of OSA-related HTN. The first section describes epidemiologic studies of the relationship of sleep-related breathing disorders, including OSA, to HTN and argues that OSA contributes to the genesis of HTN. The second section describes the known immediate physiologic consequences of 3 components of OSA that may contribute to the genesis of persistent systemic HTN. 12771270: Evidence suggests that untreated obstructive sleep apnea (OSA) can lead to hypertension, cardiovascular disease, and stroke. 15073496: PURPOSE OF REVIEW: High blood pressure and obstructive sleep apnea are closely related, and the latter is considered to induce hypertension. 16009000: CONCLUSION: beta(3)-ADR polymorphism may be involved in the development of central obesity and may be related to OSAHS by the central obesity in male OSAHS subjects of North region Han population of China, and may be induce hypertension in OSAHS patients of the population indirectly through obesity and sleep apnea. 16181037: Sleep apnea-induced hypertension: mechanisms of vascular changes. Hence, defining obstructive sleep apnea-induced hypertension and elucidating its role in cardiovascular disease will facilitate appropriate prevention and intervention. Obstructive sleep apnea-induced hypertension appears to constitute a distinct pathophysiologic entity. Obstructive sleep apnea-induced hypertension appears to be reversible in its early phases, but becomes a permanent condition with irreparable vascular changes in later stages. 16182083: Excessive daytime somnolence is a known consequence of untreated OSA, but adverse cardiovascular consequences, such as hypertension, arrhythmias, and congestive heart failure, are more serious in older patients. 16293956: Patients with obstructive sleep apnea present risk to the general public safety by causing 8-fold increase in vehicle accidents, and they may themselves also suffer from the physiologic consequences of OSA; these include hypertension, coronary artery disease, stroke, congestive heart failure, pulmonary hypertension, and cardiac arrhythmias. 16514349: OSA alone can induce hypertension, especially in younger men. A distinctive feature of OSA-induced hypertension is loss of the normal nighttime fall in blood pressure (\nondippers\). 16537671: BACKGROUND: Obstructive sleep apnoea (OSA) is a common and potentially reversible cause of systemic hypertension. 16797350: Medical history included diabetes with peripheral neuropathy and renal insufficiency, hypertension, and right-sided heart failure felt to be due to obstructive sleep apnea. 17525876: Several randomised controlled trials demonstrated a positive effect of nasal continuous positive airway pressure (CPAP) treatment on arterial blood pressure, leading the \Joint National Council on High Blood Pressure\ to list obstructive sleep apnoea as the first identifiable cause of arterial hypertension. 18001528: OBJECTIVE: To investigate the effects of intermittent hypoxia (IH) on the expression of endothelin-1 (ET-1), nitric oxide (NO), and nitric oxide synthase (NOS) in endothelium, and to evaluate the role of functional disorder of endothelium in the mechanism of obstructive sleep apnea syndrome (OSAS) induced hypertension. 18607146: Acute nocturnal blood pressure elevations associated with disordered breathing events have been reproduced from a number of observational studies, the accrual of which has also made an increasing argument for the importance of OSA in the pathogenesis of diurnal hypertension, as suggested by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which implicated OSA as a secondary cause of hypertension. 18763423: STUDY OBJECTIVES: We wanted to see if the obstructive sleep apnea hypopnea syndrome (OSAHS) causes hypertension and endothelial dysfunction through activation of the angiotensin-converting enzyme (ACE). 19185538: BACKGROUND: Obstructive sleep apnea (OSA) causes systemic hypertension. 19249449: Data from animal and human studies provide a biological plausibility to the notion that obstructive sleep apnea activates pathways that lead to insulin resistance, atherosclerosis and hypertension. 19496385: Truly drug-resistant hypertension is commonly caused by chronic kidney disease, obstructive sleep apnea, or hyperaldosteronism, all of which can lead to fluid retention. 19996187: Intermittent hypoxia, a feature of obstructive sleep apnoea, potentiates ventilatory hypoxic responses, alters heart rate variability and produces hypertension, partially owing to an enhanced carotid body responsiveness to hypoxia. 20019671: BACKGROUND: Obstructive sleep apnea (OSA) is an established cause of hypertension. 20217364: Thus, our results support the idea that the hypertension induced by CIH was preceded by alterations in the autonomic balance of HRV, associated with an enhance chemoreflex ventilatory reactivity in normotensive animals. One potential contributing mechanism to the OSA-induced hypertension is the potentiation of the carotid body chemosensory responses to hypoxia, which is responsible for the augmented sympathetic modulation of heart rate variability (HRV) and the enhanced ventilatory response to hypoxia found in OSA patients and animal exposed to chronic intermittent hypoxia (CIH). 20381666: Obstructive sleep apnea (OSA) is a secondary cause of hypertension and independently associated with target-organ damage in hypertensive patients. 21033131: OBJECTIVE: To explore the potential role of neuropeptide Y (NPY) in the pathophysiological process of hypertension caused by obstructive sleep apnea syndrome (OSAS). CONCLUSION: The increased level of serum NPY may play weakly potential roles in the pathophysiological process of hypertension caused by OSAS. 21359488: Currently, there are data suggesting that OSA is an important secondary cause of SH. 21423678: Drug-induced hypertension, obstructive sleep apnoea, primary aldosteronism, and chronic kidney disease represent the most common secondary causes of resistant hypertension. 21442254: Obstructive sleep apnea (OSA) is not only a cause of hypertension; it also possibly affects the pathogenesis and progression of aortic disease because an inspiratory effort-induced increase in negative intrathoracic pressure generates mechanical stress on the aortic wall. 21603432: Undetected obstructive sleep apnea can lead to hypertension, heart disease, depression, and even death. 21813534: For instance, OSA is a recognized secondary cause of hypertension and may contribute to insulin resistance, diabetes, and dyslipidemia. 21980836: Many studies in the literature show that OSAS due to ATH causes pulmonary hypertension, ventricular hypertrophy and systemic hypertension in the pediatric population. 22025580: PURPOSE: Obstructive sleep apnea (OSA) syndrome generates hypertension, atherosclerosis, and endothelial and autonomic dysfunction, which may mutually interact with ocular vascular regulation. 22424320: The important health-related consequences of obstructive sleep apnea include cardiovascular disorders, such as myocardial infarction and hypertension, stroke, sudden death and difficult blood sugar control related to diabetes mellitus. 22527145: Hypertension induced by obstructive sleep apnea (OSA) may be multifactorial in origin, and systemic inflammation is one of the major factors. 22800893: CONCLUSIONS: OSAS may result in higher BP levels at all four time points. 23154379: Obstructive sleep apnea is a growing public health concern because it can cause hypertension, cardiac arrhythmias, heart attack, stroke, and, in rare circumstances, sudden death if untreated. 23443912: In addition, rate of OSA-induced hypertension in Thai population is limited. Only BMI was significantly associated with OSA-induced hypertension in patients aged over or equal to 60 years. 23592126: Inhibition of NADPH oxidase activity may hopefully serve as a useful strategy for prevention and treatment of obstructive sleep apnea hypopnea syndrome-induced hypertension. 24033947: BACKGROUND: Obstructive sleep apnea is a frequent medical condition consisting of repetitive sleep-related episodes of upper air ways obstruction and can lead to hypertension. 24138362: Obstructive sleep apnoea (OSA) is a potential cause of systemic hypertension in young and middle-aged people, and treatment helps reduce blood pressure in some patients. 24321805: OSA is a common cause of systemic hypertension and should be suspected in hypertensive individuals, especially those with resistant hypertension. 24804613: Obstructive sleep apnea syndrome as a cause of resistant hypertension. 24887112: Obstructive sleep apnoea (OSA) is associated with elevated muscle sympathetic nerve activity (MSNA) during normoxic daytime wakefulness, leading to hypertension. 24952674: AIMS: Sleep disorders like obstructive sleep apnea in adults are associated with increased sympathetic activity, which induced high blood pressure and could be associated with resistant hypertension. 25125635: BACKGROUND: Obstructive sleep apnea (OSA) can result in hypertension and significantly increase cardiovascular morbidity and mortality. 25255048: Obstructive sleep apnoea (OSA) is associated with significantly increased bursts of muscle sympathetic nerve activity (MSNA), leading to hypertension and increased cardiovascular morbidity. 25379440: Muscle sympathetic nerve activity (MSNA) is greatly elevated in patients with obstructive sleep apnoea (OSA) during daytime wakefulness, leading to hypertension, but the underlying mechanisms are poorly understood. 25392136: According to recent guidelines, obstructive sleep apnea (OSA) is an important, although neglected cause of hypertension that is resistant to optimal medical therapy. 25726793: The syndrome of obstructive sleep apnea may be a cause of arterial hypertension. 25953833: Obstructive sleep apnea (OSA) is one of the most common causes of hypertension in western societies. 26096557: OSA with an apnea-hypopnea index (AHI) >=15 events/hour is present in >=30% of patients with primary hypertension and in up to 80% of those with drug resistant hypertension, suggesting that the neural, hormonal, inflammatory and vascular cascades triggered by OSA may elevate blood pressure chronically. 26144938: Prospective studies have established the adverse cardiovascular consequences of OSA, including an increased risk for developing hypertension, coronary artery disease, stroke, and heart failure. 26303488: Models of chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnoea (OSA), have demonstrated dysregulation of the cardiovascular and respiratory systems resulting in hypertension, cardiac hypertrophy and alterations in the hypoxic ventilatory response (HVR) due to changes in sympathetic and respiratory control by the carotid body. 26303489: Exposure to chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, produces autonomic and cardiorespirartory alterations, and leads to systemic hypertension. Exposure to CIH produces hypertension, increased the chemoreflex ventilatory hypoxic responses, and decreased BRS. 26409005: OSA is known to be associated with a proinflammatory state that leads to hypertension, impaired endothelial repair capacity and endothelial dysfunction. 26550503: Here, we report a case of OSA-induced hypertension with intractable hemifacial spasm in which both conditions improved after continuous positive airway pressure treatment. 26711739: Role of the Gut Microbiome in Obstructive Sleep Apnea-Induced Hypertension. These studies demonstrate a causal relationship between gut dysbiosis and hypertension, and suggest that manipulation of the microbiota may be a viable treatment for OSA-induced, and possibly other forms of, hypertension. 26874563: Obstructive sleep apnea syndrome (OSAS) causes resistant hypertension and a hypopnea-related nocturnal blood pressure (BP) surge. 26932221: This brief review focuses on the mechanism of hypertension due to OSAS and the diagnosis criteria and treatment of OSAS. OSAS can lead to hypertension by several possible mechanisms. 27051313: There is growing evidence suggesting that OSA is a secondary cause of hypertension, associated with both poor blood pressure (BP) control and target organ damage in patients with hypertension. 27127598: The Stop-Bang Questionnaire as a Screening Tool for Obstructive Sleep Apnea-Induced Hypertension in Asian Population. 27230560: INTRODUCTION Obstructive sleep apnea (OSA) is considered to be one of the major causes of resistant arterial hypertension (RAH). 27381902: Carotid Body Ablation Abrogates Hypertension and Autonomic Alterations Induced by Intermittent Hypoxia in Rats. CIH induced hypertension, enhanced ventilatory response to hypoxia, induced autonomic imbalance toward sympathetic preponderance, reduced baroreflex gain, and increased arrhythmias and atrial fibrosis. Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to hypoxia and produces autonomic dysfunction, cardiac arrhythmias, and hypertension. Present results show that autonomic alterations induced by CIH are critically dependent on the CB and support a main role for the CB in the CIH-induced hypertension. We tested whether autonomic alterations, arrhythmogenesis, and the progression of hypertension induced by CIH depend on the enhanced CB chemosensory drive, by ablation of the CB chemoreceptors. 27403143: OSA may cause hypertension, at least in part, by stimulating RAAS activity. BACKGROUND: Obstructive sleep apnea (OSA) is the most common cause of resistant hypertension, which has been proposed to result from activation of the renin-angiotensin-aldosterone system (RAAS). 27451595: Obstructive sleep apnea (OSA) has been included by European and American hypertension therapy guidelines as a common cause of high blood pressure. 27652812: RECENT FINDINGS: The cardiovascular consequences of OSA include hypertension, strokes, atrial fibrillation, and heart failure. 28003214: Sustained hypertension is an important consequence of obstructive sleep apnea. 28266781: Obstructive sleep apnea (OSA) is a common cause of high blood pressure (BP). 28345544: BACKGROUND: Obstructive sleep apnea syndrome (OSAS) has been shown to generate hypertension and endothelial dysfunction. 28365886: Evidence is now emerging that gut dysbiosis plays a causal role in the development of OSA-induced hypertension. In this review, we will examine the evidence that gut dysbiosis plays a role in OSA-induced hypertension. While this relationship has been firmly established, a detailed understanding of how OSA leads to hypertension is lacking. Obstructive Sleep Apnea-Induced Hypertension: Role of the Gut Microbiota. 28392811: OBJECTIVES: Obstructive sleep apnea (OSA) can lead to various cardiovascular disorders (CVD) such as hypertension. 29212793: Our results demonstrate that PACAP within the RVLM may contribute to the development of obstructive sleep apnea -induced hypertension. 29539254: If it is left untreated, OSA syndrome can cause hypertension, coronary artery disease congestive heart disease, insulin resistance and death. 30213534: PURPOSE: Hypoxemia and hypertension caused by obstructive sleep apnea (OSA) often result in atherosclerosis of the carotid and coronary vessels and heightened risk of stroke and myocardial infarction (MI). 30354751: Obstructive sleep apnea (OSA) is an independent cause of resistant hypertension (RH) but its association with refractory hypertension (RfH), a recently described form of severe hypertension, has not yet been investigated. 30354816: These studies identify acetate as a key player in OSA-induced hypertension. 30784906: In line with these findings, our results connect high salt diet to the gut-immune axis and highlight the gut microbiome as a potential therapeutic target to counteract the development of OSA-induced hypertension basing on a high salt diet. Here, we investigated the effect of Lactobacillus rhamnosus GG strain (LGG) on the development of hypertension induced by OSA and high salt diet. Lactobacillus rhamnosus GG strain mitigated the development of obstructive sleep apnea-induced hypertension in a high salt diet via regulating TMAO level and CD4+ T cell induced-type I inflammation. 31183617: OSA is now recognized as a cause of hypertension (especially in the case of difficult-to-treat hypertension). 31410341: In 2003, the Seventh Joint National Committee (JNC VII) recognized OSA as a secondary cause of HTN. 31596218: Neuroinflammation is a hallmark of the pathophysiology of OSA-induced SH. CONCLUSIONS: Gut dysbiosis seems to be an important factor in the pathophysiology of OSA-induced hypertension. 31970622: Obstructive sleep apnea (OSA) has been reported to be a cause of hypertension in 40-80% of hypertensive patients. 32546778: As a result, OSA induces a nighttime or morning surge in BP, and long-standing severe OSA also causes daytime hypertension. 32779153: Sprague Dawley rats were exposed to chronic intermittent hypoxia (CIH) for 8 weeks to induce OSAS-hypertension. miR-126a-3p targets HIF-1alpha and alleviates obstructive sleep apnea syndrome with hypertension.The obstructive sleep apnea syndrome (OSAS) is a common sleep-related breathing disorder and an important cause of refractory hypertension. 33231257: STUDY OBJECTIVES: Obstructive sleep apnea can induce hypertension. 33242203: PURPOSE: Intermittent hypoxia (IH), a main characteristic of obstructive sleep apnea (OSA) syndrome, has been known as a dominant cause of OSA-related endothelial dysfunction and hypertension. 33501418: Obstructive sleep apnea (OSA) is one of the most common causes of hypertension (HTN) and cardiovascular disease (CVD). 33560061: BACKGROUND AND OBJECTIVE: Chronic intermittent hypoxia (CIH), one of the main features of obstructive sleep apnea (OSA), enhances carotid body-mediated chemoreflex and induces hypertension and breathing disorders. 33960295: Untreated OSA may cause hypertension and potentially predispose even the pediatric population to develop lacunar infarcts. 33998580: The consequence of obstructive sleep apnoea (OSA) includes road traffic accidents due to drowsiness, systemic hypertension, heart disease, diabetes mellitus and neurocognitive disorders. 34162333: This study thus aimed to determine prevalence of and risk factors for hypertensive crisis in patients with hypertension caused by OSA. Hypertensive crisis in patients with obstructive sleep apnea-induced hypertension. 34184854: These mechanisms lead to sympathetic activation, inflammation, and oxidative stress, which may result in the clinical consequences of OSA such as hypertension, coronary artery disease, heart failure, and cerebrovascular disease. 34297635: Collectively, these findings indicate that KDM6B functions as a coactivator of HIF-1-mediated Nox4 transactivation and demonstrate a hitherto uncharacterized role for KDM's in IH-induced hypertension by HIF-1. Hypoxia-inducible factor (HIF)-1-dependent transcriptional activation of NADPH oxidases (Nox) and the resulting increase in reactive oxygen species (ROS) levels is a major molecular mechanism underlying IH/OSA-induced hypertension. 34580352: Obstructive sleep apnea (OSA) is a common cause of hypertension. 34650797: There were four independent factors associated with OSA-induced hypertension: age, sex, history of snoring, and history of headache. Conclusion: Age, male sex, history of snoring, and headache were independent predictors of hypertension caused by OSA. 35299627: Intervention with probiotics, prebiotics, or postbiotics in animal models simulating OSA-associated HTN restored blood pressure to normal, which allows the hypothesis that GM are involved in the pathophysiology of OSA-induced HTN patients through their metabolites' SCFAs; however, the exact regulatory mechanism is not completely clear. This review describes the potential mechanisms of SCFAs, a major metabolite of the GM, in the pathology of OSA-induced HTN, from the perspective of immune system regulation in the available studies. 35508332: The evidence for other comorbidities, such as hypertension and atrial fibrillation, support these being more a consequence of OSA with limited evidence to support a bidirectional relationship. 35560693: Blockade of Trpm7 in the Carotid Body area attenuated intermittent hypoxia-induced Hypertension. We hypothesize that IH causes hypertension acting on CB TRPM7. CONCLUSION: Our study has shown that inhibition of TRPM7in the carotid bodies abolished IH-induced hypertension. We discovered that obesity-induced hypertension is mediated via the transient receptor potential melastatin 7 (TRPM7) channel in the glomus cells of CB. FTY720 hydrogel abolished IH-induced hypertension by decreasing blood pressure to 106.6+/-1.6 mmHg (p<0.005) on Day 1 of IH and to 101.5+/-1.6 mmHg (p<0.001) on Day 5 of IH. In contrast, control hydrogel had no effect on IH-induced hypertension. Intermittent hypoxia (IH), a hallmark manifestation of OSA, is an established cause of hypertension. 35734065: The relationship between the two especially in patients with hypertension suggests the potential mechanism of OSA-induced hypertension. 35873812: Obstructive sleep apnea (OSA) is a serious breathing disorder, leading to myocardial infarction, high blood pressure, and stroke. 36246876: Both primary aldosteronism and obstructive sleep apnea are well-known causes of hypertension and contribute to increased cardiovascular morbidity and mortality independently. 36794581: This study aimed to determine if chemogenetic activation of hypothalamic OXT neurons in animals with existing obstructive sleep apnea-induced hypertension would reverse or blunt the progression of autonomic and cardiovascular dysfunction. Hypothalamic OXT (Oxytocin) Neuron Activation Attenuates Intermittent Hypoxia-Induced Hypertension and Cardiac Dysfunction in an Animal Model of Sleep Apnea. BACKGROUND: Obstructive sleep apnea is a prevalent and poorly treated cardiovascular disease that leads to hypertension and autonomic imbalance. METHODS: Two groups of rats were exposed to chronic intermittent hypoxia (CIH), a model of obstructive sleep apnea, for 4 weeks to induce hypertension. 37107242: Among the mechanisms potentially involved in OSA-induced hypertension, the role of the gut microbiome is gaining increasing attention. 37182079: OSA results in systemic hypertension, drowsiness, and driving accidents. 37260032: Obstructive Sleep Apnea-Induced Hypertension Is Associated With Increased Gut and Neuroinflammation. 37795212: Interpretation: This MR study showed that OSA is a risk factor for HBP and T2DM, and the evaluation of mediators may help further reveal the specific mechanism by which OSA causes HBP and T2DM. 37899834: By employing bibliometric tools, we analyzed critical and innovative articles in this field to provide an objective summary of the primary research directions, such as the relationship between GM and HTN, GM metabolites, high-salt diet, the developmental origins of health and disease, obstructive sleep apnea-Induced hypertension and antihypertensive peptide. 7549136: These data form direct evidence that daytime hypertension is partially induced by OSAS and is reversible with nasal CPAP treatment. 7558776: Data from recent observational and intervention studies, however, have succeeded in avoiding many of the pitfalls of earlier studies and it is now becoming evident that OSA may be a major cause of hypertension--responsible for about 30% of all cases. 8205310: The present review was prepared following a workshop aimed to critically review available scientific evidence suggesting that hypertension is a direct consequence of OSA. 8872797: In addition many other patients with EH have milder forms of sleep related breathing disorders (SRBD) like snoring, and upper airway resistance syndrome (UARS) which, while not as severe as OSA, may be severe enough to also cause systemic hypertension. 9011563: Obstructive sleep apnea as a cause of systemic hypertension. OSA resulted in acute transient increases in nighttime BP to a maximum of 13.0+/-2.0 mmHg (mean+/-SEM), and eventually produced sustained daytime hypertension to a maximum of 15.7+/-4.3 mmHg. 9363091: New evidence of a role for obstructive sleep apnea as an independent factor in the genesis of hypertension and nocturnal myocardial ischemia has been described. 9406330: It is unarguable that obstructive sleep apnea (OSA) causes pulsatile hypertension during sleep, but whether there is significant carryover of hypertension into waking hours is far from clear. 9443766: There is now strong evidence from animal studies and, in humans, from epidemiological studies as well as from retrospective and prospective intervention studies, that obstructive sleep apnea (OSA) can cause persistent hypertension not only during sleep but during waking hours as well. 10339920: [Hypertension induced by sleep apnea--diagnosis and therapy]. 11230327: Clinical studies suggest that sleep apnea causes systemic hypertension. 11706313: Sympathetic, humoral, and cellular responses to sleep apnea over the long term may cause vascular dysfunction and consequent hypertension. 11924038: The analysis of potential pathomechanisms linking sleep disordered breathing to strokes is another approach to the main topic: snoring and sleep apnea induce hypertension and arrhythmia, the carotid intima-media-thickness is increased, carotid atheromas are more common among apneics than among normals, the flow in the A. cerebri media is as well altered as the reaction to angiotensine II, noradrensine, isoproterenol and bradykinin. 15738350: We reported previously that simulating sleep apnea in rats by exposing them 7 hours per day to intermittent hypoxia/hypercapnia (IH) elevates plasma endothelin-1 and causes hypertension, which is reversed by an endothelin-1 antagonist. Augmented endothelin vasoconstriction in intermittent hypoxia-induced hypertension. We hypothesized that in this model of sleep apnea-induced hypertension, vascular sensitivity to endothelin-1 is increased in combination with the elevated plasma endothelin-1 to cause the endothelin-1-dependent hypertension. 16181037: Sleep apnea-induced hypertension: mechanisms of vascular changes. Hence, defining obstructive sleep apnea-induced hypertension and elucidating its role in cardiovascular disease will facilitate appropriate prevention and intervention. Obstructive sleep apnea-induced hypertension appears to constitute a distinct pathophysiologic entity. Obstructive sleep apnea-induced hypertension appears to be reversible in its early phases, but becomes a permanent condition with irreparable vascular changes in later stages. 16457368: [Coexistence of occupational exposure to lead and sleep apnea syndrome as a cause of hypertension and arrhythmias. A case report]. 16484362: Long-term exposure to intermittent hypoxia (IH), such as that occurring in association with sleep apnea, may result in systemic hypertension; however, the time course changes in arterial pressure, autonomic functions, and baroreflex sensitivity are still unclear. Enhanced sympathetic outflow and decreased baroreflex sensitivity are associated with intermittent hypoxia-induced systemic hypertension in conscious rats. The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats. We investigated the changes in cardiovascular neural regulations during the development of chronic IH-induced hypertension in rats. 17766485: Reactive oxygen species contribute to sleep apnea-induced hypertension in rats. Thus oxidative stress appears to contribute to increases in ET-1 production and elevated arterial pressure in this rat model of sleep apnea-induced hypertension. 1835355: The frequent association of sleep apnea syndrome and essential hypertension led to think of sleep apnea as an etiology of hypertension, especially as a good correlation has been found between the severity of both diseases. 21040717: Our results suggest that endogenous Ang peptides acting in the PVN contribute to IH-induced increases in MAP observed in this rat model of sleep apnea-induced hypertension. We investigated the role of endogenous Ang peptides within the PVN to control blood pressure in a rat model of sleep apnea-induced hypertension. 2105777: CONCLUSIONS: It is unlikely that snoring and sleep hypoxaemia from occult sleep apnoea are important causes of diurnal systemic hypertension when compared with age, obesity, and alcohol consumption. 2148005: Because sleep apnoea syndrome is often associated with arterial hypertension, it has been suggested that sleep apnoea might be responsible for hypertension. 22533344: Non drowsy obstructive sleep apnea as a potential cause of resistant hypertension: a case report. 25820844: Sleep apnoea may also be the underlying cause of high blood pressure, memory loss, poor concentration and work performance, motor vehicle accidents, and marital problems. 26838032: Chronic intermittent hypoxia is used to model the arterial hypoxemia seen in SA, and through this paradigm, the mechanisms that underlie SA-induced hypertension are becoming clear. 37198444: Mineralocorticoid receptor-associated hypertension is a broad concept of hypertension that includes not only PA, but also hypertension caused by borderline aldosteronism, obesity, diabetes, and sleep apnea syndrome. 38406843: The effect of sex on the pathophysiology of sleep apnea and associated intermittent hypoxia-induced hypertension is of important consideration in the screening, diagnosis, and treatment of the disease and its cardiovascular complications. The lack of protection in men and postmenopausal women implicates estrogen and progesterone as protective agents but testosterone as a permissive agent in sleep apnea-induced hypertension. A better understanding of how sex hormones contribute to the pathophysiology of sleep apnea-induced hypertension is important for future research and possible hormone-based interventions. 4014900: In some, sleep apnea syndrome could be the cause of hypertension, and in others it may contribute to hypertension of another cause. 8843530: Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. 9011562: Sleep apnea causes daytime hypertension. 10100688: There is substantial evidence from both observational epidemiology studies and randomized controlled trials that dietary intake of sodium and potassium is important in the etiology of hypertension. 10205243: Abnormal renal sodium transport causing excess reabsorption of sodium may be one mechanism that causes high blood pressure. 10419068: Significance of sympathetic nervous system in sodium-induced nocturnal hypertension. 11179079: We concluded that peripheral administration of losartan as well as embusartan can cause sufficient central effects to prevent the sympathetic hyperactivity and hypertension induced by chronic peripheral ouabain and central sodium. Sympathetic hyperactivity and hypertension caused by chronic treatment with ouabain or sodium-rich artificial cerebrospinal fluid (aCSF) can be prevented by central administration of an angiotensin type 1 (AT(1)) receptor blocker. 11675403: For determining the role of D(3) receptors in salt-dependent hypertension, clearance experiments were performed in anesthetized salt-sensitive (DS) and salt-resistant (DR) Dahl rats that were fed a standard diet with either normal (0.2%) or high (4%) sodium content for 21 to 26 d, which induced hypertension in DS but not in DR rats. 11785068: Mineralocorticoid hypertension refers to hypertension caused by increased sodium and water retention by the kidney, expansion of the extracellular fluid compartment, and direct effects on the vasculature and circumventricular areas of the central nervous system (CNS), which result in elevation of blood pressure. 119504: Their hypertension seems to be due to sodium overload but it is favoured by insufficient inhibition of renin secretion. 12111752: This review focuses its attention on sodium, potassium, calcium, and magnesium ions in order to investigate whether these electrolytes play a role in the pathogenesis of arterial hypertension and its treatment. 14643581: METHODS: Male Sprague-Dawley rats weighing 240 to 250 g were fed a fructose-enriched diet consisting of 21% protein, 5% fat, 60% carbohydrate, 0.49% sodium and 0.49% potassium for 5 weeks, which produced hyperinsulinemia, hypertension, and hypertriglyceridemia. 15250914: Role of sodium and volume in the pathogenesis of hypertension in hemodialysis. 15388984: We studied the effect of high sodium consumption on progression of rat experimental renal failure while sodium-induced hypertension was pharmacologically controlled. 15692166: High iCa(2+) has several vasoconstrictive effects which lead to hypertension, an indirect result of low magnesium status. Hypertension occurs when cellular Na:K ratios become too high, a consequence of a high sodium, low potassium diet or, indirectly, through a magnesium deficient state which causes a pseudo potassium deficit. Several studies on the effect of calcium on blood pressure need these added considerations of magnesium status to fully understand the impact of the Mg:Ca ratio as the primary cause of hypertension and other aspects of Syndrome X. 1582493: Regulation of sodium and body fluid homeostasis during development: implications for the pathogenesis of hypertension. 1584322: Effect of magnesium lithospermate B in rats with sodium-induced hypertension and renal failure. To evaluate the antihypertensive effect of magnesium lithospermate B isolated from Salviae miltiorrhizae radix, determinations of blood pressure and urinary excretions of sodium, potassium, prostaglandin E2 (PGE2) and kallikrein, which have been proposed to play an important role in the regulation of blood pressure, were made in rats with sodium-induced hypertension and renal failure. 17494929: Sodium and potassium in the pathogenesis of hypertension. 1791608: The results of the present study suggest that decreases in sex hormones and increased sensitivity to sodium are important factors in the genesis of postmenopausal hypertension. 18199846: Hypertonic dialysate sodium prescriptions, including sodium modeling, predispose to positive sodium balance and lead to higher blood pressure and increased interdialytic weight gain. 19109373: Mechanisms in the PVN mediating local and central sodium-induced hypertension in Wistar rats. 19262486: An ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein. It is suggested that an ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein. 1963184: These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC. 2198511: Exchangeable sodium may be variably increased in different clinical conditions associated with hypertension, thus increased sodium contents of the body is of major importance in the pathogenesis of hypertension caused by all forms of mineralocorticoid excess, and in the majority of patients with chronic renal insufficiency. 23699927: IMPORTANCE: Excess consumption of sodium is an important cause of hypertension, a major risk factor for heart disease and stroke. 23953998: Through modulation of renin secretion, glomerular filtration rate, and renal absorption of sodium, the sympathetic innervation of the kidneys plays an important role in the pathogenesis of hypertension. 2439744: Some of the critical links between sodium metabolism and vascular smooth muscle (VSM) contraction have been examined in an effort to explain the role of sodium in the etiology of hypertension. 24944029: On the other hand, excessive aldosterone levels, or those too high for sodium status, can cause hypertension and exacerbate the effects of high blood pressure on multiple organs, contributing to renal disease, stroke, visual loss, and congestive heart failure. 25560239: To evaluate the relationship between high BP induced by a high sodium (Na) diet and Mg, and other mineral balances, two experimental rat models of salt-sensitive, induced-hypertension were used: Ang-II infused and Dahl salt-sensitive (SS) rats. Blood pressure, magnesium and other mineral balance in two rat models of salt-sensitive, induced hypertension: effects of a non-peptide angiotensin II receptor type 1 antagonist. 25609366: High sodium causes hypertension: evidence from clinical trials and animal experiments. Recent studies concerning the potential pathways by which high-sodium concentration induces hypertension were reviewed. 25615575: Concordantly, lower ATP1A1 expression is expected to lower Na-reabsorption in the kidney thereby decreasing sodium-associated risk for hypertension and sodium-induced endothelial stiffness and dysfunction. 25693856: Primary renal parenchymal disease can impact on sodium and volume regulation and lead to hypertension, while arterial hypertension can induce renal parenchymal injury and precipitate renal dysfunction. 26050502: Diluted miso supernatant (in a 0.14 M sodium solution) attenuated the increased CSF sodium-induced hypertension, although pre-treatment with normal-sodium (0.14 M) saline failed to change the hypertension. We also pre-treated CPO-mice with an intracerebroventricular infusion of miso supernatant to evaluate its effect on increased cerebrospinal fluid (CSF) sodium-induced hypertension. 2658289: Nutritional deficiencies (e.g., carnitine in dogs, taurine in cats) resulting in cardiomyopathy, and nutritional excesses (e.g., calories leading to obesity, sodium leading to hypertension) have emerged as important considerations in cardiology. 2677140: Mean arterial pressure (MAP), plasma renin activity (PRA), plasma aldosterone concentration (ALDO), para-aminohippurate (PAH) clearance, glomerular filtration rate (GFR), urine volume, and sodium and potassium excretion were measured before and weekly after induction of the hypertension. 2693847: The roles of sodium, potassium and magnesium in the etiology of high blood pressure are reviewed. 2738946: The data also lend support to the contention that abnormal sodium metabolism at the cellular level may play a role in the biochemical pathway leading to hypertension. 27906749: Sodium and potassium in the pathogenesis of hypertension: focus on the brain. RECENT FINDINGS: Animal studies point to a small increase in plasma and cerebrospinal fluid (CSF) [Na], a small decrease in CSF [K], and increased levels of circulating angiotensin II, aldosterone, and endogenous ouabain as the central signals evoking hypertension. 29069584: Dendritic Cell Amiloride-Sensitive Channels Mediate Sodium-Induced Inflammation and Hypertension. 2921078: The role of sodium retention and consequent changes in cerebrospinal fluid sodium concentration in the genesis of hypertension in Dahl rats was evaluated. 2994826: These findings suggest that sodium can cause hypertension by direct stimulation of the central sympathetic nervous system without participation of peripheral mechanisms such as fluid volume expansion or alteration of the vascular wall. 3018593: In the present study, alpha-adrenoceptors and noradrenaline contents have been studied in the cerebral cortex, hypothalamus and medulla oblongata in the Sabra rat strain in order to define their role in the resistance or sensitivity to sodium-induced hypertension. 30350402: Appropriate sodium regulation is crucial for blood pressure (BP) control and disturbances in sodium balance can lead to hypo- or hypertension. 30446179: Alterations in metabolic pathways associated with the sensitivity of sodium, potassium, magnesium and calcium may lead to obesity, hypertension, and insulin resistance. 3122099: The effects of dietary sodium and moderate exercise on sodium-induced hypertension. 343905: On the assumption that the increased peripheral resistance responsible for hypertension results from an imbalance or a disturbance of the equilibrium between the sympathetic nervous system and norepinephrine on one hand, and the vascular tone, sensitivity and responsiveness of the arterial smooth muscle to norepinephrine and to angiotensin II on the other hand, three models that fit the experimental and clinical facts as known at present are described. Role of the adrenal cortex and sodium in the pathogenesis of human hypertension. 3453083: The accumulation of sodium in the extracellular bound fraction and its saturation of the tissue pools may be involved in the development of the exaggerated natriuretic response to acute sodium loading produced in SHR. 3537234: Sodium and calcium appear to be the electrolytes most closely implicated in the pathogenesis of hypertension but potassium, magnesium and chloride should not be neglected. 3584961: Abnormal sodium (Na+) and water handling by the kidney may be the cause of hypertension in rats of the Milan hypertensive strain (MHS). 3614018: Increased cell membrane permeability to sodium is proposed as the initial event leading to high blood pressure in susceptible subjects when sodium intake is increased. 3891618: The role of sodium and sodium chloride in pathogenesis of hypertension is reassessed in the light of new data from epidemiological clinical research, experimental models, and cell physiology investigations. 3916698: Such changes may alter the characteristics of (1) the renal perfusion pressure/sodium excretion curve (2) autoregulation and (3) sodium metabolism, all of which have been implicated in the pathogenesis of hypertension. 4087696: The latter seems to complement renin-angiotensin, sodium and fluid volume in the pathogenesis of high BP. 4790000: [Significance of sodium and potassium metabolism for genesis of hypertension in kidney failure]. 495153: Hemodynamic changes during the development of sodium-induced hypertension in subtotally nephrectomized rats. Hemodynamic changes during the development of sodium-induced hypertension were investigated in male Sprague-Dawley rats after about 70% of the renal mass was removed. 514119: Does exposure to elevated levels of lead enhance sodium induced hypertension? 6204132: These observations do not support the concept that body sodium and fluid volume expansion represent the initial event leading to high blood pressure in patients with essential hypertension. 6204133: Thus, the hemodynamic pattern of sodium-induced hypertension seems somehow related to the distribution of extracellular fluid over the intra- and extravascular compartments. 6204134: However, experiments have shown that it is not the accumulation of sodium per se in the body that causes hypertension. 6204158: Further, altered membrane transport of sodium may reflect factors that affect cell composition (such as age) rather than participate directly in the pathogenesis of hypertension. 6266727: It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. 6627751: Alterations observed in cell sodium concentration provide support for the hypothesis that increased dietary intake of sodium may induce hypertension by causing changes in cellular transport systems. 6872034: [The age factor in experimental sodium-induced hypertension]. 7000828: To examine the hypothesis that the renal sympathetic nerves contribute to the development and maintenance of hypertension by causing urinary sodium retention, 7-wk-old (early hypertensive) and 18-wk-old (established hypertensive) male spontaneously hypertensive rats were subjected to bilateral renal denervation and compared with sham-operated controls. 7018807: Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 7875762: These data indicate that blockade of brain \oubain\ prevents sodium-induced hypertension as well as the desensitization of the arterial baroreflex in Dahl S rats. 7924009: Studies of the cellular and subcellular handling of sodium are still in their infancy and will add much to our understanding of the physiology of volume homeostasis in normal pregnancy and its disturbance in pre-eclampsia and other causes of hypertension in pregnancy. 8401417: Since 20 years new trends seem to relate the role of sodium in the genesis of hypertension to a primary abnormality of electrolyte transport of cell membrane. 8509998: It was found that chronic treatment with i.v. losartan (3 mg/kg/day) completely prevented sodium-induced hypertension in the RRM rats, whereas neither increased salt intake nor losartan treatment affected blood pressure in the intact rats. 8743490: Substantial evidence implicates impaired renal excretion of sodium as the major culprit in the pathogenesis of hypertension. 8794827: It is unclear how sodium retention leads to a rise in blood pressure, but ouabainlike compound may act as a final common pathway in sodium-induced hypertension. 891217: However, we found that increasing the sodium stores of the body while holding volume constant does not produce hypertension, expanding fluid volume while maintaining or actually decreasing sodium concentration does lead to hypertension. 9170003: The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension. 9269532: Studies performed in our laboratory have demonstrated that chronic intravenous administration of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) selectively decreases renal medullary blood flow, causes sodium and water retention and leads to hypertension. 9443776: Ovariectomy aggravated sodium induced hypertension associated with altered platelet intracellular Ca2+ in Dahl rats. Our purpose was to determine the effect of ovariectomy on intracellular Ca2+ mobilization and platelet aggregation in sodium induced hypertension. We concluded that ovariectomy enhanced sodium induced hypertension associated with the decreased internal Ca2+ discharge capacity and increased platelet aggregation in Dahl-Iwai salt-sensitive rats. 9797195: This lower than normal expression of neuronal constitutive nitric oxide synthase gene in the hypothalamus could be an adaptive response to sodium-induced hypertension, and suggests that nitric oxide produced by hypothalamic constitutive nitric oxide synthase plays a role in maintenance of blood pressure in relation to sodium balance in rats. OBJECTIVE: To elucidate the role of brain nitric oxide produced by neuronal constitutive nitric oxide synthase in sodium-induced hypertension. 9887018: To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. 1000984: Thus, while in salt-induced hypertension no hyperlipidaemia and hyperlipoproteinaemia were established, in renal hypertension the serum lipid and lipoprotein levels were significantly increased in comparison to the controls. The remaining lipid fractions were within normal ranges or a little decreased in salt-induced hypertension, while in renal and adrenal-regeneration hypertension their quantity was significantly increased. 10070137: Inhibition of cytochrome P-450 (CYP450) enzymes with cobalt chloride (CoCl2) prevented hypertension, organ hypertrophy, and renal injury induced by DOCA and salt (1% NaCl) in uninephrectomized (UNx) rats. 10226871: Dietary NaCl-induced hypertension in uninephrectomized Wistar-Kyoto rats: role of kidney function. This study tests the hypothesis that combination of unilateral nephrectomy and a high sodium chloride (NaCl) diet causes hypertension in otherwise normotensive Wistar-Kyoto (WKY) rats and that this hypertensive response is due to a deficit in the remaining kidney's function. These data suggest that the combination of unilateral nephrectomy and dietary NaCl excess causes hypertension in the normotensive WKY rats, but the hypertensive response is not likely due to a functional deficit in the remaining kidney. 10323488: Nifedipine effectively lowers salt-induced high blood pressure in diabetic rats. 10444500: To determine the role of inducible NOS (NOS II) in salt-induced hypertension, we treated Dahl salt-resistant (DR) rats with the selective NOS II inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) for 12 days. Although recent evidence suggests that reduced nitric oxide (NO) production may be involved in salt-induced hypertension, the specific NO synthase (NOS) responsible for the conveyance of salt sensitivity remains unknown. Salt-induced hypertension in Dahl salt-resistant and salt-sensitive rats with NOS II inhibition. We, therefore, conclude from these data that NOS II is important in salt-induced hypertension. 10458644: We also examined the relationship between NPY gene expression and renin in two rat models of hypertension (two-kidney, one-clip renal hypertension (2K1C), and deoxycorticosterone-salt-induced hypertension (DOCA-salt)) characterized by a similar blood pressure elevation. 10489400: The Dahl salt-sensitive (DS) rat, a genetic model of salt-induced hypertension in humans, is more likely to develop severe vascular injuries than a rat with spontaneous hypertension. 10501091: OBJECTIVE: To determine if oxygen free radicals derived from xanthine oxidase are involved in the development of salt-induced hypertension. CONCLUSIONS: These findings indicate that xanthine oxidase-derived oxygen free radicals are involved in the pathogenesis of salt-induced hypertension. 10535697: High D2O concentrations can reduce salt- and ethanol-induced hypertension in rats and protect mice from gamma irradation. 10564212: Body fluid expansion is not essential for salt-induced hypertension in SS/Jr rats. 10622277: We have previously reported that renal xanthine oxidoreductase (XOR) activity is increased in hypertension-prone rats, and even more markedly in salt-induced experimental hypertension. 10629425: Increased (Na+K+Cl) cotransport in rat arterial smooth muscle in deoxycorticosterone (DOCA)/salt-induced hypertension. 10642341: Contribution of Ras GTPase/MAP kinase and cytochrome P450 metabolites to deoxycorticosterone-salt-induced hypertension. 1071621: Renal prostaglandin synthesis in hypertension induced by deoxycorticosterone and sodium chloride in the rat. The role of renal medullary prostaglandin E has been examined in rats with hypertension induced by sodium chloride and deoxycorticosterone (salt-DOC). 10826407: The aims of this study were to develop a rat model of combined NaCl-induced hypertension and NIDD, and to determine the contribution of the sympathetic nervous system to the development of the manifest hypertension. 10860767: AST causes hypertension, left ventricle (LV) hypertrophy and decreases plasma corticosterone level. 10912751: The results indicated that salt-induced hypertension was associated with marked alterations in the endothelial and vascular smooth muscle functions of the carotid arteries of Dahl rats. 10919359: Our findings indicate that SA7060 efficiently prevents DOCA-salt-induced hypertension and related tissue injury, mainly by inhibiting NEP. Daily administration of SA7060, candoxatril or enalapril significantly suppressed the development of hypertension induced by DOCA and salt, although the effect of enalapril was less potent at 4-weeks of the treatment period. Effects of SA7060, a novel dual inhibitor of neutral endopeptidase and angiotensin-converting enzyme, on deoxycorticosterone acetate-salt-induced hypertension in rats. 10950402: We conclude that the development of spontaneous and salt-induced hypertension is not associated with decreased activity of 11betaHSD. The role of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) in hypertension remains unknown even if it appears that the inappropriately decreased 11betaHSD activity might be involved in a process that leads to high blood pressure. The possible changes of 11betaHSD were therefore investigated in rats with spontaneous or salt-induced hypertension. 10995524: The associated dysfunction in water and salt handling often induces hypertension. 1107451: Salt-induced hypertension in rats with hereditary hydronephrosis: the effect of renomedullary transplantation. 11187987: The authors investigate the ovemse of salt by pregnant women in two aspects--as a detrimental nutritive habit and as a factor in the pathogenesis of hypertensive disorders during pregnancy. 11243413: This effect may contribute to the development of salt-induced hypertension in Dahl S rats. 11244027: In the present study, we tested the hypothesis that chronic peripheral administration of an AT(1) receptor blocker inhibits the salt-induced hypertension relative to the extent of central AT(1) receptor blockade that is induced. 11258674: It was found that ingestion of a low sodium diet or infusion of NaCl in doses slightly above 0.15 M caused hypertension and sodium accumulation in erythrocytes and the cerebrospinal fluid of kininogen-deficient BN-Ka rats. 11304511: This study investigated the effect of omapatrilat in comparison to the ACE inhibitor captopril on systolic blood pressure and endothelial function in salt-induced hypertension. Vasopeptidase inhibition exhibits endothelial protection in salt-induced hypertension. 11339690: To evaluate gender differences in salt-induced hypertension, female and male Dahl salt-sensitive rats were fed high (8.0% NaCl, HS) and low (0.3% NaCl, LS) salt diets. Thus, salt-induced hypertension is associated with a reduction in levels of nitric oxide regardless of gender. 11390023: To assess the role of Ang-(1-7) in salt-induced hypertension, Ang-(1-7) (24 microg/kg/hr) or saline was administered chronically via osmotic minipump into the jugular vein of 5-6 wk-old male (M) and female (F) Dahl salt-sensitive rats placed on a high-salt (8% NaCl) diet for 2 weeks. 11390717: In salt-induced hypertension, functional ECE activity (calculated as the ratio of the contraction to big ET-1 divided by the contraction to ET-1) in renal arteries (0.46+/-0.05) and in aorta (0.68+/-0.05) was reduced as compared with control animals (0.9+/-0.05 and 0.99+/-0.04, respectively; P<0.05). CONCLUSIONS: In salt-induced hypertension, vasopeptidase inhibition restores alterations in the endothelin system, such as renovascular ECE activity and responsiveness to ET-1 and big ET-1 with chronic but not acute in vitro application. The present study investigated the effect of the vasopeptidase inhibitor omapatrilat on endothelin-1 (ET-1)-mediated vascular function in salt-induced hypertension. Chronic vasopeptidase inhibition restores endothelin-converting enzyme activity and normalizes endothelin levels in salt-induced hypertension. 11398281: Salt-induced hypertension in rats alters the response of isolated aortic rings to cromakalim. 11476758: We investigated the potential of natural occurring antioxidant alpha-lipoic acid to prevent hypertension and hypertensive tissue injury induced by deoxycorticosterone acetate (DOCA) and salt in rats. 11675404: Vasopeptidase inhibition restores renovascular endothelial dysfunction in salt-induced hypertension. The effect of the vasopeptidase inhibitor omapatrilat (O) and the ACE-inhibitor captopril (C) on endothelial function in the renal circulation in salt-induced hypertension were investigated. In salt-induced hypertension, endothelium-dependent relaxations in renal arteries (56 +/- 6 versus 100 +/- 6%; P < 0.05) as well as contractions to endothelin-1 (ET-1) (98 +/- 5% versus 128 +/- 5%; P < 0.05) and big ET-1 (47 +/- 6% versus 116 +/- 7%; P < 0.05) were markedly reduced as compared with control animals, whereas standardized aortic weight and heart weight (4.9 +/- 0.4 versus 3.2 +/- 0.3 g/kg; P < 0.05) increased. In conclusion, O restored renovascular endothelial function and prevented vascular hypertrophy in salt-induced hypertension and therefore may advance as a beneficial approach in the therapy of various forms of hypertension. 11714878: Conversely, the presence of this receptor in SBN rats and its up-regulation could be protective change against the increase of alpha(2)B-adrenoceptors induced by the salt overload and could consequently be responsible for the resistance to salt-induced hypertension. 11725152: The animal experiments have led us to conclude that the sympathetic outflow is regulated by activation of the presynaptic alpha2A-AR subtype, which is the predominant alpha2-AR subtype in the central nervous system and exerts a sympathoinhibitory (hypotensive) action; on the contrary, activation of the central alpha2B-AR elicits a sympathoexcitatory response (such as seen in salt-induced hypertension, which requires functionally intact alpha2B-AR). 11752095: This study investigated the importance of the male sex hormone testosterone on salt-induced hypertension, renal alpha(2)-adrenoceptor subtype distribution, and gene expression in salt-sensitive (SBH) male Sabra rats. In conclusion, testosterone is needed for the full expression of salt-induced hypertension in male salt-sensitive Sabra rats. In gonadectomized rats, testosterone replacement restores salt-induced hypertension, density of renal alpha(2B)-adrenoceptors, and gene expression to the intact levels observed both under normal and high salt diet. 11814618: In the present study, we have examined the acute effect of Ang-(1-7) in salt-induced hypertension using Dahl salt-sensitive rats placed on low (0.3%) or high (8.0% NaCl) salt diets for 2 weeks. 11858800: In conclusion, these results demonstrate that in rats with hypertension induced by DOCA-salt, brain mineralocorticoid receptor blockade affects renal function and blood pressure regulation. In the present study, the coordinate cardiovascular and renal effects of brain mineralocorticoid receptor blockade were examined by intracerebroventricular (i.c.v.) administration of a selective mineralocorticoid receptor antagonist (RU28318; 3,3-oxo-7 propyl-17-hydroxy-androstan-4-en-17yl-propionic acid lactone) in rats with hypertension induced by deoxycorticosterone acetate (DOCA) and salt. 1185940: [Significance of excessive consumption of salt in the etiology of arterial hypertension]. 11875309: OBJECTIVE: To investigate whether chronic selective beta1-blockade with nebivolol could prevent endothelial dysfunction in salt-induced hypertension, and to compare it with atenolol. Nitric-oxide-mediated relaxations in salt-induced hypertension: effect of chronic beta1 -selective receptor blockade. 11878010: The results of this study show that meals given by mass catering institutions can increase risk of hypertension, strokes and gastric cancers because of high sodium chloride content. 11884268: This review discusses the view that the renal genotype is not the only determinant of salt-induced sympathetic hyperactivity and hypertension, and that changes in genetic control of neuronal responses to cerebrospinal fluid Na(+) may play a primary role. Neural mechanisms play an essential role in salt-induced hypertension, and recent studies indicate that centrally induced sympathetic hyperactivity actually causes the hypertension. 11907647: It thus appears that mild, chronic overproduction of ET-1 does not primarily cause hypertension but triggers damaging changes in the kidney which lead to the susceptibility to salt-induced hypertension. 1192615: Animal studies show that the amount of excess body water and salt required to cause hypertension is exceedingly small, and that the hypertensive effect of the excess water and salt may not develop for days or weeks. When vascular constriciton occurs simultaneously, as occurs in the presence of large quantities of angiotensin, the blood volume may be less than normal, but even in these circumstances the fluid volume is relatively increased and is responsible for the hypertension because the vascular constrictont has decreased the capacity of the circulation to a greater extent than the decrease in blood volume. 11961577: Therefore, it is concluded that inducible NOS is an important modulator of blood pressure in case of NaCl-induced hypertension. 12045297: To determine the effect of salt loading, animals were provided with 8% NaCl in chow, causing hypertension in SBH/y but not in SBN/y. 12105146: In an attempt to elucidate whether there is a specific alpha1-adrenergic receptor (alpha1-AR) subtype involved in the genesis or maintenance of hypertension, the alpha1D-AR subtype was evaluated in a model of salt-induced hypertension. Role of the alpha1D-adrenergic receptor in the development of salt-induced hypertension. 1218518: The authors examined the changes in arterial blood pressure and the content of Noradrenaline in the myocardium, brain and aorta of rats with hypertension due to nephrectomy and treatment with desoxycorticosterone and NaCl, and after a chronic 6-month treatment of hypertension with various antihypertensive means. 1225988: The effects of various doses of 6-hydroxydopamine (6-OHDA) injected into the hypothalamus on DOCA-salt-induced hypertension were studied. 12382034: We examined the time course of gene expression and the activity of PDE3 and PDE4 in an animal model of salt-induced hypertension, left ventricular hypertrophy, and congestive heart failure (CHF). 12384457: Thus aldosterone and salt treatment in uninephrectomized rats led to severe hypertension and the development of a vascular inflammatory phenotype in the heart, which may represent one mechanism by which aldosterone contributes to myocardial disease. Aldosterone induced severe hypertension at 4 wk [systolic blood pressure (SBP), 210 +/- 3 mmHg vs. vehicle, 131 +/- 2 mmHg, P < 0.001], which was partially attenuated by eplerenone (SBP, 180 +/- 7 mmHg; P < 0.001 vs. aldosterone alone and vehicle). 12409964: Increased sensitivity of the obese Zucker rat to deoxycorticosterone-salt-induced hypertension. 12511545: These results suggest that elevated levels of endogenous CO contribute to arteriolar NO dysfunction in DS rats with salt-induced hypertension. 12564647: Vitamin C lowers blood pressure and alters vascular responsiveness in salt-induced hypertension. The present study was undertaken to investigate the effect of vitamin C treatment on blood pressure and vascular reactivity in salt-induced hypertension. 12675855: RESULTS: Aldosterone/salt induced severe hypertension compared to controls (220 +/- 4 mm Hg vs. 131 +/- 4 mm Hg, P < 0.05), which was partially attenuated by eplerenone (179 +/- 4 mm Hg, P < 0.05). 12714871: OBJECTIVE: Previous studies have shown that a fully functional alpha(2B)-adrenergic receptor (AR) is necessary for the development of salt-induced hypertension. 12782645: Endothelin A (ETA) receptor blockade has prevented vascular remodeling in aldosterone and salt-induced hypertension. 12842816: Because the brain renin-angiotensin system only contributes to salt-induced hypertension in Dahl S rats, further studies are needed to determine which of the salt-induced increases in brain AT1 receptor densities contribute to the hypertension and which to other aspects of body homeostasis. 12854358: It is concluded that benidipine may be useful for improving the development of salt-induced hypertension and its accompanying haemodynamic responses. 12924625: We examined the effect of the dihydropyridine calcium channel blocker (CCB) benidipine, the angiotensin II type 1 receptor blocker (ARB) candesartan, and the combination of these drugs on blood pressure and kidney and vascular function in rats with salt-induced hypertension. 1338308: Although most workers in the field agree that salt causes hypertension, but there is no well-established mechanism(s) explaining how salt works. 1345215: There is considerable evidence that salt is an important cause of hypertension. Salt-induced hypertension has been produced in both man and experimental animals. 13473553: [Significance of sodium chloride in the etiology of edema and hypertension]. 13513919: Hypertension induced by renal artery constriction also intensified the hypercholesterolemia and hyperlipemia. The induction of hypertension by desoxycorticosterone and salt accelerated the development of hypercholesterolemia, hyperlipemia, increase in tissue cholesterol content, and atherosclerotic changes in the intima. 13547894: [Relation of essential hypertension to sodium chloride. II. Clinical & experimental animal experiments on the dependence of high blood pressure caused by sodium chloride or its separated sodium & chloride ions in essential hypertension & in salt water hypertension in rats]. 13550917: Hypertensive vascular disease produced by salt. 13719314: The hypertension produced by sea salt was more pronounced than that caused by sodium chloride alone, although the average amount of sodium chloride contained in the sea salt feeding was slightly less. 1387228: The objective of this study was to determine the effect of treatment with graded levels of dietary NaCl on the induction of hypertension during chronic exposure to cold. 1387762: Conversely, the ability of calcium channel blockade to reverse salt-induced hypertension is related to its ability to prevent these transmembrane ionic effects. 1418847: Since the SBP of DSR and Fischer 344 rats are not influenced to any great extent by high salt intake, even after prolonged exposure, the SBP rise associated with the high sugar/low protein diet may be via a mechanism different from salt-induced hypertension. 1423012: Since rats of the Long-Evans (LE) strain are known to be resistant to the induction of deoxycorticosterone salt induced hypertension, their cardiovascular responses to chronic exposure to cold were compared with those of rats of the Sprague-Dawley (SD) strain. 1423019: Surprisingly, the renal nerves do not contribute to dietary NaCl exacerbated hypertension in the spontaneously hypertensive rat, dietary NaCl-induced hypertension in the Dahl NaCl-sensitive rat, or the chronic hypertensive and nephrotoxic effects of cyclosporine A therapy in the rat, despite the finding that in all three forms of hypertension, overactivity of the sympathetic nervous system is prominent. 14269643: HYPERTENSION DUE TO COMMON SALT. 1452951: The test has three phases: unrestricted salt, to document hypertension and customary salt intake; restricted salt (2 g/day), to identify the salt-sensitive patient; and stepwise increased salt (each step = 1 g/day), to find the level that precipitates hypertension. 14567044: The role of salt in the genesis of hypertension has been well documented. 14597594: Differential effects of selective cyclooxygenase-2 inhibitors on endothelial function in salt-induced hypertension. 14600213: These data demonstrate a significant influence of diet composition on salt-induced hypertension and renal disease in the Dahl SS/Mcw rat. 14654751: CONCLUSION: 'Optimal' dietary KCl (2.6%) prevents hypertension and preserves cerebral and renal hemodynamics in DSS rats fed a diet containing 1% NaCl for 8 months, which causes hypertension when dietary KCl is limited or excessive. 14654758: Resistance to salt-induced hypertension in catechol-O-methyltransferase-gene-disrupted mice. OBJECTIVE: To test the hypothesis that COMT blockade protects from salt-induced hypertension. CONCLUSION: Our findings suggest that COMT deficiency in mice increases the availability of L-DOPA, leading to enhanced dopaminergic tone, which may be associated with resistance to salt-induced hypertension. 14674712: Salt-induced hypertension in WKY rats: prevention by alpha-lipoic acid supplementation. 14700508: This study tests the hypothesis that cardiac HO-1 expression is increased in DS rats with salt-induced hypertension and provides cardioprotection by promoting coronary vasodilation. CONCLUSIONS: These findings suggest that coronary HO-1 expression is increased to promote enhanced coronary vasodilation in DS rats with salt-induced hypertension. 14703303: Effects of vitamin C on high blood pressure induced by salt in spontaneously hypertensive rats. 1477292: Treatment with deoxycorticosterone acetate (DOCA) and salt for 12 weeks consistently induced hypertension in rats. 14913745: [Hypertension in rabbits, caused by salt and its relation to the adrenals]. 15032461: Alcohol, tobacco, Obesity, use of non-steroidal anti-inflammatory drugs and excessive use of salt were not found as key factors responsible for resistant hypertension in this study. 1507547: Reassessment of noradrenergic function in salt-induced hypertension in Dahl rats. 15130889: Thus, in both Dahl S and SHR on H-Na, increases in CSF [Na+] preceded the increases in BP and HR, consistent with a primary role of increased CSF [Na+] in the salt-induced hypertension. 151509: These data indicate that genetic differences influence the pathogenesis of cadmium-induced hypertension. Dahl hypertension-resistant (R) and hypertension-sensitive (S) rats were used to determine whether cadmium-induced hypertension is dependent on genetic predisposition. Genetic influence on cadmium-induced hypertension. Also, the development of salt-induced hypertension was accelerated in cadmium-fed (1 and 2.5 mg/liter) S rats. 15191416: The hypertension is mediated by enhanced volume expansion due to enhanced salt and water retention by the kidney. 15458970: The intracerebroventricular, but not subcutaneous, infusion of 0.3 microg/h trilostane effectively blocked the increase in systolic blood pressure and reversed the hypertension produced by drinking 0.9% saline. Salt-induced hypertension in the Dahl inbred salt-sensitive (SS/jr) rat is associated with normal to low levels of circulating aldosterone, yet it is abrogated by the central infusion of mineralocorticoid receptor antagonists. These studies suggest that the synthesis in the brain of a mineralocorticoid receptor agonist, probably aldosterone, is responsible in part for the salt-induced hypertension of the inbred Dahl SS/jr rat. To test the hypothesis that de novo synthesis of aldosterone in the brain has a pathophysiological role in the salt-induced hypertension of the SS rat, the 3beta-steroid dehydrogenase antagonist trilostane was infused continuously intracerebroventricularly or subcutaneously in two different cohorts of Dahl SS/jr rats, one female, the other male, during and after the development of salt-induced hypertension. 1548054: Unaltered arteriolar responsiveness to sodium nitroprusside in hypertensive DS rats also suggests that salt-induced hypertension is not accompanied by a change in the responsiveness of arteriolar smooth muscle to nitric oxide. These results indicate that basal release of nitric oxide, presumably from the endothelium, normally influences arteriolar tone in skeletal muscle of DS rats and that this influence is suppressed in established salt-induced hypertension. 15528397: Furthermore, administration of an HO inhibitor lowered blood pressure in Dahl-S rats with salt-induced hypertension but did not do so in low-salt control rats. 15591155: Dahl salt-sensitive (Dahl-S) rats with salt-induced hypertension show endothelial dysfunction, including decreased vascular nitric oxide formation. Arginase inhibition restores arteriolar endothelial function in Dahl rats with salt-induced hypertension. These results suggest that enhanced vascular arginase activity contributes to endothelial dysfunction in Dahl-S rats with salt-induced hypertension and identifies arginase as a potential therapeutic target to prevent endothelial dysfunction. 15699443: Renal medullary prostanoids mediate vascular tone, salt and water balance, and renin release and, as a result, are involved in the maintenance of renal blood flow and the pathogenesis of hypertension. 1571527: Publicity surrounding the salt and hypertension debate evoked fear in workers at a Salt Mine that their working conditions may lead to high blood pressure. 15715924: The processes of induction of hypertension, possible pathogenesis, characteristics, advantages, and limitations of these animal models are reviewed. Hypertension and related cardiovascular diseases are the leading causes of death in many countries. These models are classified as genetically-induced, environmentally-induced, pharmacologically-induced, and renal-induced hypertension according to the way of induction; the typical representatives of each of these major types of experimental hypertension are spontaneous hypertension, cold-induced hypertension, DOCA-salt-induced hypertension, and renal-induced hypertension, respectively. 15808808: Evidence is now compelling that inappropriate aldosterone for salt status can cause not only hypertension, but vascular inflammation and end-organ damage, preventable by mineralocorticoid receptor blockade. Primary aldosteronism was considered rare, but recent work beginning in 1992 suggests that it might be the most common curable cause of hypertension, worth screening for in every hypertensive. 15831365: CONCLUSIONS: High-salt diet in DS rats increased renal APA activity, although renal injury remained mild, but then reduced it along with the progression of glomerulosclerosis, suggesting that reduced APA activity may be involved in the deterioration of salt-induced hypertension and renal injury. 15834283: This indicates that, in this model, salt-induced hypertension is not mediated by endothelial dysfunction. 15837830: Contributions of sodium and chloride to NaCl-induced hypertension. 15838988: Vitamin D metabolism in the Dahl salt-sensitive (S) rat, a model of salt-induced hypertension, differs from that in the Dahl salt-resistant (R) rat. 15860534: During saline infusion, hypoxaemia induced hypertension, bradycardia, femoral vasoconstriction, hyperglycaemia and an increase in haemoglobin, catecholamines and neuropeptide Y (NPY). 1590468: Renal nerves contribute to salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits. The objective of this study was to investigate the role of the renal nerves in the pathogenesis of salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits. 15921072: Alterations in aldosterone and angiotensin II levels in salt-induced hypertension. 15965362: The data supports the view that Cl handling and Ca-dependent Cl channels seem to undergo modification as a consequence of salt-induced hypertension. 1599633: However, increases in the availability and consumption of dietary salt have raised concerns that excessive intakes may cause hypertension. Among the topics we examine are the effects of salt on fluid and electrolyte homoeostasis; potential mechanisms of salt-induced hypertension; the epidemiology of salt intake and blood pressure; the effects of salt restriction and supplementation on blood pressure regulation; the potential roles of sodium and chloride ions, as well as interactions with dietary potassium, calcium, and magnesium; current theories of salt sensitivity; the clinical risks of dietary salt depletion; and the dietary sources of salt. 1600637: In a second study, neonatal castration of males slowed the onset of salt-induced hypertension, and females that were treated neonatally with testosterone developed somewhat higher pressures that did untreated females. 16280288: Simvastatin and losartan enhance nitric oxide and reduce oxidative stress in salt-induced hypertension. 16361843: It has been known for decades that salt (NaCl) determines extracellular volume as well as blood pressure and is one cause of hypertension. 16546838: The renin-angiotensin-aldosterone system (RAAS) has been implicated in the pathophysiology of salt-induced hypertension. The purpose of this study was to examine the effects of enalapril, an angiotensin II converting enzyme inhibitor; eplerenone, a selective aldosterone receptor antagonist; and tempol, a superoxide dismutase mimetic, on salt-induced hypertension in Dahl Salt-Sensitive rats. 16584850: Based on epidemiologic studies, minimal effective dose of salt, producing hypertension is estimated as 1.76 g/d. 1665759: Altered responses of aortic smooth muscle from Sprague-Dawley rats with salt-induced hypertension. 16685193: The beneficial effects of spironolactone, eplerenone, amiloride and potassium in preventing cardiovascular damage in various experimental models of salt-induced hypertension can be dissociated from blood pressure effects, and have drawn attention to the direct genomic and non-genomic actions of aldosterone at the level of the vessels, the heart and the kidneys. 16685463: Low ethanol intake prevents salt-induced hypertension in WKY rats. These results suggest that chronic low ethanol intake prevents salt-induced hypertension and attenuates renal vascular changes in WKY rats by preventing an increase in tissue aldehyde conjugates and cytosolic [Ca2+]i. 16741004: Vascular endothelin (ET)-1 is upregulated in several forms of salt-induced hypertension. 16862820: INTRODUCTION: The involvement of central alpha2B adrenoceptors (AR) in the maintenance of hypertension has been proven by a series of previous experiments, at least in a particular model of nephrogenic salt-induced hypertension. 16877963: Distinct rapid and slow phases of salt-induced hypertension in Dahl salt-sensitive rats. METHODS: Blood pressure (BP) telemetry was used to describe the detailed time course of salt-induced hypertension in Dahl-S rats and in hybrid rats derived from Dahl-S and Dahl salt-resistant strains. Our data also suggest that short-term measures of salt-sensitivity may be predictive of the effect of salt on the eventual progression of salt-induced hypertension. CONCLUSIONS: Two phases of salt sensitivity coexist and provide distinct contributions to salt-induced hypertension in Dahl-S rats. 16923758: These data suggest that angiotensin II via angiotensin type 1 receptor activation contributes to organ damage in nitric oxide-deficient salt-independent hypertension but is protective in salt-induced hypertension. 17070424: In alpha(2B)-AR gene knockout mice, blood pressure (BP) does not rise with salt loading, and in rats with salt-induced hypertension, BP decreases transiently with antisense (AS) treatment targeting the alpha(2B)-AR gene. BACKGROUND: Salt-induced hypertension is mediated via the alpha(2B)-adrenergic receptor (AR) subtype. CONCLUSIONS: These results indicate that our construct, when given by ICV means, could reach multiple sites of the central nervous system relevant to BP regulation and could safely inhibit the central alpha(2B)-adrenergic receptor, thereby achieving prolonged reversal of salt-induced hypertension. 1719285: We designed experiments to investigate the effects of cicletanine, a novel antihypertensive drug, on medial hypertrophy in Dahl rats susceptible to salt-induced hypertension (Dahl S rats). 17209324: Impaired baroreflex sensitivity and responses to angiotensin converting enzyme inhibitor in salt-induced hypertension and its prevention by dietary calcium supplement in Sprague-Dawley rats. 17220029: Furthermore, in the Sabra rat model of salt-induced hypertension, priming of PMNLs, oxidative stress and inflammation antecede the development of hypertension. 1733341: However, other mechanisms can increase sodium excretion independent of pressure natriuresis and suppression of ANG II during salt-induced hypertension. Pressure natriuresis and angiotensin II in reduced kidney mass, salt-induced hypertension. 17342193: MANAGEMENT: Saline-induced hypertension resulting in rapid restoration of cortical perfusion and a resolution of the initial speech and language deficits. 17553846: The effects of salt-induced hypertension on alpha1-adrenoreceptor expression and cardiovascular physiology in the rainbow trout (Oncorhynchus mykiss). 17689201: The consequences of salt exposure during early life of human beings have not been investigated as detailed as in experimental animals, however, there are some clinical trials and epidemiological observations indicating that, similar to experimental animals, irreversible and reversible components are also developed in man during the genesis of HT. 1773501: These rats are fairly NaCl-resistant on a 2.1% high K diet, whereas they are quite susceptible to NaCl-induced hypertension and deaths on a 0.5% normal K diet. 1773504: High vs low oral Ca (2.0 vs 0.4% Ca, 8-13 rats/diet) significantly (p less than 0.05) attenuated salt-induced hypertension (7% NaCl intake) in female spSHR (mean arterial pressure = 137 vs 175 mmHg) but aggravated such hypertension in female DS rats (141 vs 124 mmHg). Interest in effects of oral calcium (Ca) on blood pressure is now generally focused on salt-induced hypertension. 1773519: The current study sought to determine whether exercise might also exert a similar protective effect on salt-induced hypertension. 17906684: Here, we assessed the effects of chronic angiotensin converting enzyme (ACE) inhibition on salt-induced hypertension and cardiovascular and renal hypertrophy and fibrosis, relative to the extent of ACE blockade. Prevention of salt induced hypertension and fibrosis by angiotensin converting enzyme inhibitors in Dahl S rats. 18209918: Persistent hypertension and progressive renal injury induced by salt overload after short term nitric oxide inhibition. 1833320: The salt-induced plasticity of cardiopulmonary baroreceptor reflexes may exert a protective effect against the development of salt-induced hypertension by augmenting the reflex vasodilatory response to volume expansion. 18377762: Clofibrate (clof) prevents this salt induced hypertension. Older animals are resistant to both salt induced hypertension and oxidative stress. 18414066: Dahl salt-sensitive rats, models of salt-induced hypertension, excrete protein-bound vitamin D metabolites into urine, a process that is accelerated during high salt intake. 18417720: During the development of salt-induced hypertension over 2 wk, the RPP to the left kidney was maintained at control levels (125 +/- 2 mmHg) by continuous servocontrol inflation of an aortic balloon implanted between the renal arteries; during the same period, the RPP to the right kidney rose to 164 +/- 8 mmHg. 18418273: In Dahl S but not R rats, the high-salt diet caused marked hypertension, cardiac and kidney hypertrophy, and fibrosis. Prevention of salt-induced hypertension and fibrosis by AT1-receptor blockers in Dahl S rats. 18535843: In the following we marshal the current evidence that salt plays a definite role in the genesis of hypertension and target organ damage, point to practical problems of salt restriction, and report on novel pathomechanisms of how salt affects blood pressure and causes target organ damage. 18551017: Hypertension was induced by adding 6% salt to the chow (n = 8-11/group). 18554900: The Dahl salt-sensitive rat, a model for salt-induced hypertension, develops hypovitaminosis D during high salt intake, which is caused by loss of protein-bound vitamin D metabolites into urine. 18574600: Our data suggest that diabetes during intrauterine development and salt overload beginning at an early age can cause hypertension and renal injury. 18596730: To determine if clofibrate affects blood pressure regulation we studied mice with DOCA-salt induced hypertension in wild-type and PPAR alpha knockout mice. 1873017: This study attempted to evaluate the effect of anion associated with sodium loading on the development of angiotensin II (AII)-induced hypertension in rats. Importance of chloride in the development of salt-induced angiotensin II hypertension in rats. 18815205: In Dahl S rats with high-salt-induced hypertension, this system maintained RPP at 100-120 mmHg over 10 days, while systemic arterial pressures were 150 +/- 5.9 mmHg in uncontrolled animals. 18826995: Knockdown of renal medullary 11 beta-hydroxysteroid dehydrogenase type 1 with small-interfering RNA attenuated the early phase of salt-induced hypertension in Dahl salt-sensitive rats and reduced urinary excretion of corticosterone. In summary, we have demonstrated that suppression of 11 beta-hydroxysteroid dehydrogenase type 1 expression in the renal medulla attenuates salt-induced hypertension in Dahl salt-sensitive rats. Long-term attenuation of salt-induced hypertension was achieved with small hairpin RNA targeting renal medullary 11 beta-hydroxysteroid dehydrogenase type 1. 19079278: These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. The time course of salt-induced hypertension, and why it matters. 19118098: Role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt-induced hypertension in Dahl salt-sensitive rats. 19225142: Trilostane, FAD286, and the role of aldosterone in the central regulation of blood pressure: focus on \Role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt-induced hypertension in Dahl salt-sensitive rats\. 19270192: Taken together, the results indicate that central estrogen plays a protective role in the development of Aldo/NaCl-induced hypertension and that this may result from reduced sympathetic outflow. Gonadectomy augmented Aldo/NaCl-induced hypertension in females (Delta18.2 +/- 2.0 mmHg) but had no effect in males (Delta23.1 +/- 2.9 mmHg). 1928439: Different muscles undergo similar increases in vascular resistance, despite differences in the microvascular abnormalities accompanying salt-induced hypertension. 19321237: Hypertension was induced by DOCA-salt. 1934539: The present study was performed to determine if chronic administration of a high salt diet induces hypertension similarly in young and adult rats and if treatment with DSP-4 alters the development of the hypertension. Age-dependent salt-induced hypertension in the rat: prevention with DSP-4, a selective noradrenergic neurotoxin. 19483387: The drinking water contained 10 g/l sodium chloride to induce early hypertension. 19546378: Little is known about the pathophysiological significance of fumarate metabolism in cardiovascular and renal functions, including salt-induced hypertension. The infusion significantly exacerbated salt-induced hypertension in SS-13(BN) rats (140+/-3 vs125+/-2 mm Hg in vehicle control at day 5 on a 4% NaCl diet; P<0.05). These data suggest a novel role for fumarate metabolism in salt-induced hypertension and renal medullary oxidative stress. 19841522: CONCLUSIONS: Co-administration of vitamin C and E does not have an additive beneficial effect on reducing the kidney damage and hypertension compared to either vitamin C or E alone in DOCA-salt-induced hypertension. Unilateral nephrectomy was carried out in the study groups and hypertension was induced by deoxycorticosterone injection and 1% sodium chloride and 0.2% potassium chloride added to the drinking water. INTRODUCTION: We assessed whether co-supplementation of vitamins C and E has additive beneficial effects on reducing the kidney damage and attenuation of the arterial pressure elevation compared to administration of either vitamin C or vitamin E alone in deoxycorticosterone acetate-salt-induced hypertension. Reduction of kidney damage by supplementation of vitamins C and E in rats with deoxycorticosterone-salt-induced hypertension. 1986980: The sympathetic nervous system but not vasopressin may play an important role in the chronic phase of central NaCl-induced hypertension. These results indicate that sustained sodium stimulus on the central nervous system causes mild hypertension and alters water and sodium balance. 1986988: A substantial body of epidemiological and experimental data has accumulated that strongly implicates NaCl as having a causal role in the genesis of arterial hypertension. 1986995: This observation has implications for understanding mechanisms contributing to NaCl-induced hypertension. 1987017: Based on early experiments, it was thought that hypertension in Dahl salt-sensitive rats epitomized the overriding importance of renal and humoral mechanisms in salt-induced hypertension, but studies in the past 15 years have demonstrated that alterations in sympathetic neural mechanisms also participate critically in the genetic predisposition to salt-induced hypertension in Dahl salt-sensitive rats. This article briefly reviews sympathetic neural mechanisms in Dahl rats, including evidence for a role of afferent baroreceptor as well as central neural and peripheral adrenergic mechanisms in salt-induced hypertension in Dahl salt-sensitive rats. The Dahl strain provides a model for examining mechanisms involved in the genetic sensitivity or resistance to salt-induced hypertension. Sympathetic neural contribution to salt-induced hypertension in Dahl rats. 19874603: A multi-component model of the dynamics of salt-induced hypertension in Dahl-S rats. CONCLUSION: Our results suggest that the slow process of development of salt-induced hypertension in Dahl-S rats over a period of many weeks can be well represented by a combination of three components that differ in their timing, reversibility, and their associated effect on the chronic pressure natriuresis relationship. Detailed time course data collected in the Dahl salt-sensitive rat strain suggest that the development of salt-induced hypertension may consist of several distinct phases or components that differ in their timing and reversibility. These components are important to distinguish since each may represent a unique set of underlying mechanisms of salt-induced hypertension. To better understand these components, the present study sought to model the dynamics of salt-induced hypertension in the Dahl salt sensitive (Dahl-S) rat using 3 sets of time course data. 19969025: As the association of Rho kinase and oxidative stress was reported in Ald-NaCl-induced hypertension of rats, we investigated the effects of an MR antagonist (eplerenone) and a Rho kinase inhibitor (fasudil) on Ald-NaCl-induced cardiac fibrosis in AT1aR-KOs. 2010576: However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. 20118201: Decreased susceptibility to salt-induced hypertension in subtotally nephrectomized mice lacking the vasopressin V1a receptor. The present study was undertaken to elucidate the role of the V1aR in salt-induced hypertension. 2013478: Intravenous administration of a blocker of thromboxane A2/prostaglandin endoperoxide receptors, SQ29548 (2 mg/kg bolus injection plus 2 mg/kg/hr for 3 hours), reduced from 162 +/- 4 to 144 +/- 5 mm Hg (p less than 0.05) the blood pressure of rats with aortic coarctation-induced hypertension at 7-14 days after coarctation when plasma renin activity is greatly increased. Accordingly, the blood pressure of rats with aortic coarctation-induced hypertension is influenced by the interplay of prostanoid-mediated pressor and vasodepressor mechanisms. Also prostanoid-mediated vasodepressor mechanisms are operational in the early phase of aortic coarctation-induced hypertension since the blood pressure of rats pretreated with SQ29548 was increased by the subsequent administration of indomethacin. The blood pressure-lowering effect of SQ29548 in the early phase of aortic coarctation-induced hypertension was positively correlated with the prevailing plasma renin activity and could not be demonstrated in hypertensive rats pretreated with indomethacin. In contrast, treatment with SQ29548 was without effect on the blood pressure of either normotensive or hypertensive rats (i.e., aortic coarctation-induced hypertension at 90-113 days after coarctation, deoxycorticosterone-salt-induced hypertension) having normal or depressed values of plasma renin activity. 2015070: The results suggest that salt-induced hypertension is associated with impairment of endothelium-dependent relaxation to histamine but not to ACh. 20194297: Thus, HS-induced enhancement of TRPV4 function and expression in sensory neurons and resistant vessels in DR rats may prevent salt-induced hypertension possibly via activation of Maxikappa channels given that blockade of TRPV4 elevates mean arterial pressure. 20194304: Salt-induced hypertension and renal injury in Dahl salt-sensitive rats, particularly medullary interstitial fibrosis, have been shown previously to be substantially attenuated in SS-13(BN) rats. 20374182: Evaluation of renal oxidative stress in the development of DOCA-salt induced hypertension and its renal damage. 20396348: CONCLUSION: The elevated expression of sEH in kidney may play a role in high-salt induced hypertension. [Renal over expression of soluble epoxide hydrolase in rat with hypertension induced by high-salt]. 2045141: The Dahl salt-sensitive rat was used to investigate the effect of hypertension on indexes of copper status and to determine the extent to which dietary manipulation of copper attenuated, or exacerbated, the rate of sodium chloride-induced hypertension. These results suggest that altered copper metabolism is secondary, rather than primary, to the development of sodium chloride-induced hypertension in the salt-sensitive rat. At the lower levels of copper intake, sodium chloride-induced hypertension increased red blood cell superoxide dismutase activity in a manner consistent with the plasma copper and ceruloplasmin changes observed. 2045150: Dual hemodynamic mechanisms for salt-induced hypertension in Dahl salt-sensitive rats. 2045153: These results imply that vasopressin plays a crucial role in the expression of salt-induced hypertension in rabbits with compromised baroreceptor and renal function. To elucidate the contributions of renal, humoral, and arterial baroreceptor reflex components to salt-induced hypertension, we administered 10% NaCl intravenously for 10 days to sinoaortic-denervated rabbits with unilateral nephrectomy (n = 7), sinoaortic-denervated rabbits with intact kidneys (n = 7), and sham-operated sinoaortic-denervated rabbits with unilateral nephrectomy (n = 7). 20466668: CONCLUSIONS: Dahl SS rats exposed to excessive salt in prepubescence show a permanent increase in susceptibility to salt-induced hypertension and proteinuria. We examined the role that the mineralocorticoid receptor (MR) plays in the salt-induced hypertension and renal damage of prepubertal Dahl salt-sensitive (SS) rats. 20538365: This work builds upon a recent study, which developed a grey-box multi-component model of salt-induced hypertension in the Dahl-S rat. Salt-induced hypertension has been demonstrated in a variety of species including rats, monkeys, chimpanzees and humans. A 5-component mathematical model for salt-induced hypertension in Dahl-S and Dahl-R rats. 20586949: Current evidence documents that salt is crucial to the genesis of hypertension. 2058718: The purpose of this study was to determine the effect of salt-induced hypertension on the microvascular pressure profile in skeletal muscle. Effect of salt-induced hypertension on microvascular pressures in skeletal muscle of Dahl rats. Pressures in the collecting and draining venules were not elevated in DS on 7% NaCl, suggesting that increased precapillary resistance in salt-induced hypertension effectively shields the skeletal muscle capillary and venular networks from high hydrostatic pressures. 2066893: It has been shown that dietary sodium restriction reduces blood pressure in hypertensive patients and that a diet high in sodium chloride produces hypertension in the population predisposed to the disease. 20672822: Oral dosing of 3S,3aR-27d (PF-3882845) in the Dahl salt sensitive preclinical model of salt-induced hypertension and nephropathy showed blood pressure attenuation significantly greater than that with eplerenone, reduction in urinary albumin, and renal protection. 20852048: This study was conducted to determine the contribution of CYP1B1 to hypertension and associated pathophysiological changes produced by DOCA (30 mg/kg) given subcutaneously per week with 1% NaCl + 0.1% KCl in drinking water to uninephrectomized rats for 6 wk. 2,3',4,5'-Tetramethoxystilbene prevents deoxycorticosterone-salt-induced hypertension: contribution of cytochrome P-450 1B1. These data suggest that CYP1B1 contributes to DOCA-salt-induced hypertension and associated pathophysiological changes, most likely as a result of increased ROS production and ERK1/2 and p38 MAPK activity, and could serve as a novel target for the development of agents like TMS to treat hypertension. Reactive oxygen species (ROS) contribute to various models of hypertension, including deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 2101067: Hypertension caused by deoxycorticosterone-salt (DOC-salt) may involve enhanced sympathetic tone and some diuretics may exert their antihypertensive action by modulating presynaptic adrenergic sensitivity. 21097806: Dietary nitrate attenuates oxidative stress, prevents cardiac and renal injuries, and reduces blood pressure in salt-induced hypertension. 2112004: Relevance of vascular PGI2 synthase to vascular prostacyclin production in Dahl rats susceptible to salt-induced hypertension. 21143427: Recent studies demonstrated that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload and thus causing hypertension. This article will discuss the interaction of Glut5 with salt-absorbing transporters and review the role of dietary fructose in enhanced salt absorption in intestine and kidney as it relates to the pathogenesis of hypertension in metabolic syndrome. 21214402: Salt and nitric oxide inhibition induced hypertension: the role of prostacycline and 8-isoprostane. 21292834: INTRODUCTION: Salt-induced hypertension in the Dahl rat is associated with increases in angiotensin II, aldosterone, free radical generation and endothelial dysfunction. 21388436: Interestingly, it is also suggested that, in obesity-induced hypertension models, increases in BP are caused by brain ROS-induced central sympathoexcitation. There are multiple and complex mechanisms of salt-induced hypertension; however, central sympathoexcitation plays an important role. Reactive oxygen species and the central nervous system in salt-sensitive hypertension: possible relationship with obesity-induced hypertension. Recent studies suggest that increased ROS production in the brain and central sympathoexcitation may share a common pathway that increases BP in both salt- and obesity-induced hypertension. 2139470: This study was designed to contrast the effects of prolonged treatment with a thromboxane (Tx) synthase inhibitor (UK 38485 or SC 41156) and a Tx receptor antagonist (SQ 29548) on the development of angiotensin II (Ang II)-salt-induced hypertension. Ang II infusion (125 ng/min i.p. for 12 days) in rats drinking 0.15 M NaCl resulted in severe hypertension accompanied by proteinuria, reduction of urinary creatinine excretion and augmentation of urinary TxB2 excretion and TxB2 release from aortic rings and renal cortex slices. Contrasting effect of thromboxane synthase inhibitors and a thromboxane receptor antagonist on the development of angiotensin II-salt-induced hypertension in rats. 214053: The two weeks of desoxycorticosterone and 1% saline-induced hypertension caused myocarditis and hyalinization of the coronary arteries of the nonarteriosclerotic (virgin) rats and definite exacerbation of the preexisting arteriosclerosis in breeder rats, severe myocarditis, and polyarteritis nodosa. 21445721: This concept parallels results observed in other models of neurogenic hypertension, such as spontaneously hypertensive rats and rats with angiotensin II-salt-induced hypertension, pointing out alterations in the central coupling of respiratory and sympathetic activities as a novel mechanism underlying the development of neurogenic hypertension. 21478481: Mineralocorticoid receptor activation: a major contributor to salt-induced renal injury and hypertension in young rats. 21539470: Bilateral orchidectomy attenuated the impaired endothelial function induced by the high-salt diet in rats, but this was reversed by concomitant administration of testosterone, suggesting a role for androgens in enhancing long-term vascular smooth muscle tone and hence maintenance of high blood pressure in salt-induced hypertension. 2157760: Renal function in rats with angiotensin II-salt-induced hypertension: effect of thromboxane synthesis inhibition and receptor blockade. 21585422: The salt-induced hypertension of the Dahl salt-sensitive rat is mitigated by the central infusion of a mineralocorticoid antagonist even though circulating aldosterone is normal or reduced in salt-sensitive (SS). The central infusion of inhibitors of aldosterone synthesis lowers salt-induced hypertension in the Dahl salt-sensitive rat, suggesting a role for excessive Dahl salt-sensitive synthesis in the brain. The mechanisms by which excessive salt causes hypertension involve more than retention of sodium and water by the kidneys and are far from clear. 2174236: The parallel increase in vascular 22Na uptake and blood pressure suggests a possible, key role of Na+ influx in the mechanism of salt induced hypertension of DS rats. 21748534: Emblica officinalis exerts antihypertensive effect in a rat model of DOCA-salt-induced hypertension: role of (p) eNOS, NO and oxidative stress. We determined whether hydroalcoholic lyophilized extract of EO may influence DOCA/HS-induced hypertension by modulating activity of (p) eNOS and endogenous antioxidants. Our results demonstrate that EO reduces oxidative stress, prevents development and progression of hypertension as well as cardiac and renal hypertrophy in DOCA/HS-induced hypertension via modulation of activated eNOS, endogenous antioxidants, serum NO and electrolyte levels. Emblica officinalis (EO) has antioxidant properties that could improve redox-sensitive vascular, cardiac and renal changes associated with deoxycorticosterone acetate/1% NaCl high salt (DOCA/HS)-induced hypertension. 2176807: Thus in order to explain salt-induced hypertension, a delayed remote indirect vasoconstrictor action must be postulated. 21789281: This paper will focus on synergistic roles of fructose and salt in the pathogenesis of hypertension resulting from salt overload. Recent studies in rodents demonstrate that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload, thus setting in motion a cascade of events that will lead to hypertension. The role of salt in the pathogenesis of fructose-induced hypertension. 21824999: In rats with salt-induced hypertension or postmyocardial infarction, angiotensin II type 1 receptor (AT(1)R) densities and oxidative stress increase and neuronal NO synthase (nNOS) levels decrease in the paraventricular nucleus (PVN). 21844822: CONCLUSIONS: These results indicate that prepubertal transient blockade of AT1R signaling exerts a long-term therapeutic effect on salt-induced hypertension and renal injury in Dahl Iwai salt-sensitive rats, partly through a sustained enhancement of renal ATRAP expression, thereby suggesting ATRAP a novel molecular target in salt-induced hypertension and renal injury. In this study we examined whether the regulation of renal ATRAP expression is related to the development of salt-induced hypertension and renal injury as well as to the beneficial effects of AT1R blockade. 22210049: Moreover, CYP1B1 contributes to the development and/or maintenance of hypertension produced by Ang II-, deoxycorticosterone (DOCA)-salt-, and N(omega)-nitro-L-arginine methyl ester-induced hypertension and in spontaneously hypertensive rats. The pathophysiological changes, including cardiovascular hypertrophy, increased vascular reactivity, endothelial and renal dysfunction, injury and inflammation associated with Ang II- and/or DOCA-salt induced hypertension in rats, and Ang II-induced hypertension in mice are minimized by inhibition of CYP1B1 activity with 2,4,3',5'-tetramethoxystilbene or by Cyp1b1 gene disruption in mice. 2222964: Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl-induced hypertension in the Dahl salt-sensitive (S) rat. 22262304: These results indicate that intracerebroventricular infusions of aliskiren and an AT(1) receptor blocker are similarly effective in preventing salt-induced sympathetic hyperactivity and hypertension in Dahl S rats, suggesting that renin in the brain plays an essential role in the salt-induced hypertension. 22262479: The renal sympathetic nervous system is known to play a key role in the development of salt-induced hypertension. 2232308: Among the risk factors, hypertension has gradually decreased due to treatment and lower intake salt in Japan. 22467312: In angiotensin II-induced hypertension, however, aortic endothelial SPR expression was not affected. DOCA-salt-induced hypertension is associated with H(4)B oxidation and uncoupling of eNOS. 2250596: These data indicate that compared to normotensive DR, the DS rat with salt-induced hypertension exhibits a lower vascular density within both the arcading and the transverse portions of the gracilis muscle arteriolar network. Arteriolar network morphology in gracilis muscle of rats with salt-induced hypertension. The purpose of this study was to determine if structural rarefaction of arterioles occurs in the gracilis muscle of Dahl salt-sensitive (DS) rats with salt-induced hypertension. The lower arcade vessel density reflects an inherent characteristic of the DS strain, whereas the lower transverse arteriole density reflects a true structural rarefaction associated with salt-induced hypertension. 22573381: High nephron endowment protects against salt-induced hypertension. 2261149: Immunohistochemical study of vascular lesions in severe hypertension induced by DOCA and salt administration to spontaneously hypertensive rats. 22744228: About one third of the population worldwide is supposed to be salt sensitive which is a major cause for arterial hypertension later in life. 22796734: There is a widely held belief that hypervolaemia due to excess intake or inadequate removal of salt and water is the principal cause of hypertension in dialysis patients. 22802227: Salt-induced hypertension in a mouse model of Liddle syndrome is mediated by epithelial sodium channels in the brain. These findings highlight the possible causative contribution of central nervous system ENaC in the etiology of salt-induced hypertension. 22805345: The results reveal the importance of a largely unexplored role for deficiencies of mTAL mitochondrial metabolism and oxygen utilization in salt-induced hypertension and renal medullary oxidative stress. 22861813: Pharmacological inhibition of CatA by the natural product ebelactone B increased renal bradykinin levels and prevented the development of salt-induced hypertension. 22914542: OBJECTIVES: To elucidate the roles that renal mineralocorticoid receptor-Rac1 interactions and oxidative stress play in salt-induced hypertension and renal injury in prepubertal rats. 23024265: This study tests the hypothesis that activation of the NK-1Rs by SP occurs during hypertension induced by deoxycorticosterone (DOCA)-salt treatment, which contributes to renal injury in this model. 23096235: We conclude that activation of the MR/ENaCs pathway in the CP contributes to hypertension via an increase in CSF [Na(+)], thereby exaggerating salt-induced hypertension with sympathetic hyperactivation in SHRSP. Increase in cerebrospinal fluid (CSF) Na(+) concentration ([Na(+)]) precedes hypertension and is a key step in the development of salt-induced hypertension. 23110194: METHODOLOGY/PRINCIPAL FINDINGS: Therefore, we investigated the role of ADMA and DDAH1 in hypertension-induced end organ damage using the uninephrectomized, deoxycorticosterone actetate salt, and angiotensin II-induced hypertension model in human DDAH1 (hDDAH1) overexpressing and wild-type (WT) mice. 23112808: A simple test system is now available that evaluates vascular salt sensitivity in humans and identifies individuals who are at risk of salt-induced hypertension. 2318522: The purpose of this study was to identify microvascular alterations that could contribute to increased peripheral vascular resistance in the Dahl salt-sensitive rat with salt-induced hypertension. The similarity in vascular densities among groups indicates that structural rarefaction of arterioles does not contribute to any increase in spinotrapezius muscle resistance at this stage of salt-induced hypertension. 2318525: Recent studies indicate that extrarenal factors, including the sympathetic nervous system, play a critical role in the development of NaCl-induced hypertension in DS rats. To assess the contribution of extrarenal and renal factors in the development of NaCl-induced hypertension in Dahl rats, we performed renal transplantation in DS and DR rats. The fact that DS rats with a DR kidney (DSR) also developed hypertension indicates that extrarenal factors also contribute significantly to NaCl-induced hypertension in DS rats. 23224155: Altered lymphatic function and architecture in salt-induced hypertension assessed by near-infrared fluorescence imaging. Thus, we longitudinally characterized lymphatic contractile function and vessel remodeling noninvasively using dynamic near-infrared fluorescence imaging in animal models of salt-induced hypertension. Lymphatic contractile function and vessel remodeling occurs in response to salt-induced hypertension suggesting a possible role for the lymphatics in the regulation of vascular blood pressure. 23328675: This study sought to determine the effects of long-term treatment with ghrelin (10 nmol/kg, twice a day, intraperitoneally) on the hypertension induced by high salt (8.0% NaCl) diet in Dahl salt-sensitive hypertensive (DS) rats. These results demonstrate that long-term ghrelin treatment counteracts salt-induced hypertension in DS rats primarily through diuretic action associated with increased renal NO production, thereby exerting cardio-protective effects. 23460283: Our data support a differential microRNAs expression profile in salt-induced hypertension. 23484864: Sodium alginate oligosaccharide treatment via the subcutaneous route almost completely abolished salt-induced hypertension in Dahl S rats fed a high-salt diet. Subcutaneous administration of sodium alginate oligosaccharides prevents salt-induced hypertension in Dahl salt-sensitive rats. 23572029: This has been well documented experimentally for cardiac ischaemia, diabetes renal disease, peripheral ischaemia and aldosterone-salt induced hypertension. 23652235: These results suggest that HS attenuated the development of salt-induced hypertension and this attenuation may be associated with its high K+ content or high potassium: sodium ratio and not with altered pressor/depressor response to noradrenalin or acetylcholine. Attenuation of salt-induced hypertension by aqueous calyx extract of Hibiscus sabdariffa. 2369498: These rats are fairly NaCl-resistant on a 2.1% high K diet, whereas they are quite susceptible to NaCl-induced hypertension and stroke deaths on a 0.5% normal K diet. 23702776: In this study, we tested the hypothesis that components of the SWI/SNF complex are activated and recruited to promoters that regulate the fetal cardiac gene program in hearts that become hypertrophic as a result of salt induced hypertension. Our data implicate SWI/SNF chromatin remodeling enzymes as regulators of gene expression in cardiac hypertrophy resulting from salt induced hypertension. Thus we provide novel insights into the epigenetic mechanisms by which salt induced hypertension leads to cardiac hypertrophy. 23713522: BACKGROUND AND PURPOSE: The contribution of endothelin-1 (ET-1) in a B2KO mouse model of a high salt-induced arterial hypertension was investigated. High salt-induced hypertension in B2 knockout mice is corrected by the ETA antagonist, A127722. 23766534: In summary, chloride transport in the distal nephron can play a primary role in driving NaCl transport in this part of the kidney, and a primary abnormality in renal chloride transport can provoke arterial hypertension. 2393103: This study was designed to investigate the GABAergic neurons in specific regions of the brain possibly linked to salt-induced hypertension. This study provides new evidence to support further the idea that central GABAergic neurons are closely associated with pathogenesis of salt-induced hypertension. Different hypertensive mechanisms between salt-induced hypertension and genetic hypertension are also discussed. It is not clear, however, which GABAergic systems are involved in salt-induced hypertension. 23933891: We have previously shown that a high salt diet causes hypertension in MnSOD-deficient (MnSOD(+/-)) mice but not in wild-type mice. CONCLUSION: Salt-induced hypertension in MnSOD(+/-) mice is associated with activation of intra-renal inflammatory and ROS generating pathways. 23966951: P2X7 antagonism has been shown to ameliorate rodent models of DOCA salt-induced hypertension and P2X4 null mice are hypertensive. 23981445: Treatment with high salt diet increased BP (P<0.01) and caused LV hypertrophy (P<0.001) and interstitial myocardial fibrosis only in ANP+/-(WT) and not ANP+/-(KO) offspring, suggesting gestational hypertension programs the offspring to show resistance to salt-induced hypertension and LV remodeling. 24047246: OBJECTIVES: We investigated the antihypertensive mechanism of long-term Miso soup consumption in Dahl salt-sensitive (Dahl S) rats with salt-induced hypertension. CONCLUSIONS: Long-term consumption of Miso soup attenuated blood pressure elevation in Dahl salt-sensitive rats with salt-induced hypertension. 24048492: The combination of excess aldosterone and salt loading induces hypertension and cardiac damage. 2412086: These data suggest that alterations in the dihydropyridine binding sites associated with calcium channels in the brainstem may be involved in the etiology of DOCA-NaCl-induced hypertension. 24161401: CONCLUSIONS: Our data supports a differential miRNA expression profile in salt-induced hypertension. 24164386: This study was designed to determine the effect of Liu-Wei-Di-Huang-Fang (L-W-D-H-F), a compound used in traditional Chinese herbal medicine, to treat salt-sensitive hypertension (SSHT) induced by a high-salt and high-fat diet. 24303192: We conclude that (1) the OVLT regulates the basal levels of MAP in rats consuming a high-salt and (2) the OVLT is an important brain site of action for the pathogenesis of AngII-salt hypertension in the rat. Therefore, the objective of this study was to investigate the role of the OVLT during AngII-induced hypertension in rats fed a high-salt diet. 2431416: It was the objective of this paper to integrate recent findings concerning Ca-dependent 42K effluxes from rat aorta with observations of elevated basal 42K efflux and supersensitivity to norepinephrine (NE) stimulation of 42K effluxes during aldosterone-salt induced hypertension (Aldo). 2441184: Renal vascular reactivity to both BAY-K-8644 and its agonist isomer were greatly magnified following salt-induced DS rat hypertension. 24578129: This review provides an in-depth discussion of the evidence supporting these conclusions and considers the significance with regard to treating salt-sensitive hypertension and salt-induced cardiorenal injury. 24695748: Aldosterone-salt treatment induces not only hypertension but also extensive inflammation that contributes to fibrosis in the rat kidney. 24808538: Enhanced tubular reabsorption of salt is important in the pathogenesis of obesity-related hypertension, but the mechanisms remain poorly defined. 24990139: Excessive or high salt or sodium intake is known to cause hypertension and other diseases. 25177670: It has been well established that excessive intake of sodium chloride (salt) induced hypertension in some populations. 2525523: Comparison of the responses of DS and DR rats to high salt diets, ANF infusion, and acute volume expansion indicates that the salt-induced hypertension in DS rats is initiated by a diminished renal response to ANF. It is concluded that the primary hemodynamic disturbance in DS rats with salt-induced hypertension is an increase in cardiac output caused by blood volume expansion in the absence of any vasodilation. Salt-induced hypertension in Dahl salt-sensitive rats. 2527974: These findings suggest that the combination of cyclosporine, corticosteroids, and, in some patients, an elevated plasma renin activity prevents the kidney from responding to the acute volume and salt overload with an appropriate diuresis and natriuresis, thus leading to systemic hypertension. 2531119: This observation has implications for understanding mechanisms contributing to NaCl-induced hypertension in the susceptible host. 25391363: Molecular adaptations in vasoactive systems during acute stroke in salt-induced hypertension. 25452472: We found that hypertension and renal injury induced by a high-salt diet were substantially attenuated in Dahl SS/JrHsdMcwiCrl (SS/Crl) rats that had been maintained for many generations on the grain-based 5L2F diet compared with SS/JrHsdMcwi rats (SS/Mcw) maintained on the casein-based AIN-76A diet (mean arterial pressure, 116+/-9 versus 154+/-25 mm Hg; urinary albumin excretion, 23+/-12 versus 170+/-80 mg/d). Together, the data suggest that maternal diet during the gestational-lactational period has substantial effects on the development of salt-induced hypertension and renal injury in adult SS rats. Conversely, salt-induced hypertension and renal injury were significantly attenuated in rats developed from SS/Mcw embryos transferred to SS/Crl surrogate mothers. Salt-induced hypertension and renal injury were substantially exacerbated in rats developed from SS/Crl embryos transferred to SS/Mcw surrogate mothers. 2547398: In isolated perfused mesenteric vasculatures of spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, seven- to ten-weeks-old) and age-matched Wistar Kyoto rats (WKY), the effects of ouabain, a potent Na+,K+-ATPase inhibitor, or partially purified plasma obtained from salt-induced hypertension on pressor responses and norepinephrine overflow were investigated. 25531334: BACKGROUND/AIMS: To investigate the change of intrarenal renin-agiotensin system (RAS) and its role in high-salt induced hypertension. 2557032: These results suggest that: (1) in the kidneys, the receptor density and not the receptor affinity was different between S and R strains whether they were fed a low or high salt diet; (2) in the brain, the receptor density and affinity were the same between S and R rats regardless of the diet (low or high salt), indicating that the sodium salt diet modulates the peripheral but not the central alpha 2-adrenoreceptors; and this modulatory effect was observed only in S rats; (3) Na+ was able to reduce the affinity of the agonist (epinephrine) for the receptors in both S and R rats, and this effect of Na+ on central and peripheral alpha 2-adrenoreceptors was similar in prehypertensive rats and rats with salt-induced hypertension; and (4) the resistance of R rats to salt-induced hypertension was not due to the absence of Na+ binding component involved in the regulation of alpha 2-adrenoreceptor-adenylate cyclase complex. 2558064: This property may represent a genetically-mediated change responsible for the resistance to the development of salt-induced hypertension. These results also suggest an association between absence of sodium regulation of alpha 2-adrenoceptors and resistance to salt-induced hypertension. 25617698: BACKGROUND: The study was designed to explore the significance of endogenous H2S in the development of high-salt-induced hypertension in rats. Down-regulated CBS/H2S pathway is involved in high-salt-induced hypertension in Dahl rats. METHODS: High-salt-induced hypertension rat model was made by feeding Dahl rat high-salt diet containing 8% NaCl for 8 weeks with SD rats as control. 25626872: SM-NCX1 KO mice exhibit significantly lower blood pressure and attenuated angiotensin II (Ang II)-salt-induced hypertension (measured by radio telemetry and intra-arterial catheterization). 25632109: In this study, salt-induced hypertension was used as a model to retrieve blood pressure records of Brown Norway, Fawn-Hooded Hypertensive (FHH) and Dahl salt-sensitive (SS) rat strains. 2567707: Aggravation of salt-induced hypertension in Dahl rats by 2% supplemental dietary calcium. Thus, 2.0% supplemental calcium intake enhances salt-induced hypertension in DS rats. 25681084: We present a case of a 12-month-old infant initially diagnosed with tachyarrhythmia requiring defibrillation, subsequent presentation with hypertension and hyponatraemia secondary to renal salt loss and presumed inappropriate ADH secretion. 25686347: OBJECTIVE: To test the hypothesis that in a high-salt induced hypertension in normal rats, whether the changes of intrarenal renin-agiotensin system (RAS) play a critical role in renal damage and could be reflected by urinary angiotensinogen (AGT). 2569295: These findings suggest that Na+ regulation of alpha 2-adrenoceptor-agonist interactions was not altered with age and it was found to be similar in prehypertensive rats and rats with severe hypertension; further, the resistance of R rats to salt-induced hypertension was not due to the absence of Na+ binding component in the alpha 2-adrenoceptor-adenylate cyclase complex. 25802361: However, we now report that salt-induced hypertension is not different between sexes when measured by telemetry. 2583797: Lesions of the anteroventral third ventricle prevent salt-induced hypertension in the borderline hypertensive rat. The current investigation examined the extent to which this forebrain area is necessary for the elaboration of salt-induced hypertension in the borderline hypertensive rat. 25891026: Endogenous hydrogen peroxide in the hypothalamic paraventricular nucleus regulates neurohormonal excitation in high salt-induced hypertension. The aim of this study is to explore whether endogenous H2O2 changed by polyethylene glycol-catalase (PEG-CAT) and aminotriazole (ATZ) in the hypothalamic paraventricular nucleus (PVN) regulates neurotransmitters, renin-angiotensin system (RAS), and cytokines, and whether subsequently affects the renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) in high salt-induced hypertension. Our findings demonstrate that ROS component H2O2 in the PVN regulating MAP and RSNA are partly due to modulate neurotransmitters, renin-angiotensin system, and cytokines within the PVN in salt-induced hypertension. 2589496: In summary, the salt-induced hypertension was consistently related to small but significant fluid retention, blood volume expansion, elevations of cardiac output, and a gradual increase in TPR. 25937175: The protective effects of GSP on blood pressure and cardiovascular remodeling in rats with DOCA-salt-induced hypertension were investigated. Our results indicated that DOCA-salt could induce hypertension, cardiovascular remodeling and dysfunction, oxidative stress and the release of endothelin-1 (ET-1) and could increase JNK1/2 and p38MAPK phosphorylation. These findings demonstrate that GSP has protective effects against increase of blood pressure induced by DOCA-salt hypertension and cardiovascular remodeling by inhibiting the reactive oxygen species/mitogen-activated protein kinase pathway via restraining the release of ET-1. 25953742: Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels. 25994957: We reported that brain (pro)renin receptor (PRR) expression levels are elevated in DOCA-salt-induced hypertension; however, the underlying mechanism remained unknown. 26432844: Depressor effect of chymase inhibitor in mice with high salt-induced moderate hypertension. The aim of the present study was to determine whether long-term high salt intake in the drinking water induces hypertension in wild-type (WT) mice and whether a chymase inhibitor or other antihypertensive drugs could reverse the increase of blood pressure. 26447210: However, little is known about the effects of fructose in renal salt handling and whether combined intake of high fructose and salt can lead to salt-sensitive hypertension before the development of metabolic abnormalities. 26518973: In this study, we determined whether ALA supplementation attenuates oxidative stress in hypothalamic paraventricular nucleus (PVN), decreases the sympathetic activity and arterial pressure in high salt-induced hypertension by cross-talking with renin-angiotensin system (RAS) and pro-inflammatory cytokines (PICs). Alpha lipoic acid supplementation attenuates reactive oxygen species in hypothalamic paraventricular nucleus and sympathoexcitation in high salt-induced hypertension. CONCLUSION: These findings suggest that supplementation of ALA obviously decreases the sympathetic activity and arterial pressure in high salt-induced hypertension by improving the superoxide inhibitory property, suppressing the activation of RAS and restoring the balance between pro- and anti-inflammatory cytokines in the PVN. 26534937: The goal of the present study was to further narrow that region to identify the gene(s) most likely to protect from salt-induced hypertension. A 1.37 Mbp region of chromosome 13 previously identified by exclusion mapping was consistently associated with a reduction of salt-induced hypertension in the Dahl salt-sensitive (SS) rat. We conclude that we have identified a variant form of Pappa2 that can protect against salt-induced hypertension in the Dahl S rat. The studies yielded a subcongenic SS rat strain containing a 0.71 Mbp insert from BN (26-P strain) in which salt-induced hypertension was reduced by 24 mmHg. 26553126: We found that mRNA and protein levels of renalase in the kidneys of SS and SS-13BN rats were significantly decreased (P < 0.05) after high salt intervention, whereas dopamine in plasma was increased (P < 0.05) compared with rats received normal salt, suggesting that salt may induce salt-sensitive hypertension through inhibition of renalase expression. 26607702: CONCLUSION: Postnatal HS intake exacerbated prenatal HF-induced programmed hypertension. HF and HS induced programmed hypertension by differentially inducing renin-angiotensin system and sodium transporters in the kidneys. 26644237: SS(Nox4-/-) rats exhibited a significant reduction of salt-induced hypertension compared with SS rats after 21 days of 4.0% NaCl diet (134+/-5 versus 151+/-3 mm Hg in SS) and a significant reduction of albuminuria, tubular casts, and glomerular injury. 26656220: Central blockade of mineralocorticoid receptors (MRs) or angiotensin II type 1 receptors (AT1Rs) attenuates aldosterone (aldo)-salt induced hypertension. 26671951: CONCLUSIONS: Colectomy did not reduce the general risk of CVD, but reduced the risk of hypertensive disorders, most likely due to salt and water depletion induced by colectomy. 26783414: Central Infusion of Angiotensin II Type 2 Receptor Agonist Compound 21 Attenuates DOCA/NaCl-Induced Hypertension in Female Rats. 2681406: Salt-induced hypertension: the interactive role of vasopressin and of the sympathetic nervous system. 26927006: Vasodysfunction That Involves Renal Vasodysfunction, Not Abnormally Increased Renal Retention of Sodium, Accounts for the Initiation of Salt-Induced Hypertension. 27088730: METHODS: The present work was designed in an attempt to determine guidelines in the field of salt-induced hypertension by recording continuously blood pressure by telemetry in mice submitted to different sodium and potassium loaded diets and changing experimental conditions in both C57BL/6N and C57BL/6J mice strain (Normal salt vs. Low salt vs. High-salt/normal potassium vs. High salt/low potassium, standard vs. modified light cycle, Non-invasive tail cuff blood pressure vs. telemetry). Indeed, in this condition, salt-induced hypertension can also be detected during light period even though this BP increase is lower compared to the one occurring during the dark period. CONCLUSIONS: Therefore, to carry investigations on salt-induced hypertension in mice, chronic telemetry and studies in the active phase are essential prerequisites. 27173481: Chronic consumption of caffeine attenuates hypertension induced by high salt without affecting sympathetic nerve activity in Dahl-S rats. 2718107: A very low percentage were informed of the role played by sodium chloride in the genesis of hypertension. 27220372: The present study investigated the importance of periostin in hypertension-induced myocardial fibrosis. Periostin expression induced by oxidative stress contributes to myocardial fibrosis in a rat model of high salt-induced hypertension. 27288061: We assessed the hypothesis that the complexity of beat-to-beat BPV will be differentially altered in salt-sensitive hypertensive Dahl rats (SS) versus rats protected from salt-induced hypertension (SSBN13) maintained on high-salt versus low-salt diet. 2737713: How is the NaCl signal transmitted in NaCl-induced hypertension? 27402668: Salt-induced hypertension leads to development of left ventricular hypertrophy in the Dahl salt-sensitive (Dahl/SS) rat. Despite these differences, no significant effect of salt-induced hypertension was observed for either peak work output or peak mechanical efficiency during compensated hypertrophy. 27452860: The purpose of this work was to know if oral administration of anti-oxidant and free-radical scavenger CoQ10 may attenuate high salt-induced hypertension via regulating neurotransmitters and cytokines in the hypothalamic paraventricular nucleus (PVN). Adult male Sprague-Dawley (SD) rats were fed with a normal salt diet (NS, 0.3% NaCl) or a high salt diet (HS, 8% NaCl) for 15 weeks to induce hypertension. 27588564: We investigated the effect of DOCA-salt induced hypertension on endothelial function and artery structure in PAs and MCAs. 2766092: Development of salt-induced hypertension in Dahl salt-sensitive (S) rats is dependent on sympathetic overactivity which may be partially related to arterial baroreflex dysfunction and, therefore, is regionally selective. 27679494: Long-term radiotelemetry studies demonstrated that oral 8-aminoguanosine and 8-aminoguanine (5 mg/kg/day) suppressed deoxycorticosterone/salt-induced hypertension. 27720848: MATERIALS AND METHODS: SHR, DOCA-salt- and L-NAME-induced hypertension models were used. 27774451: The popularization of low salt may not be justified in people with normal kidney function in whom the compatible statistically based evidence that salt causes hypertension has been challenged by experimental evidence to the contrary. 27777356: Prolonged Baroreflex Activation Abolishes Salt-Induced Hypertension After Reductions in Kidney Mass. During 7 days of baroreflex activation, the hypertension induced by high salt was abolished (103+/-6 mm Hg) along with striking suppression of plasma norepinephrine concentration from 139+/-21 to 81+/-9 pg/mL, but despite pronounced blood pressure lowering, there were no significant changes in glomerular filtration rate (43+/-2 mL/min). 2790213: Vascular changes associated with deoxycorticosterone-NaCl-induced hypertension. Alterations were observed in the arteries, some of which were related to hypertension, but not to treatment, and some were due to treatment alone. 27986554: Anakinra reduced renal collagen content (n=6, P<0.01) but paradoxically appeared to exacerbate the renal and glomerular hypertrophy (n=8-9, P<0.001) that accompanied 1K/DOCA/salt-induced hypertension. CONCLUSION: Despite its anti-hypertensive and renal anti-fibrotic actions, anakinra had minimal effects on inflammation and leukocyte infiltration in mice with 1K/DOCA/salt-induced hypertension. 28003189: It is commonly accepted that increased renal sodium handling and plasma volume expansion are necessary factors for the development of salt-induced hypertension. 28035366: Inhibitory effects of alpha-lipoic acid on oxidative stress in the rostral ventrolateral medulla in rats with salt-induced hypertension. 2803669: Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl induced hypertension in the Dahl salt sensitive (S) rat. 2807513: This likely contributes to NaCl-induced hypertension in SHR-S on a high NaCl diet. 28185984: Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension. These findings suggest that endogenous or exogenous H2S in the PVN attenuates sympathetic activity and hypertensive response, which are partly due to decrease of ROS and PICs within the PVN in high salt-induced hypertension. 282036: Administration of DOCA-salt to H and N rats, while causing marked hypertension in the former, had no effect on noradrenaline in either strain. 28325999: Our findings show that consumption of natural sea salt induces less hypertension compared to refined salt in the Dahl salt-sensitive rat. 28338001: This study was designed to explore the precise mechanisms of RAS acting on reactive oxygen species (ROS) in salt-induced hypertension. These results, for the first time, identified that the precise signaling pathway of RAS regulating ROS in PVN is via AT1R/PKCgamma/Rac1 in salt-induced hypertension. Male Wistar rats were administered with a high-salt diet (HS, 8.0% NaCl) for 8 weeks to induced hypertension. Renin-angiotensin system acting on reactive oxygen species in paraventricular nucleus induces sympathetic activation via AT1R/PKCgamma/Rac1 pathway in salt-induced hypertension. 28373112: The present review article suggests that the consumption of a high-salt diet is not the cause of hypertension and that there are other factors, such as added sugars, which are causative for inducing hypertension and cardiovascular disease. For decades the notion that an excessive consumption of salt (NaCl) leads to hypertension has persisted. 2839785: [Hereditary resistance to salt-induced hypertension. What mechanisms?]. The demonstration of a similar pattern of response in the Dahl rats suggests that alpha 2 adrenoreceptor may be involved in the sensitivity or resistance to salt induced hypertension. 28404591: Therefore, development of salt-induced hypertension can be triggered by fast and progressive pathogenic remodeling of PT epithelia, which can be associated with changes in albumin handling. To determine the relative contributions of the glomerulus and proximal tubule (PT) to albuminuria, we applied intravital two-photon-based imaging to investigate the complex renal physiological changes that occur during salt-induced hypertension. 2842021: Correlation of left ventricular hypertrophy and its regression by lisinopril with salt-induced hypertension. The interaction of salt with hypertension-induced left ventricular hypertrophy and its reversal by inhibition of angiotensin converting enzyme were studied in salt sensitive and salt resistant Dahl rats. 28479261: Next, we explain how any physiological state that reduces urinary sodium concentrating ability may increase an individual's risk for salt-induced hypertension. 2849788: The role of vascular Na,K-ATPase activity in salt induced hypertension in Dahl rats. 2853754: These differences may play a primary role in the resistance or in the sensitivity of salt-induced hypertension. 2856782: These renin-calcium metabolic deviations may both predict and contribute to the pathophysiology of salt-induced hypertension, the blood pressure effects of oral calcium supplementation, as well as the short and longer term effectiveness of calcium channel blockade. 28637271: Although the theory itself is not a tautology, it does not appear to be testable because it holds that abnormal pressure natriuresis causes salt-induced hypertension to be sustained through abnormal increases in cardiac output that are too small to be detected. 28696224: An aortic balloon occluder placed around the aorta between the renal arteries was used to maintain perfusion pressure to the left kidney at control levels, ~128 mm Hg, during 7 days of salt-induced hypertension, whereas the right kidney was exposed to increased renal perfusion pressure that averaged 157+/-4 mm Hg by day 7 of high-salt diet. 28827472: We conclude that enhancement of intrarenal H2O2 with a 4.0% NaCl diet stimulates the mTORC1 pathway that is necessary for the full development of the salt-induced hypertension and kidney injury in the SS rat. Inhibition of Mammalian Target of Rapamycin Complex 1 Attenuates Salt-Induced Hypertension and Kidney Injury in Dahl Salt-Sensitive Rats. 28844481: These data suggest that the protective effects of tBHQ in salt induced hypertension are partly due to inhibiting oxidative stress and inflammation in PVN. Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension. Excessive oxidative stress and inflammation in hypothalamic paraventricular nucleus (PVN) are implicated in the pathogenesis of hypertension. The objective of this study was to investigate the effects of tBHQ in high salt induced hypertension and to identify whether the beneficial effects were induced by inhibiting PVN oxidative stress and inflammation. 28922660: BACKGROUND/AIMS: The kidney plays a critical role in the control of blood pressure and its elevation in salt-induced hypertension. 28927660: In literature, since many decades, it is often believed and condoned that excessive common salt (Nacl) ingestion can lead to hypertension. 28978980: In conclusion, BM ameliorated tubulointerstitial damage in the Ald- and salt-induced hypertension model through suppression of both ROS production and intrarenal renin-angiotensin system activation. 2901269: The inbred S/JR rat is characterized by a genetic predisposition to NaCl-induced hypertension. 2910816: Systemic and regional hemodynamic measurements were determined by the radioactive microsphere technique in conscious and unrestrained rats (kidneys intact) with DOC-salt-induced hypertension that were pair-fed either a normal calcium (0.6% by weight, n = 12) or a calcium-supplemented (high-calcium) diet (2.5% by weight, n = 12). 29109190: PLA2 assay and Western blotting showed that cPLA2 activity was higher in salt-induced hypertension and HC067047 or a Ca2+ chelator inhibited cPLA2 activity. 29130499: Fumarase insufficiencies were associated with increased levels of fumarate, decreased levels of malate and exacerbated salt-induced hypertension. 2920307: To investigate the role of these factors on calcium homeostasis in salt induced hypertension, calcium uptake was measured in aortae of Sprague-Dawley rats by plasma derived from Dahl salt sensitive and resistant rats given high (8.0%) and low (0.4%) salt diets, respectively, for four weeks. 29278541: PURPOSE OF REVIEW: For decades, it has been widely accepted that initiation of salt-induced hypertension involves a type of kidney dysfunction (natriuretic handicap), which causes salt-sensitive subjects to initially excrete less of a sodium load than normal subjects and undergo abnormal increases in cardiac output, and therefore blood pressure. SUMMARY: To advance discovery, prevention, and treatment of primary abnormalities causing salt-induced hypertension, greater research emphasis should be placed on identifying mechanisms mediating subnormal renal vasodilation and abnormally increased renal vascular resistance in response to high-salt diets. Mounting evidence indicates that in most salt-sensitive subjects, renal vasodysfunction, defined as impaired renal vasodilation and abnormally increased renal vascular resistance in response to increased salt intake, in the absence of greater sodium retention than in salt-loaded normal subjects, is involved in initiation of salt-induced hypertension. Here we discuss emerging views that renal vasodysfunction, not natriuretic dysfunction (subnormal sodium excretion), is usually a critical factor initiating salt-induced hypertension. The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced hypertension. 29307050: Role of Acetyl Salicylic Acid in Controlling the DOCA-Salt Induced Hypertension in Rats by Stimulating the Synthesis of r-Cortexin in the Kidney. 2937835: Increased concentration of plasma immunoreactive atrial natriuretic factor in Dahl salt sensitive rats with sodium chloride-induced hypertension. 2953170: In order to assess the possible role of atrial natriuretic peptide (ANP) in the development of deoxycorticosterone (DOCA)-NaCl-induced hypertension, plasma immunoreactive ANP concentration was compared with sodium balance and blood pressure in NaCl- or DOCA-NaCl-treated rats. 2953783: Therefore, our findings do not support the notion that ANF is important in the development or maintenance of chronic salt-induced hypertension in S rats. 29544657: In addition, recent studies in animal models have demonstrated that modest increases in nitrate intake can protect against the initiation of salt-induced hypertension. Functional foods for augmenting nitric oxide activity and reducing the risk for salt-induced hypertension and cardiovascular disease in Japan. 29567533: Our findings provide comprehensive biochemical details about the metabolic responses to a high salt diet, which may contribute to the understanding of renal disease and salt-induced hypertension in SS rats. 29570433: Targeted disruption of regulated endocrine-specific protein ( Resp18) in Dahl SS/Mcw rats aggravates salt-induced hypertension and renal injury. 29604087: Uteroplacental insufficiency temporally exacerbates salt-induced hypertension associated with a reduced natriuretic response in male rat offspring. Salt-induced hypertension was exacerbated in Restricted offspring, reaching a peak systolic pressure of ~175 mmHg earlier than normal weight counterparts. 2964946: Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). 2968870: The results of this study would suggest that the vascular alterations to vasopressin are probably post receptor mediated and result from the DOCA/NaCl-induced hypertension. 2968955: We examined the consequences of genetic susceptibility or resistance to NaCl-induced hypertension and of prior salt loading (high or low NaCl intake) on the responses of isolated perfused Dahl salt-sensitive (DS) and Dahl salt-resistant rat (DR) kidneys to atriopeptin II. The natriuretic response to atriopeptin II was blunted in kidneys from rats genetically susceptible to NaCl-induced hypertension, independently of their NaCl consumption. Therefore, the glomerular filtration rate response to atriopeptin II varied globally with dietary NaCl, independently of genetic predisposition or resistance to NaCl-induced hypertension. 29694982: CONCLUSION: UCP3 protein was involved in the incidence of high-salt induced hypertension and the progression of cardiac dysfunction in the early stages of heart failure. 29710536: Over all, we found that the young leaves of Polygonum hydropiper suppressed salt-induced hypertension. Therefore, we examined the hypothesis that chymase inhibitory dried young leaves of Polygonum hydropiper (PPH) or young leaves extract of Polygonum hydropiper (PHE) could reduce salt-induced hypertension. 2975694: Our data would not permit conclusion as to whether the different capacity of these agents to prevent salt-induced hypertension was due to a different degree of penetration into the central nervous system, or to some other property. Renin-angiotensin and vasopressin in the development of salt-induced hypertension. The purpose of this study was to assess the participation and interaction of the renin-angiotensin system and vasopressin in the early stages of the development of salt-induced hypertension. 2983159: Replacing dietary NaCl with a near equimolar amount of dietary NaHCO3 corrects both the hypercalciuria and the hypertension initially induced by NaCl. In rats given desoxycorticosterone (DOC), the recently reported finding that a normal amount of dietary sodium chloride (NaCl) induces hypertension but an equimolar amount of sodium bicarbonate (NaHCO3) does not, might be a consequence of the differing effects of the two sodium salts on the metabolism of calcium. In accord with this hypothesis, we have found that, in uninephrectomized rats given DOC: Dietary NaCl induces persisting hypercalciuria and hypertension whereas an approximately equimolar amount of dietary NaHCO3 induces neither hypercalciuria nor hypertension. 2990968: Moreover, the absence of sodium regulation of alpha 2-adrenoceptors in SBN rats may be responsible for the resistance to salt-induced hypertension. 3002978: This article proposes the theory that sodium exerts its hypertensive action by decreasing the state of affinity of the alpha 2-adrenergic receptors of the central nervous system for locally occurring agonist neurotransmitters, which results in disinhibition of sympathoinhibitory neurons and leads to the hyperadrenergic state characteristic of salt-induced hypertension. 30048986: Therefore, this study aimed to investigate the mechanisms within RVLM that can influence exercise training induced effects in salt-induced hypertension. METHODS: Male Wistar rats were fed with a normal salt (0.3%) (NS) or a high salt (8%) (HS) diet for 12 weeks to induce hypertension. 30049682: Kidney-specific inhibition of miR-214-3p significantly attenuated salt-induced hypertension and albuminuria in SS rats. 30059752: However, the molecular mechanism of high-salt diet induced hypertension and the serious complications in cardiovascular system still remain unknown. CONCLUSION: Our study provided new insight about molecular mechanism of high-salt induced hypertension and heart and kidney damage. Differential expression gene (DEG) analysis and further functional annotation including Ingenuity Pathway Analysis (IPA) was performed to reveal the molecular mechanism of high-salt induced hypertension and organ injury. 30078015: CONCLUSION: Activation of TRPV1 plays an anti-inflammatory and anti-oxidative stress role in preventing renal tissue damage and salt-induced hypertension after I/R injury, indicating that TRPV1 conveys preconditioning protection that may have therapeutic implication. 3013775: This apparent inability of DS to modulate prostaglandin receptors may contribute to their susceptibility to salt-induced hypertension. 3013968: The density of alpha 1-adrenoceptors was reduced in the left ventricle but not consistently affected in the ventricular septum, right ventricle, or atria of S/JR offspring with NaCl-induced HT. 30290168: Administering DOCA and offering saline to uninephrectomized rats, induced hypertension and associated abnormalities of diastolic dysfunction, CV and renal hypertrophy and fibrosis via activating local renin angiotensin system. To address this, we aimed to determine the effect of deoxycorticosterone acetate (DOCA) -salt (sodium chloride)-induced hypertension on the alterations in renin-angiotensin system, leading to CV and renal dysfunction in uninephrectomized male Sprague Dawley rats. 3031700: In the second experiment, similar rats were assigned to 1 of 3 treatment groups: control diet plus Nphx and Sal, control diet plus Nphx, DOCA and Sal, and Tyr plus DOCA, Nphx, and Sal; however, Tyr was not started until DOCA-salt-induced hypertension developed (4 weeks). 30328008: These results suggest that the increased MAP and sympathetic activity in salt-induced hypertension can be suppressed by blockade of endogenous Ang-(1-7) in the PVN, through modulation of PICs and oxidative stress. This study was designed to determine whether inhibition of Ang-(1-7) in the hypothalamic paraventricular nucleus (PVN) attenuates sympathetic activity and elevates blood pressure by modulating pro-inflammatory cytokines (PICs) and oxidative stress in the PVN in salt-induced hypertension. 30355112: Methods- Intracranial aneurysms were induced by a combination of deoxycorticosterone-salt induced hypertension and a single-dose elastase injection into cerebrospinal fluid in mice. 30390036: Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity. Among the most promising approaches are dietary strategies for reducing the risk for salt-induced hypertension that do not depend on reducing salt consumption in the population. According to this theory, initiation of salt-induced hypertension usually involves abnormal vascular resistance responses to increased salt intake, not greater renal retention of a salt load in salt-sensitive subjects than in normal subjects. By shifting the focus from the historical theory to a contemporary final common pathway for the pathogenesis of salt sensitivity, research from Japan is building the scientific foundation for more effective approaches to the prevention and treatment of salt-induced hypertension. 30401628: Zamicastat (10, 30 and 100 mg/kg body weight) was tested acutely against salt-induced hypertension in the Dahl SS rat. The aim of the present study was to evaluate the effects of zamicastat, a novel DbetaH inhibitor that decreases noradrenaline and increases dopamine levels in peripheral sympathetically innervated tissues, on the hemodynamic and cardiometabolic parameters in salt-induced hypertension and heart failure in the Dahl salt-sensitive (SS) rat. 3108964: Alterations of vascular prostacyclin and thromboxane A2 in Dahl genetical strain susceptible to salt-induced hypertension. 31107610: In the obesity, diabetes, and hypertension triad (ODHT), deregulation of glucose and NaCl homeostasis, respectively, causes diabetes and hypertension. 3157848: Aldosterone binding in the aortae of these rats is contrasted to that of age- and sex-matched rats of the Dahl salt-susceptible strain in an effort to identify a mechanism for resistance to salt induced hypertension. 3164706: Role of pressor prostanoids in rats with angiotensin II-salt-induced hypertension. 3183369: In conclusion, AVP has a compensatory pressor role in SN rats after acute diuresis, with or without salt-induced hypertension, but not in the normal rat. This study was performed to determine if vasopressin has a compensatory pressor role following acute diuresis in both normal rats and in rats with subtotal nephrectomy (SN) or in rats with SN-salt induced hypertension. 3284820: We investigated the status of circulating kinins in rats with severe hypertension caused by drinking 1% NaCl (saline) and treatment with deoxycorticosterone (DOC, 25 mg/kg/wk s.c.) for 5 weeks. 3351295: The relation of cellular sodium to the onset of hypertension induced by DOCA-saline in the rat. 3375267: Pulmonary vascular efflux of norepinephrine in Dahl rats susceptible or resistant to salt-induced hypertension. These data indicate that impaired accumulation and efflux of norepinephrine by the lungs does not contribute to the pathogenesis of hypertension in Dahl S rats. 3379301: These results are discussed in terms of the mechanism of salt-induced hypertension and dehydration natriuresis. 3395338: The aim of this study was to show whether [Ca2+]i is elevated in salt induced hypertension. 3419540: A disturbance of GABA-5-HT interactions between GABA and 5-HT in brainstem sites may also contribute to the pathogenesis of hypertension induced by DOCA/NaCl. Central serotonergic alterations in deoxycorticosterone acetate/NaCl (DOCA/NaCl)-induced hypertension. Treatment with DOCA/NaCl produced changes in the metabolism of 5-HT that may be important in the genesis of hypertension, but are not required for the maintenance of elevated arterial pressure. 3422633: The underproduction of prostaglandin E2 in the papillary collecting tubule of DS may play a role in their inadequate renal natriuretic capacity and contribute to the onset and maintenance of salt-induced hypertension in this strain. 3471900: A diet rich in either monounsaturated or polyunsaturated fatty acids produced a significant lowering of blood pressure compared with the relatively saturated palm-oil diet in NaCl-induced hypertension in Dahl-S rats. 3481633: The calcium agonist BAY K 8644 accelerated the development of salt-induced hypertension in S rats. Calcium antagonism of nifedipine, nitrendipine or nisoldipine prevented salt-induced hypertension, renovascular damage and mortality in Dahl salt-sensitive (S) rats. 3539403: An absence of this compensatory adjustment or plasticity in cardiac baroreflex function in DS rats may predispose to salt-induced hypertension. 3596769: Absence of salt-induced baroreceptor sensitization in DS was not due to the hypertensive state because the sensitization also failed to occur in separate groups of DS in which salt-induced hypertension had been prevented by chemical sympathectomy with 6-OH-dopamine. 3596786: Antihypertensive treatment normalizes decreased endothelium-dependent relaxations in rats with salt-induced hypertension. 3690408: Unilateral nephrectomy, DOCA, plus NaCl resulted in hypertension by increasing arteriolar resistance in a vascular compartment with a fast time constant for venous return. 3721557: Plasma from Dahl rats susceptible to salt-induced hypertension (Dahl S rats) contains inhibitory factors that reduce the release of thromboxane A2 from thrombin-activated platelets. 3731505: However, the results suggest that the central and peripheral cholinergic systems participate in the development of salt-induced HT in the S/JR rat. The effect of atropine or atropine methylnitrate on salt-induced hypertension in the inbred S/JR and R/JR Dahl rat. 3734445: Male Dahl-S rats were randomly assigned to either normal chow (NC) or high-salt (HS) diets to induce hypertension. Effect of exercise on the development of salt-induced hypertension in Dahl-S rats. 3762307: Previously, altered aldosterone binding to corticoid receptor I was found in aortic smooth muscle cells cultured from Fischer 344 rats which are extremely resistant to steroid and salt induced hypertension. Rat models of genetic hypertension include spontaneous hypertension and resistance or sensitivity to mineralocorticoid and salt induced hypertension. 3783445: The Dahl selected rat lines, one susceptible to salt-induced hypertension (DS) and the other resistant to salt-induced hypertension (DR), were subchronically exposed to filtered air, 0.4, 1.4, or 4.0 ppm acrolein. 3793203: The possible role of catecholamines in the abnormal renal response to salt loading, a genetic defect resulting in hypertension in the salt-sensitive strain of Dahl rats, was investigated by measuring the adrenal synthesis of norepinephrine, epinephrine, and dopamine as well as their content in several tissues and the urinary excretion of these catecholamines as well as some of their metabolites at the height of salt-induced hypertension. 3826392: Contribution of AV3V region in anephric NaCl-induced hypertension in the rat. 3884235: Salt-induced hypertension in the 'Sabra' rat strain: influence of nifedipine treatment. Salt diet for 12 weeks resulted in a sustained hypertension and heart hypertrophy only in SBH. 3891618: The role of sodium and sodium chloride in pathogenesis of hypertension is reassessed in the light of new data from epidemiological clinical research, experimental models, and cell physiology investigations. 3910171: Radiofrequency lesions were placed in the anteromedial hypothalamus in Dahl rats to investigate the role of this area in salt-induced hypertension. 3955390: The dynamics of hypothalamic arginine vasopressin (AVP) release was examined during the development of hypertension in rats with deoxycorticosterone (DOCA)-NaCL induced hypertension. 4008866: Sprague-Dawley rats susceptible (DS) to NaCl-induced hypertension suffer higher mortality when exposed daily to 2.0 ppm ozone than do hypertension-resistant (DR) rats, independent of salt in the diet or systemic blood pressure. 4009486: GABAergic inhibition of hypertonic saline-induced vasopressin-dependent hypertension. 4020131: The aim of this work was to look for similar changes in a model of salt induced hypertension, the Dahl salt sensitive (DS) rat, using the sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis. 4039776: How salt causes hypertension: the natriuretic hormone-Na/Ca exchange--hypertension hypothesis. 434186: Essential role of mean circulatory filling pressure in salt-induced hypertension. 4457083: [Ultrastructure of the kidney in salt-induced hypertension]. 477232: Sodium distribution in mesenteric arterial wall of rats with hypertension induced by drinking saline. 488040: Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. 5092176: [Electrolyte changes following a long-term parenteral administration of NaCl to rabbits. Pathogenesis of salt hypertension]. 535885: Prevention of NaCl-induced hypertension in Dahl 'S' rats with thiazide. 5477379: Sympathetic nerve function and DOCA-NaCl induced hypertension. 551897: The absence of salt-induced hypertension was observed regardless of whether the animals were anesthetized with ether or pentobarbital or had the blood pressures determined in an unanesthetized state. 5594457: [Taste threshold for NaCl, its genetic bond and possible significance in the etiology of hypertension]. 5636623: Tissue electrolyte alterations with hypertension induced by L-triiodothyronine and salt. 5671482: Adrenal plasma levels of corticosterone and deoxycorticosterone in methylandrostenediol-salt induced hypertension (1). 5766945: We suspect that this correlation exists only during the period when cortical tissue is regenerating; it does not exist among intact animals with and without hypertension induced by salt. 5870364: Effects of hypertension induced by norepinephrine and sodium chloride upon the arteries and various organs of rats. 5903139: Salt-induced hypertension in the dog. 5970317: Salt hypertension induced by drinking saline and the effect of different concentrations of sucrose and maltose upon its development. 6027929: Plasma levels of corticosterone in methylandrostenediol-salt-induced hypertension. 6084117: In contrast, the marked decrease in cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension. 6085890: Although an increased calcium influx seems to be involved in salt-induced hypertension, the presence of high sodium chloride is apparently essential for its development. 6093159: Changes in arterial collagen synthesis and the effects of P-1894B, a potent inhibitor of prolyl hydroxylase, were investigated on rat hypertension, induced by deoxycorticosterone acetate (DOCA) and salt. 6100736: Conversely, the marked decrease of cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension. 6100744: Replacing dietary NaHCO3 with a near equimolar amount of NaCl induced hypertension. 6111849: Cerebral aneurysms were induced in rats treated with unilateral ligation of the common carotid artery and hypertension produced by renal infarction with or without beta-aminopropionitrile, one of the lathyrogens. In this experiment, cerebral aneurysms developed more frequently than in the previous experiments in which hypertension induced by deoxycorticosterone and salt had been used. 6114922: This defect augments responses to pressor stimuli and may contribute to the development of salt-induced hypertension in the Dahl strain. 6115031: Whole brain tyrosine hydroxylase activity during the development of deoxycorticosterone acetate-1% sodium chloride-induced hypertension in rats. 6117975: Regional aortic differences in atherosclerosis-susceptibility: changes in prostaglandin biosynthesis and cholesterol accumulation in response to desoxycorticosterone (DOCA)-salt induced hypertension. 6136351: The second animal model examined was the deoxycorticosterone/salt-induced hypertension (DOCA) in uninephrectomized rats. 6141125: [Effects of several beta-blockers and penfluzide, a thiazide diuretic, on the blood pressure, urinary water output and excretion of Na and K in DOCA-saline-induced hypertension in rats]. 6243503: Pain sensitivity was studied in renal and DOCA-salt hypertensive rats, and in two strains of rats derived from the same parental strain for their sensitivity (H) or immunity (N) to hypertension induced by DOCA-salt treatment. 6325798: The role of a natriuresis in the protective effect of potassium against the development and maintenance of salt-induced hypertension was studied. 6345356: Three models of hypertension are discussed: 1) deoxycorticosterone-salt (DOCA-salt)-induced hypertension; 2) low-renin (presumably volume expanded) renal hypertension (LRRH); and 3) the spontaneously hypertensive rat (SHR) of the Okamoto-Aoki Kyoto-Wistar strain and its normotensive genetic control (WKY). 6467642: Contractile responses to norepinephrine (NE) of strips of vasa deferentia from prostatic end isolated from rats with genetic hypertension and deoxycorticosterone (DOC)-salt induced hypertension were examined. 6495330: Carbon monoxide exposures affected blood pressure only in DS rats fed a high NaCl diet, where it enhanced the development of NaCl-induced hypertension. The influence of carbon monoxide (CO) on the development of systemic hypertension was studied in Dahl rats selectively bred for susceptibility (DS) and resistance (DR) to NaCl-induced hypertension. 6543221: Also strips from regular normotensive Wistar rats (NWR) which failed to develop hypertension after deoxycorticosterone (DOC)-salt treatment (DNR) were compared to those from NWR with DOC-salt induced hypertension (DHR). 6599690: Neural mechanisms contribute to salt-induced hypertension in Dahl salt-sensitive (DS) rats. 6628892: Two lines of Dahl rats, one resistant to salt-induced hypertension (DR) and one susceptible to salt-induced hypertension (DS) were subchronically exposed to SO2 (50 ppm, 6 hr/d, 5 d/wk for 31 weeks) or ozone (2.0 ppm, 6 hr/d, 5 d/wk for 20 weeks). 6662415: [Antihypertensive action of K in rats with DOCA-salt-induced hypertension]. 6681043: Membrane abnormalities occur in vascular smooth muscle but not in non-vascular smooth muscle from rats with deoxycorticosterone-salt induced hypertension. 6729836: The Dahl selected rat lines, one susceptible to salt-induced hypertension (DS) and the other resistant to salt-induced hypertension (DR), were exposed to filtered air, 0.4, 1.4, or 4.0 ppm acrolein for 6 h/day, 5 days/week for 62 days. 6822291: Nitrendipine is highly effective in normalizing blood pressure, reducing heart hypertrophy, and preventing mortality in salt-related hypertension (two-kidney renal hypertension, salt-induced hypertension in Dahl rats), which are rather refractory to the effect of vasodilators. 6827908: Salt-induced hypertension in chronic renal failure: evidence for a neurogenic mechanism. 6848463: The age factor and salt-induced hypertension in the Brattleboro rat. 6862570: Previous studies have shown that a combination of avoidance conditioning schedules and increased intake of salt and water results in progressive hypertension in dogs within 14 days. 6862573: Hypothalamic pressor responses and salt-induced hypertension in Dahl rats. 688554: Subpressor angiotensin infusion, renal sodium handling, and salt-induced hypertension in the dog. 7018493: Plasma renin activity (PRA) was studied in the rats bred by Dahl for susceptibility (S-strain) or resistance (R-strain) to salt (NaCl) induced hypertension. A qualitative difference in plasma renin activity in Dahl rats susceptible or resistant to salt-induced hypertension. 7068202: Vasopressin in salt-induced hypertension of experimental renal insufficiency. 7116668: These experiments were intended to elucidate the role of central mechanisms in the maintenance of high blood pressure produced by deoxycorticosterone (DOC) and salt in rats. 7124969: The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. 7137945: The effects of LA on hypertension of SHR appear to be opposite to those observed during salt-induced hypertension. 7152633: The Brattleboro rat and salt-induced hypertension. 7246746: Role of vasopressin, catecholamines, and plasma volume in hypertonic saline-induced hypertension. 7249877: We conclude that diabetic rats have no greater susceptibility to salt-induced hypertension than rats receiving only salt. 7250299: Recognising on the one hand the interaction between the coagulation system and the vessel wall and on the other hand the fibrinolysis-blocking properties of EACA, it can be assumed that derangements of the coagulation system are aetiologically involved i hypertension induced by salt/DOCA. The development of hypertension induced by DOCA/salt in rats can be reduced by epsilon-aminocaproic acid. 7290277: Combined nephritis-DOCA-NaCl resulted in severe hypertension and shortened life span, whereas nephritis-NaCl combination failed to induce hypertension or shorten life span. 7318356: Paraventricular--suprachiasmatic lesions prevent salt-induced hypertension in Dahl rats. 7318357: These results show that NaCl-induced hypertension in Dahl salt-sensitive rats requires the integrity of the central nervous system catecholaminergic neurones and the paraventricular nuclei for its full expression. 7389263: Parathyroid hormone- and deoxycorticosterone acetate-induced hypertension in the rat. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 742305: The influence of a linoleic acid-rich diet and of acetyl salicylic acid on NaCl induced hypertension, Na+--and H2O-blance and urinary prostaglandin excretion in rats. 7437522: Previous studies showed that aortic strips from rats with either spontaneous (SHR) or DOCA/salt-induced hypertension developed less stress (force/area) in response to noradrenaline (NA) when compared to aortic strips from normotensive rats. 7449256: By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. 7449267: Rats genetically sensitive to salt-induced hypertension showed higher levels of plasma noradrenaline and adrenaline than rats genetically resistant to hypertension. 7462901: Cadmium enhanced the rate and the degree of salt-induced hypertension development. These data indicate that differences in genetic background influence the development of cadmium-induced hypertension in weanling rats, and that cadmium exacerbates the severity of salt-induced hypertension. 7503314: To determine whether abnormal cellular Ca2+ handling is involved in salt-induced hypertension of Dahl salt-sensitive rats (DS), we investigated Ca2+ handling in fura 2-loaded platelets of DS and Dahl salt-resistant rats (DR) fed a high-NaCl (8%) or a low-NacL (0.3%) diet for 4 wk from 5 wk of age. 7508060: Oxygen radical scavengers and renal protection by indapamide diuretic in salt-induced hypertension of Dahl strain rats. 7546624: In salt-induced hypertension NO production may be impaired. 7581263: The modulation of alpha 2-adrenoceptors by a high salt intake may be essential particularly in the early phase of the development of salt-induced hypertension. AIM: To clarify the role of those factors in the sympathetic nervous system, we examined the regulation of alpha2-adrenoceptors in the lower brainstem and the renal tubular basolateral membranes simultaneously during the development of salt-induced hypertension in Dahl-Iwai salt-sensitive rats. 7609515: Lacidipine is a second-generation 1,4-dihydropyridine calcium antagonist, whose potent and long-lasting antihypertensive properties prompted us to investigate whether its chronic administration to Dahl-S rats prevented salt-induced hypertension, vasculopathy, and accelerated mortality. 7611490: In conclusion, a continuous infusion of L-arginine prevented both the changes in the pressure-natriuresis relationship and the development of salt-induced hypertension in Dahl S rats. The aim of this study was to determine the role of nitric oxide (NO) in the development of salt-induced hypertension in the Brookhaven strain of Dahl rats. 7734140: The study examined the effect of salt-induced hypertension on vascular relaxation in response to magnesium sulphate during pregnancy. The mechanism of relaxation in response to magnesium by the aorta of pregnant rats with salt-induced hypertension. The results suggest that the relaxation of isolated rat aortic rings contracted with phenylephrine is enhanced in pregnant rats with salt-induced hypertension. 7759856: Such a mechanism might underlie a predisposition to hypertension-induced organ damage seen in Dahl-S rats with salt-induced hypertension. 7768565: Studies in animals suggest that nitric oxide production is increased under conditions of salt loading and that this increase protects against the development of salt-induced hypertension. 7814850: OBJECTIVE: To investigate whether and how renin-angiotensin inhibition attenuates renal injury seen in salt-induced hypertension in Dahl salt-sensitive (Dahl-S) rats. 7850963: Direct measurements of endothelium-derived nitric oxide release by stimulation of endothelin receptors in rat kidney and its alteration in salt-induced hypertension. 7915651: Norepinephrine (NE) infused at doses of 0.7, 2.2 and 6.7 micrograms/min/kg body weight into conscious, salt and water loaded ducks dose-dependently induced arterial hypertension, reflex bradycardia and diuresis/natriuresis at unchanged glomerular filtration and reduced renal blood flow. 7963490: CONCLUSION: These results suggest that taurine is an effective antihypertensive agent for salt-induced hypertension. RESULTS: Administration of taurine (3% in drinking water) for 4 weeks retarded the development of salt (4% sodium chloride diet)-induced hypertension. Taurine amplifies renal kallikrein and prevents salt-induced hypertension in Dahl rats. 7966936: [Role of centro-renal noradrenergic systems in the development of salt-induced hypertension]. 7995636: We investigated whether long-term infusion of kallikrein would attenuate renal injury in salt-induced hypertension in Dahl salt-sensitive rats. 8021475: DESIGN: The relationship between blood pressure and membrane dynamics was investigated in erythrocytes from three different rat strains with experimental hypertension, namely two models of salt-induced hypertension (Sabra and Dahl rats) and Lyon hypertensive rats with spontaneous hypertension. 8030619: Antihypertensive property and renal protection by shichimotsu-koka-to extract in salt-induced hypertension in Dahl strain rats. We determined whether or not the kampo formula, Shichimotsu-koka-to extract, attenuates the development of salt-induced hypertension and provides renal protection against hypertensive injury in Dahl salt-sensitive (Dahl S) rats. 8069408: These experiments demonstrate that chronic administration of RO 40-5967 potentiates endothelium-dependent relaxations in arteries from animals with salt-induced hypertension. 8091016: Enhanced sensitivity to salt-induced high blood pressure in diabetes mellitus. The enhanced state of vascular reactivity in the diabetic rats was probably responsible for their enhanced sensitivity to salt-induced high blood pressure. Salt-induced high blood pressure in diabetic rats was compared with that in non-diabetic (control) rats. 8097749: OBJECTIVE: To investigate the effects of a salt diet and of salt-induced hypertension on hepatic atrial natriuretic peptide (ANP) receptors in Dahl salt-resistant (DR) and Dahl salt-sensitive (DS) rats. 8141153: Calcium restriction accelerates salt-induced hypertension in young spontaneously hypertensive rats. These results indicate that Ca restriction accelerates salt-induced hypertension in young spontaneously hypertensive rats, and the cellular impairment in vascular smooth muscle might, at least in part, participate in the enhanced blood pressure elevation under this condition. 8144221: Sodium chloride-induced hypertension may be due in part to calcium wasting and subsequent elevation of calcium-regulating hormones. 8157859: The effects of high sugar diets on SBP were not due to angiotensin II inhibition, however, decreased availability of vasodilatory prostaglandins may play a role in the renal events and sugar-induced hypertension in SHR. OBJECTIVE: We examined whether sugar-induced systolic blood pressure (SBP) elevations in rats may develop, in part, through a mechanism common to salt-induced hypertension, i.e., renal retention of water and salt. CONCLUSIONS: Salt and water retention occur early during sugar-induced hypertension due to reduced renal excretion, consistent with some part in the pathogenesis. 8206572: That pressor and aortic constrictor responsiveness to L-NAME are increased after aortic coarctation suggests that a mechanism of vasodilation, mediated by nitric oxide, is preferentially manifested in rats with aortic coarctation-induced hypertension. NG-Nitro-L-arginine methyl ester (L-NAME) (3 x 10(-4) mol/L) increased tension (82 +/- 11% of the response to 120 mmol/L potassium chloride) in rings of thoracic aorta taken from hypertensive rats 7 to 14 days after aortic coarctation, whereas rings of abdominal aorta from below the coarctation were unresponsive, as were rings of thoracic aorta from rats with deoxycorticosterone-salt-induced hypertension and from the corresponding normotensive controls of either model of hypertension. 8206579: Salt-induced hypertension in normotensive spontaneously hypertensive rats. 8307708: These results suggest that a hyperresponsiveness to the actions of blood-borne or tissue oxygen could contribute to increased arcade arteriolar tone in the spinotrapezius muscle of Dahl rats with salt-induced hypertension. 8343228: These data indicate that cicletanine is an antioxidant that protects the kidney from salt-induced hypertension in Dahl salt-sensitive strain rats. 8479344: Enhanced arteriolar vasomotion in rats with chronic salt-induced hypertension. Therefore, cyclic variations in arcade arteriole diameter are normally limited by basal nitric oxide, and the enhancement of these variations in animals with salt-induced hypertension may be attributable to the loss of this nitric oxide influence. 8500974: In addition, distal arteriole rarefaction (functional or structural) does not contribute to increased spinotrapezius muscle resistance at this stage of salt-induced hypertension. 8541008: To examine that possibility, we assessed the depressor responses to Digibind, an antibody Fab directed against digoxin, in a volume-dependent model--DOCA-salt-induced hypertension in rats. 8557966: CONCLUSION: The integrity of the brain renin-angiotensin system is necessary for the development of salt-induced hypertension in DIS rats. OBJECTIVE: To examine the role of brain angiotensin II in the development of salt-induced hypertension in Dahl-Iwai salt-sensitive (DIS) rats. 8569214: To determine whether the vasopressor and antidiuretic actions of arginine vasopressin (AVP) may participate in the development of salt-induced hypertension, we examined the long-term effects of AVP V1 and V2 receptor antagonists on blood pressure (BP) in Dahl-Iwai salt-sensitive (DS) and salt-resistant (DR) rats. Our results indicate that even if AVP plays a role in salt-induced hypertension peripheral blockade of either subtype of AVP receptors does not prevent the development of hypertension in DS rats. Effects of vasopressin V1 and V2 receptor antagonists on the development of salt-induced hypertension in Dahl rats. 8576787: In salt-induced hypertension, nitric oxide production may be impaired. 8698443: In sabra rats sensitive (n=6) or resistant (n=6) to salt-induced hypertension and maintained on a normal salt diet, the percentage and level of each receptor subtype mRNA in cortex and outer stripe were similar in the two strains and comparable to those observed in Sprague-Dawley rats. 8747306: We examined the role of central GABAergic mechanisms in salt-induced hypertension and exaggerated responses to stress in borderline hypertensive rats (BHR), the first offspring of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Central GABAergic mechanisms are defective in salt-induced hypertension in borderline hypertensive rats. 8761026: The results suggested that marked changes in electrolyte levels of erythrocytes, serum, heart and kidney tissues in NaCl loaded rats may play a definite role in the development of salt induced hypertension. 8777835: Since they display several of the characteristics of salt-sensitive hypertensive humans, i.e. salt retention, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II are an appropriate model of human salt-induced hypertension. 8799479: These results demonstrate that AT III has preventive action against salt-induced hypertension and proteinuria in pregnancy through a mechanism largely independent of its anticoagulant action. 8808210: DOCA-NaCl treatment causes hypertension, accelerates development of proteinuria, and leads to glomerulosclerosis in rats with autoimmune Heymann nephritis. Thus in autoimmune Heymann nephritis, DOCA-NaCl treatment causes hypertension and increased renal mass together with upregulation of local cytokine and growth factor production, which may further aggravate hypertension and accelerate progression of renal damage. To study the mechanisms of kidney injury induced by renal haemodynamic load in chronic nephritis, we studied by immunohistochemistry the local expression of various cytokines, growth factors and adhesion molecules in the kidneys of Heymann nephritic rats with or without DOCA-NaCl-induced hypertension. 8822232: The results suggest that MaxEPA can attenuate salt-induced hypertension, reduce salt-induced mortality and protect the integrity of kidney NBMPR binding sites in salt-induced hypertension. 8851168: These findings indicate that cholesterol feeding strikingly enhances the impaired endothelium-dependent relaxations and the slightly impaired endothelium-independent relaxations in the aorta of DS rats with salt-induced hypertension, parallel to the development of hypertension, hypercholesterolemia and cholesterol deposition. 8888962: This study demonstrates the effects of hypertension produced by deoxicorticosterone acetate (DOCA) and salt load on the extensor digitorum longus (EDL) and soleus muscles of the rat. 8931838: Thus, hyporeactivity to insulin may play a role in the development of salt-induced hypertension in young SHR, possibly through a reduced suppression of norepinephrine overflow from sympathetic nerve endings. To determine how the effect of insulin is related to the development of salt-induced hypertension, and whether a hyporesponse to insulin exists in the peripheral sympathetic nerves of a hypertensive model rat, we measured norepinephrine overflow from the periarterial nerve of isolated mesenteric arteries exposed to insulin in spontaneously hypertensive rats (SHR) as well as Wistar-Kyoto rats (WKY) fed diets that were high and low in salt. 8969897: The effect of 19-ethynyldeoxycorticosterone was dose dependent, with the lower doses preventing salt-induced hypertension and the higher doses having no effect or increasing the blood pressure. 8982436: We investigated whether the Chinese herbal remedy, Hachimi-jio-gan extract, attenuates the renal injury seen in salt-induced hypertension in Dahl salt-sensitive (Dahl S) rats. These data suggest that Hachimi-jio-gan extract exhibits an antihypertensive effect, which is associated with partial resolution of renal injury in salt-induced hypertension. 8986457: Restoration of endothelial cell function by chronic cicletanine treatment in Dahl salt-sensitive rats with salt-induced hypertension. 8998253: These data indicate that adenosine A1 receptor antagonism reduces salt-induced hypertension and the consequent renal injuries. 9028581: The aim of our study was not only to search for the occurrence of such alterations in platelets of rats with salt-induced hypertension but also to investigate whether these changes might precede blood pressure rise in this form of experimental hypertension. 9039143: Cardiopulmonary baroreflex in NaCl-induced hypertension in borderline hypertensive rats. To determine whether decreased cardiopulmonary baroreflex sensitivity, as seen in other models of NaCl-induced hypertension, develops later in the course of the disease, we studied an older backcross population derived from borderline hypertensive rats and Wistar-Kyoto rats. Attenuated renal sympathoinhibition during acute increases in intravascular volume is not involved in the development or maintenance of NaCl-induced hypertension in borderline hypertensive rats. 9072378: These results suggest that hypercholesterolaemia causes greater impairment of endothelium-dependent relaxation in rat aorta with salt-induced hypertension than genetic hypertension. 9098545: These results indicate that salt-induced hypertension in Dahl salt-sensitive rats is not associated with enhanced responsiveness of the RVLM to EAA. 9139995: Thus the supplementation of L-arginine prevented the increase in blood pressure in S rats on a high-salt diet and normalized the abnormality of renal hemodynamics accompanying salt-induced hypertension. 9160787: We investigated whether long-term infusion of kallikrein would attenuate renal injury in salt-induced hypertension in Dahl salt-sensitive (Dahl S) rats. 9160788: It is suggested that the disturbance in the production of nitric oxide may induce salt-sensitive hypertension and the abnormality of renal hemodynamics in the S rats. Thus, the supplementation of L-arginine normalized the abnormality of renal hemodynamics accompanying salt-induced hypertension. 9160791: Multivariate analysis revealed that activity of the renin-angiotensin system is an independent risk factor to glomerular injury in salt-induced hypertension. To test this hypothesis, we investigated, using Dahl salt-sensitive (Dahl S) rats, whether subpressor dose of Ang II progresses to cardiovascular injury observed in salt-induced hypertension. 9181257: We investigated the role of lipid metabolism in renal protection by chronic cicletanine treatment in Dahl salt-sensitive (Dahl S) rats with salt-induced hypertension. Lipid metabolism and renal protection by chronic cicletanine treatment in Dahl salt-sensitive rats with salt-induced hypertension. Thus, it is suggested that cicletanine treatment lowers the levels of LDL cholesterol in Dahl salt-sensitive rats, and that besides blood pressure reduction, this decrease in LDL cholesterol level contributes, in part, to regression of glomerular injury in salt-induced hypertension. 9181258: Further studies to characterize this factor and its possible relation to salt-induced hypertension are warranted. 9220272: We investigated the effects of the immunosuppressant HR-325 on arterial lesions in Dahl rats with salt-induced hypertension. 9228552: Infusion of ebelactone B, (a selective inhibitor of carboxypeptidase Y-like exopeptidase, a kininase in rat urine), to normal BN-Ki rats during induction of hypertension with DOCA and salt, resulted in the reduction of the raised blood pressure, indicating that a site of action of kinins was at the luminal membrane of the renal tubule cells. 9270081: Preventive effect of iganidipine on renal and cerebral injuries in salt-induced hypertension. 9275484: OBJECTIVE: To determine the effect of area postrema AP on DOCA-salt induced hypertension in rat, with emphasis on renal hemodynamics. [Role of area postrema on DOCA-salt induced hypertension in rat]. 9288538: It may be a secondary phenomenon of salt induced hypertension. 9294102: 25 d after the induction of severe hypertension with deoxycorticosterone acetate and salt, proteinuria, impaired glomerular filtration rate, and extensive vascular and glomerular injury were observed in the Brown Norway donor kidneys, but not in the SHR-RT1.N kidneys. 9314425: The molecular mechanisms of salt sensitivity and the contribution of the kidney to salt-induced hypertension in Sabra rats are imperfectly defined. 9336391: Structure and function of small arteries in salt-induced hypertension: effects of chronic endothelin-subtype-A-receptor blockade. 9353164: In this study, we examined the time course changes in the glomerulus associated with salt-induced hypertension using the inbred Dahl salt-sensitive rats. These findings indicate that salt-induced hypertension accelerates the age-dependent progression of glomerulosclerosis in Dahl salt-sensitive rats, and fibronectin may play a role in the pathogenesis, development, and progression of glomerulosclerosis associated with salt-induced hypertension. Progression of glomerulosclerosis, renal hypertrophy, and an increased expression of fibronectin in the renal cortex associated with aging and salt-induced hypertension in Dahl salt-sensitive rats. This age-dependent progression was further accelerated by the co-existence of salt-induced hypertension in the high salt diet group. 9447248: Cardiac hypertrophy was produced in the Dahl S but not R rat through NaCl-induced hypertension. 9453334: These data suggest that in subtotal nephrectomy-salt-induced hypertension, CGRP may play a compensatory depressor role in an attempt to lower the elevated blood pressure. 9453352: These results suggest that ET-1 acts as a local mediator of vascular dysfunction and aortic hypertrophy in Dahl salt-induced hypertension. 950759: The administration of DOC to rats with unilateral nephrectomy resulted in more distinct hypertension than in those with both kidneys preserved. [Renal prostaglandins in DOCA-sodium chloride-induced hypertension in rats]. 9529170: Intra-abdominal hypertension was induced by saline infusion and maintained for 30 minutes. 9582108: Ouabain has been isolated as an endogenous pathogenetic factor in salt-induced hypertension and has been shown to be rich in the adrenals. 9622141: Thus, sodium chloride may directly induce AT1 receptor upregulation in vitro as well as in vivo; this suggests a potential mechanism participating in salt-induced hypertension because the AT1 receptor activation is tightly coupled to blood pressure regulation. 9683039: In conclusion, the salt-induced high blood pressure of salt-sensitive Sabra rats is not associated with hyperinsulinemia and insulin resistance. This possibility has been tested in this study on Sabra rats, an animal model of salt-induced hypertension. 9744523: Spontaneously hypertensive rats did not have low plasma 25-hydroxyvitamin D concentrations, suggesting that reduction of plasma 25-hydroxyvitamin D concentration might be specific to salt-induced hypertension. 9784919: To investigate whether the kidney releases a hypertensinogenic factor for developing salt-induced hypertension in S rats, we examined a pressor effect, or vascular contractive activity of a kidney extract from S rats using a conscious recipient rat or an isolated aortic ring. These results suggest that the kidney of S rats may not release an active hypertensinogenic factor that would cause salt-induced hypertension. 9791089: Studies were designed to examine the effects of renal medullary interstitial infusion of L-arginine (L-Arg) on the development of high-salt-induced hypertension in Dahl salt-sensitive/Rapp (DS) rats. The same amount of L-Arg that prevented salt-induced hypertension in DS rats when infused into the renal medulla (300 micrograms . kg-1 . min-1) failed to blunt salt-induced hypertension when administered intravenously to DS rats. 9822451: Increased kidney xanthine oxidoreductase activity in salt-induced experimental hypertension. 9877424: Possible mechanisms of salt-induced hypertension in Dahl salt-sensitive rats. To further understand the mechanisms involved in salt-induced hypertension, cardiovascular, hemodynamics, and biochemical parameters in Dahl salt-sensitive rats were evaluated in animals on high- and low-sodium diets. 9931075: Role of the alpha2B-adrenergic receptor in the development of salt-induced hypertension. 9931158: We conclude that functional abnormalities in DS rat kidneys may cause retention of NaCl and that an increased blood-brain barrier permeability to NaCl may enhance its access to sites in the brain that are then activated and induce hypertension. Handling 22NaCl by the blood-brain barrier and kidney: its relevance to salt-induced hypertension in dahl rats. 9933754: CONCLUSION: Long-term infusion of subdepressor dose of rat urinary kallikrein attenuates functionally and morphologically the progression of renal injury in Dahl rats susceptible to salt-induced hypertension, and that the protection is mediated by stimulation of bradykinin B2 receptor. 11211741: Salt-induced hypertension experiment using alpha 2B-KO and alpha 2C-KO revealed that alpha 2B AR subtype is necessary to raise BP in response to dietary salt loading. 11243307: Thus, chronic consumption of a high salt diet resulted in moderate HTN in normotensive Sprague-Dawley rats. Consumption of a high salt diet for 3 weeks induced hypertension (HTN) (158 +/- 6 v 115 +/- 5 mm Hg, P < .01) and widespread downregulation of iNOS expression in renal cortex, renal medulla, aorta, and heart. 11370798: These data suggest that salt-induced hypertension and salt-induced alterations in the vitamin D endocrine system of male S rats do not affect the calciuric response to dietary salt. 11948016: Exogenous 24,25-dihydroxycholecalciferol (24,25-(OH)(2)D(3)), administered at a level that increased plasma 24,25-(OH)(2)D concentration to five times normal, did not attenuate the salt-induced hypertension of salt-sensitive rats. 15633617: On the other hand, risk factors such as an increased BMI, smoking, alcohol abuse, lack of exercise and a diet high in salt and fatty foods can themselves play an instrumental role in the etiology of hypertension. 1599633: However, increases in the availability and consumption of dietary salt have raised concerns that excessive intakes may cause hypertension. Among the topics we examine are the effects of salt on fluid and electrolyte homoeostasis; potential mechanisms of salt-induced hypertension; the epidemiology of salt intake and blood pressure; the effects of salt restriction and supplementation on blood pressure regulation; the potential roles of sodium and chloride ions, as well as interactions with dietary potassium, calcium, and magnesium; current theories of salt sensitivity; the clinical risks of dietary salt depletion; and the dietary sources of salt. 16647629: These data suggest that Nox activation may not be the sole factor or alternatively, that a constitutively active isoform of Nox is involved in oxidative stress mechanism that is associated with dietary salt or ANG II-induced hypertension. To examine the hypothesis that NAD(P)H oxidase (Nox)-derived superoxide generation is involved in the development of angiotensin II (ANG II)-induced hypertension, we evaluated the responses to ANG II infusion (65 ng/min; osmotic mini-pump) for 2 weeks in rats treated with or without apocynin (APO) (inhibitor of Nox subunits assembly) in drinking water (12 mmol/L). 17203116: INTRODUCTION: The mechanisms responsible for genesis of salt-induced hypertension and its prevention by dietary calcium supplementation are still not clear. 18330898: Maternal and infantile dietary salt exposure may cause hypertension later in life. 19079278: These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. The time course of salt-induced hypertension, and why it matters. 19420288: These results suggest that VEGF receptor inhibition enhances dietary salt-induced hypertension and kidney injury, possibly by direct damage on renal cells and decreasing NO production by eNOS. Vascular endothelial growth factor receptor inhibitor enhances dietary salt-induced hypertension in Sprague-Dawley rats. 19786377: Excess dietary salt is a well established cause of high blood pressure and vascular disease. 19806432: Fructose and moderately high dietary salt-induced hypertension: prevention by a combination of N-acetylcysteine and L-arginine. 19811354: Moreover, excessive salt (8% salt diet: 8 weeks)-induced hypertension and proteinuria was accelerated in HF-fed rats. Salt sensitivity of blood pressure (BP) is speculated to be a characteristic in obesity-induced hypertension. 20596792: In this model, a high-salt diet induced high blood pressure and increased ghrelin levels but reduced food intake. 21642952: RESULTS: In rats injected with control shRNA, high-salt diet (HS) caused higher systolic blood pressure compared with normal-salt diet (NS) (HS:149 +/- 4 mmHg; NS:126 +/- 2 mmHg, P<0.05). 22058154: Excess dietary salt is a major cause of hypertension. 22261579: CONCLUSION: We found that long-term miso soup drinking attenuates the blood pressure increase in salt-induced hypertension with organ damage. 23029690: High-salt diet may cause hypertension. 2347624: High salt induced hypertension in young and adult but not in old DS rats although red blood cell Na+ was slightly increased in all age groups of DS rats fed a high salt diet. 24047246: OBJECTIVES: We investigated the antihypertensive mechanism of long-term Miso soup consumption in Dahl salt-sensitive (Dahl S) rats with salt-induced hypertension. CONCLUSIONS: Long-term consumption of Miso soup attenuated blood pressure elevation in Dahl salt-sensitive rats with salt-induced hypertension. 24322818: RESULTS: Eighty-three percent of adults strongly agreed or agreed that most of the sodium we eat comes from packaged, processed, store-bought, and restaurant foods, and 93.0% thought that a high-salt diet could cause hypertension. 24535442: The intrarenal generation of active glucocorticoid by 11betaHSD1 stimulates Na(+) reabsorption; failure to downregulate the enzyme during adaption to high dietary salt causes salt-sensitive hypertension. 2459549: These results could mean that dietary salt loading eventually increases sympathetic activity and thereby induces hypertension by stimulating the ventromedial hypothalamus. 25452472: We found that hypertension and renal injury induced by a high-salt diet were substantially attenuated in Dahl SS/JrHsdMcwiCrl (SS/Crl) rats that had been maintained for many generations on the grain-based 5L2F diet compared with SS/JrHsdMcwi rats (SS/Mcw) maintained on the casein-based AIN-76A diet (mean arterial pressure, 116+/-9 versus 154+/-25 mm Hg; urinary albumin excretion, 23+/-12 versus 170+/-80 mg/d). Together, the data suggest that maternal diet during the gestational-lactational period has substantial effects on the development of salt-induced hypertension and renal injury in adult SS rats. Conversely, salt-induced hypertension and renal injury were significantly attenuated in rats developed from SS/Mcw embryos transferred to SS/Crl surrogate mothers. Salt-induced hypertension and renal injury were substantially exacerbated in rats developed from SS/Crl embryos transferred to SS/Mcw surrogate mothers. 25617698: BACKGROUND: The study was designed to explore the significance of endogenous H2S in the development of high-salt-induced hypertension in rats. Down-regulated CBS/H2S pathway is involved in high-salt-induced hypertension in Dahl rats. METHODS: High-salt-induced hypertension rat model was made by feeding Dahl rat high-salt diet containing 8% NaCl for 8 weeks with SD rats as control. 25631641: The results showed that the edible salt induced hypertension, but the SPS did not. 25878490: PURPOSE: High intake of dietary salt increases extracellular osmolarity, which results in hypertension, a risk factor of neovascular age-related macular degeneration. 25991719: These mice exhibit enhanced pressor responses to CSF [Na(+)] as well as dietary salt-induced hypertension which both can be blocked by central infusion of the ENaC blocker benzamil. 26038832: Male Sprague Dawley rats were fed with a normal salt diet (NS, 0.3%) or a high salt diet (HS, 8%) for 8 weeks to induce hypertension. 26238503: In the present study, the effects of Yiqi Huaju formula (YQ; a compound used in traditional Chinese herbal medicine) were observed in salt-sensitive hypertension, which was induced by a high-salt and high-fat (HSF) diet and the potential mechanism was investigated. 26261587: Salt-sensitive hypertension was successfully induced by 12-week high salt diet in BHR model. 27452860: The purpose of this work was to know if oral administration of anti-oxidant and free-radical scavenger CoQ10 may attenuate high salt-induced hypertension via regulating neurotransmitters and cytokines in the hypothalamic paraventricular nucleus (PVN). Adult male Sprague-Dawley (SD) rats were fed with a normal salt diet (NS, 0.3% NaCl) or a high salt diet (HS, 8% NaCl) for 15 weeks to induce hypertension. 27457879: The protective effect of a buckwheat-enriched diet on renal injury in high salt-induced hypertension in rats. An excess of dietary salt is the most common factor that contributes to the pathogenesis of hypertension. 2747426: Dietary N-6 and N-3 fatty acids and salt-induced hypertension in the borderline hypertensive rat. 27628063: High intake of dietary salt increases extracellular osmolarity resulting in systemic hypertension. 28730828: A high-salt diet induces hypertension in the salt-sensitive strain, but not in the salt-resistant strain. The high-salt diet led to salt-induced hypertension, but did not affect the level of adult neurogenesis in the dentate gyrus of the hippocampus. 29544657: In addition, recent studies in animal models have demonstrated that modest increases in nitrate intake can protect against the initiation of salt-induced hypertension. Functional foods for augmenting nitric oxide activity and reducing the risk for salt-induced hypertension and cardiovascular disease in Japan. 2983159: Replacing dietary NaCl with a near equimolar amount of dietary NaHCO3 corrects both the hypercalciuria and the hypertension initially induced by NaCl. In rats given desoxycorticosterone (DOC), the recently reported finding that a normal amount of dietary sodium chloride (NaCl) induces hypertension but an equimolar amount of sodium bicarbonate (NaHCO3) does not, might be a consequence of the differing effects of the two sodium salts on the metabolism of calcium. In accord with this hypothesis, we have found that, in uninephrectomized rats given DOC: Dietary NaCl induces persisting hypercalciuria and hypertension whereas an approximately equimolar amount of dietary NaHCO3 induces neither hypercalciuria nor hypertension. 30390036: Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity. Among the most promising approaches are dietary strategies for reducing the risk for salt-induced hypertension that do not depend on reducing salt consumption in the population. According to this theory, initiation of salt-induced hypertension usually involves abnormal vascular resistance responses to increased salt intake, not greater renal retention of a salt load in salt-sensitive subjects than in normal subjects. By shifting the focus from the historical theory to a contemporary final common pathway for the pathogenesis of salt sensitivity, research from Japan is building the scientific foundation for more effective approaches to the prevention and treatment of salt-induced hypertension. 30426340: Salt-sensitive rats received a high-salt (HS) diet to induce hypertension, or a normal-salt (NS) diet as control. 30704040: We discuss the role of endogenous cardiotonic steroids in mediating the dietary salt-induced hypertension and organ damage. 31162138: We hypothesized that excess dietary salt alters the gut microbiome leading to hypertension and this is associated with increased immunogenic IsoLG-adduct formation in myeloid antigen presenting cells. 34232678: Immune Mechanisms of Dietary Salt-Induced Hypertension and Kidney Disease: Harry Goldblatt Award for Early Career Investigators 2020. 3737739: Dietary salt (NaCl) has been implicated in the etiology of hypertension and atherosclerosis, although its role remains controversial. 5043414: It was concluded that the dietary Na/K molar ratio can be an important determinant for the severity, or even development, of salt-induced hypertension. 6648527: A normal amount of dietary sodium chloride induced hypertension, whereas an equimolar amount of sodium bicarbonate did not increase blood pressure. 704206: Some physicians and consumer groups have encouraged mothers to prepare their own baby foods, in part because of their concern that the physiologically unnecessary salt that is added by some commercial baby food manufacturers may lead to hypertension in adult life. 7296385: Chronic excess intake of NaCl (3.75% in the diet) was associated with a significant elevation of blood pressure on all three diets but a low level of LA in the diet exaggerated the salt-induced hypertension. Dietary linoleic acid and salt-induced hypertension. 7437746: These data provide no support for the hypothesis that dietary salt is a major cause of hypertension. 7454130: Salt-induced hypertension in rats can be prevented and cured by a high linoleic acid diet. 7852744: OBJECTIVE: To test the hypothesis that chronic exposure to psychosocial stress, alone or in combination with elevated levels of dietary salt, leads to hypertension and cardiac pathology in a susceptible strain of rats. 9353164: In this study, we examined the time course changes in the glomerulus associated with salt-induced hypertension using the inbred Dahl salt-sensitive rats. These findings indicate that salt-induced hypertension accelerates the age-dependent progression of glomerulosclerosis in Dahl salt-sensitive rats, and fibronectin may play a role in the pathogenesis, development, and progression of glomerulosclerosis associated with salt-induced hypertension. Progression of glomerulosclerosis, renal hypertrophy, and an increased expression of fibronectin in the renal cortex associated with aging and salt-induced hypertension in Dahl salt-sensitive rats. This age-dependent progression was further accelerated by the co-existence of salt-induced hypertension in the high salt diet group. 10024986: Although intracranial hemorrhage associated with neurofibromatosis type 1 is a rare condition, fine telangiectatic collateral vessels caused by occlusive cerebrovascular disease, intracranial aneurysms, brain tumors, or hypertension caused by pheochromocytoma or stenosis of the renal artery should be considered as the cause of hemorrhage. 1036677: The autopsy findings in a 2-year-old girl with severe hypertension resulting from stenosis of the lower part of the thoracic and the abdominal aorta were reviewed. 10548900: Hypertension induced by the stenosis is best approached by captopril renal MAG 3 scintigraphy. 1105838: Renal artery stenosis with resultant hypertension may occur secondary to stenosis at the anastomosis, atherosclerotic plaque formation or intimal fibrosis of the renal artery. 11082685: Valuable facts have been obtained in vasorenal hypertension caused by stenoses, occlusions, extravasal compressions, additional arteries, and in the portal system (thrombosis of the main trunk and branches of the portal vein, signs of portal hypertension). 11190295: Hypertension secondary to the stenosis, still incorrectly called renovascular hypertension, is, however rare, affecting less than 0.5% of hypertensives. 12929009: Doppler ultrasound showed an elevation of blood flow in the main artery of the functioning kidney consistent with stenosis as a cause of hypertension. 13152962: [Experimental hypertension produced by stenosis of the thoracic aorta]. 13222516: [Experimental hypertension produced by stenosis of the thoracic aorta]. 13412493: [Experimental hypertension induced by stenosis of the portal vein]. 13695386: Hypertension due to stenosis of the renal artery. 13707669: [Arterial hypertension due to stenosis of a renal artery]. 13724651: [Arterial hypertension caused by stenosis of a renal artery (5 cases)]. 13798587: [Arterial hypertension caused by stenosis of the renal arteries. Surgical treatment]. 13839344: [Arterial hypertension and renal ischemia. Apropos of a case of hypertension caused by stenosis of the renal artery, treated by plastic arterial graft]. 13846514: The diagnosis and treatment of renal hypertension; with special reference to a case of hypertension due to stenosis of both renal arteries. 13846989: [Arterial hypertension of the Goldblatt type caused by stenosis of the renal artery during thrombosis of the terminal aorta]. 13924815: Hypertension secondary to cogenital stenosis of the renal artery. 13947778: Hypertension resulting from stenosis of the renal artery. 14073251: [THE SURGICAL TREATMENT OF ARTERIAL HYPERTENSION CAUSED BY STENOSIS OF THE RENAL ARTERY]. 14187758: [SURGICAL TREATMENT OF HYPERTENSION CAUSED BY STENOSIS OR OBSTRUCTION OF THE RENAL ARTERY]. 14280178: [VALUE OF THE SURGICAL TREATMENT OF HYPERTENSION CAUSED BY STENOSIS OF THE RENAL ARTERY]. 2132037: Surgical repair is indicated in tight stenoses with impending thrombosis and in stenoses responsible for severe hypertension which does not respond to anti-hypertensive treatment. 21446982: Posttransplantation, she developed mild hypertension due to a postanastomotic stenosis, which was easily controlled with antihypertensives. 21629344: Arterial hypertension induced by pyeloureteral stenosis in horseshoe kidney. 23247786: Arterial hypertension due to stenosis of the renal arteries was noted in 4 cases. 23835240: However, it could be that the currently accepted belief, i.e. that only stenoses greater than 50-70% of the luminal surface result in ischaemic changes leading to hypertension and renal insufficiency, needs rethinking. 24130628: A 67-year-old woman admitted with severe hypertension, atrial fibrillation, and dyspnea was found to have hypertension and congestive heart failure due to stenosis of the descending aorta. 26893910: Resistant hypertension caused by stenosis of the aorta in elderly women: three case reports. 29944948: These findings support the conclusion that a tonic excitatory neurotransmission exerted by angiotensin II, and mostly by glutamate in the MnPO could participate in the modulation of blood pressure and RSNA independent on whether hypertension is primarily neurogenic or is secondary to stenosis in renal artery. 3099694: These cases are three young women (20, 40 and 42 years old) with severe hypertension secondary to atherosclerosis with stenosis of renal arteries, one or both sided, and in association in one case with diffuse arterial stenosis. [Essential thrombocythemia and hypertension as a result of stenosis of the renal artery]. 32774955: Conclusion: Though hypertension secondary to accessory renal artery stenosis is rare and not well published in medical literature, few case reports, including this one, demonstrate that accessory renal artery stenosis can be an underlying etiology of hypertension. Hypertension was suspected to be secondary to stenosis of the accessory renal artery. 350193: Stenosis of the renal artery is increasingly being recognized as a cause of hypertension and renal failure after kidney transplantation. 3551789: Moderate stenosis of the renal artery in one case resulted in systemic hypertension which was well controlled by medical treatment. 37415991: We hypothesize that vessel compression from the large mass created functional stenosis, resulting in persistent hypertension. 4628246: [Severe arterial hypertension due to stenosis of the aorta below the diaphragm. Surgical cure]. 4714961: Hypertension as a result of stenosis of a renal artery was diagnosed in three patients, aged 20, 17, and 9 respectively, among 14 siblings from one family. 4849867: [Systemic arterial hypertension secondary to stenosis of the renal artery caused by Takayasu's arteritis]. 5146508: [Nephrovascular hypertension due to stenosis of the renal artery branches. Apropos of a case]. 5744981: [On the clinical meaning of urography with intravenous infusion of urea (wash-out test) in arterial hypertension due to stenosis of the renal artery]. 5826194: [Surgical treatment of hypertension due to the stenosis of renal artery]. 5968067: [Importance of intravenous urography in the diagnosis of hypertension caused by stenosis of the renal artery]. 5978558: [Operative treatment of hypertension due to the stenosis of renal arteries]. 5988817: [The adrenal glomerular area during hypertension due to stenosis of the renal artery. Experimental studies in dogs. II]. 6664354: Stenoses of the abdominal aorta or stenoses of other arteries causing hypertension are rare in comparison to classical coarctation. 6794123: [Arterial hypertension caused by stenosis of the renal artery in neurofibromatosis]. 6868233: Hypertension secondary to stenosis of the left renal artery developed in a thirteen-year-old male six years after completion of inverted Y irradiation (3,600 rad) for abdominal Hodgkin disease. 7719110: [Effects of acupuncture on blood pressure, SOD,LPO and five kinds of trace elements to stenosis of renal artery caused hypertension in rats]. 781308: However, because of definite risk to the graft we believe that operative intervention should be undertaken only if hypertension is uncontrolled or if declining renal function is present and attributable to the stenosis. 788069: [Renal autotransplant by arterial hypertension secondary to stenosis of the right renal artery]. 8064789: Hypertension in neurofibromatosis is mostly a consequence of a stenosis of the renal artery or is due to phaeochromocytoma. 8151548: We conclude that PTA is an effective treatment at long term of hypertension and of decline in renal function due to stenoses of renal transplant arteries. 8369186: Untreated, these stenoses lead to intractable hypertension and impairment or loss of renal function. 841806: This is a report of hypertension caused by stenosis of a segmental renal artery and cured by simple ligation of the stenotic artery. Hypertension secondary to segmental renal ischemia caused by segmental renal artery stenosis has been relieved by nephrectomy, partial nephrectomy, excision of atrophic segments, or repair of the segmental vessels. 8730448: Therefore, we concluded that her hypertension resulted from stenosis of the right renal artery due to neurofibromatosis. 9539845: This case report has two particularities: an exceptionally long interval, 50 years after nephrectomy, and a severe hypertension due to stenosis of the contra-lateral renal artery. 10742426: Since her transplant kidney was based off the right external iliac artery, it was felt that this high-grade stenosis was responsible for her severe hypertension. 11737726: The mechanisms for hypertension are not clear, but residual stenosis, even mild, may result in upper body hypertension. 13722855: [On a case of arterial hypertension caused by arteriosclerotic stenosis of a renal artery]. 13877351: Hypertension and kidney: hypertension secondary to atheromatous stenosis of renal artery. 1443767: This article reports the case of a rapidly severe stenosis of the right renal artery, causing uncontrolled hypertension. 14488041: [The importance of renal vasography in hypertension due to renal stenosis]. 14653044: A 51-year-old patient suffering from Buerger's disease with bilateral lower limb amputation and Leriche syndrome presented with uncontrollable hypertension and renal failure caused by right renal artery subocclusive stenosis associated with an occluded left renal artery and atrophic kidney. 14767092: In this case study stenosis of a main renal artery, an unusual finding in classical PAN, is believed to be the cause of hypertension. 1491913: At the age of 10 months the patient developed arterial hypertension caused by left renal artery stenosis. 18134001: Arterial hypertension produced by experimental stenosis of the thoracic aorta. 183521: Embolic control of hypertension caused by segmental renal artery stenosis. 24991947: A 52-year-old female patient with a history of polycythaemia vera under treatment with hydroxyurea and phlebotomy presented in our outpatient clinic with newly diagnosed hypertension caused by left renal artery stenosis. 25907506: Intuitively, one could surmise that stenosis removal should void both the hypertension and the kidney damage resulting from the obstructive stenosis. 31360915: Renal artery dissections (RADs) are lesions that disrupt vessels that primarily occur in patients with a known history of hypertension and caused by stenosis or enlargement of the renal artery typically due to underlying connective tissue disorders. 5142285: [Multiple stenosis of a renal artery responsible for arterial hypertension in children. Cure with aortorenal bypass. Review of literature]. 5400373: [Arterial hypertension due to right renal artery stenosis: vascular prosthesis; normal delivery at term]. 5992325: [Casuistic contribution to the knowledge of arterial hypertension caused by intrinsic stenosis of the renal artery]. 6794509: Unusual features are the absence of craniofacial abnormalities, normal intelligence, and the left-sided dominance aggravated by hypertension due to curable intimal stenosis of the renal artery. 7019844: Hypertension caused by 90% stenosis of a transplant renal artery was effectively treated by percutaneous transluminal angioplasty of the stenosed artery. 10213637: Steroid-induced hypertension and its complications were the most expensive side effect ($93,900), followed closely by posttransplantation diabetes ($89,700) and avascular necrosis of the hip ($61,700). 11560123: Telemetric monitoring of adrenocorticotrophin-induced hypertension in mice. This model will allow the selective use of transgenic and/or knockout mice to further elucidate the mechanism of ACTH- and steroid-induced hypertension. We have studied adrenocorticotrophin (ACTH)- and steroid-induced hypertension in both rat and humans. The aim of the present study was to develop a model of ACTH-induced hypertension in the mouse and to assess a chronically implanted telemetric device for measurement of blood pressure (BP). 12538613: However, the steroid(s) responsible for hypertension in MR(L810) carriers (men and nonpregnant women) has not yet been identified. 1321309: Adrenocorticotrophin and steroid-induced hypertension in humans. The role of this increased pressor responsiveness in ACTH/steroid-induced hypertension remains to be determined. 1513024: [Disease models of steroid-induced hypertension]. 15257557: A 37-year-old black woman with nephritis secondary to systemic lupus erythematosus, steroid-induced diabetes mellitus, and hypertension presented with fever, nausea, vomiting, and right upper quadrant abdominal pain with distension. 1661608: In this group of patients, rejection was delayed and the incidence of hypercholesterolemia, hypertension, and steroid-induced complications was decreased. 16635442: Empiric treatments include the use of calcium channel blockers, steroids, induced hypertension or blood pressure lowering, and rarely endovascular therapy. 16980198: Lack of adrenal steroids in Addison's disease causes life-threatening hypotension, whereas glucocorticoid excess in Cushing's syndrome invariably results in high blood pressure. Mutations in the 11beta-HSD2 gene cause a rare form of inherited hypertension, the syndrome of apparent mineralocorticoid excess (AME), in which cortisol activates the MR resulting in severe hypertension and hypokalemia. 17459031: Steroid-induced intraocular hypertension was not observed in either group. 18496130: Genetic predictors of glucocorticoid-induced hypertension in children with acute lymphoblastic leukemia. Our aim was to define the frequency of and clinical and genetic risk factors for steroid-induced hypertension. 187612: These studies suggest that a steroid other than aldosterone, 18-OH-DOC, or DOC may be the cause of the ACTH-induced hypertension in this patient. Evidence for an unidentified ACTH-induced steroid hormone causing hypertension. 19803968: It is very clear that comorbidities such as steroid-induced diabetes mellitus, hypertension and osteonecrosis have been responsible for a great deal of the morbidity associated with systemic lupus erythematosus and must be aggressively managed. 23960949: Gene therapy strategies in glaucoma and application for steroid-induced hypertension. 25216697: It is strongly related to hypertension induced by steroids and other immunosuppressive agents. 25239629: Amlodipine was started for steroid-induced hypertension; 11 days after its initiation, alanine aminotransferase and aspartate aminotransferase peaked at 630 and 421 IU/L, respectively. 2558826: This study examined which of these adrenocortical steroids were necessary for the initiation of the hypertension produced by these steroids in sheep. Hypertension resulting from the combined steroid infusion in the sheep appears to be produced by a mechanism which involves a complex interaction between ALDO, F, 17 alpha OHP and 17 alpha 20 alpha OHP. 26424219: Steroid-induced hypertension and glaucoma is associated with increased extracellular meshwork (ECM) deposition in trabecular meshwork (TM). 27049792: Renal denervation substantially ameliorates the development of hypertension in animal models such as renovascular, spontaneously hypertensive, and steroid-induced hypertension in rats and aortic coarctation in dogs. 2764136: Hypertension was induced by unilateral nephrectomy plus steroid and salt water administration. 28801709: DEX implant intravitreal injection, sustained intraocular hypertension, and steroid-induced glaucoma in patients with no risk factors. 29189508: Steroid-induced Hypertension During Induction Chemotherapy for Acute Lymphoblastic Leukemia in US Children's Hospitals. 3011328: As 9 alpha FF did not cause a further increment in blood pressure in sheep with ACTH-induced hypertension it is possible that both ACTH and 9 alpha FF may produce hypertension by similar mechanisms. The effect of treatment with 9 alpha-fluorocortisol (9 alpha FF), a steroid which causes hypertension in sheep, was examined in sheep with ACTH-induced hypertension. The effect of the 'hypertensinogenic' steroid, 9 alpha-fluorocortisol on blood pressure in sheep with ACTH-induced hypertension. 3015460: Pressor responsiveness in steroid-induced hypertension in man. 30234749: CONCLUSIONS: XEN gel stent would seem to represent a safe and effective solution for treating steroid-induced hypertension. 31129643: This severe case of acute intraocular hypertension due to systemic steroids highlights the need to consider monitoring of IOPs for children on high-dose topical and systemic steroids with risk factors for raised IOP. 31809283: We found information regarding the role of the brain-gut--bone marrow axis, the brain-gut--kidney axis, the high-salt diet, short-chain fatty acids (SCFAs), neurotransitters, such as serotonin, dopamine and norepinephrine, nitric oxide, endothelin and steroids in modulating gut microbiota and in contributing to the pathogenesis of hypertension. 323586: The hypothesis that a steroid can produce hypertension was tested in an 18-year-old man with dexamethasone-suppressible hypertension. 3283584: In 7 patients (all with NS) steroid-induced hypertension has developed. Steroid-induced hypertension in patients with nephrotic syndrome. 3346052: Characteristics of hormonal and neurogenic mechanisms of deoxycorticosterone-induced hypertension. We characterized the hemodynamic and endocrine changes associated with the evolution of steroid-induced hypertension in conscious, trained, instrumented dogs given intramuscular injections of deoxycorticosterone (DOC) pivalate on Days 1 (20 mg/kg) and 14 (10 mg/kg) of the study. The data suggest that DOC-induced hypertension changes central hormonal influences of cardiovascular function, and also alters cardiopulmonary baroreceptor reflex control of peripheral sympathetic nerve activity. Compared to normal animals, dogs with DOC-induced hypertension showed a reduced pressor response to carotid occlusion associated with suppression of reflex tachycardia; vagotomy partially restored the pressor response to normal levels. 3698922: Experiments were done to evaluate whether 19-hydroxyandrostenedione (19-OH-A) is a steroid which produces hypertension and amplifies the mineralocorticoid effects of aldosterone. 3762307: Previously, altered aldosterone binding to corticoid receptor I was found in aortic smooth muscle cells cultured from Fischer 344 rats which are extremely resistant to steroid and salt induced hypertension. Rat models of genetic hypertension include spontaneous hypertension and resistance or sensitivity to mineralocorticoid and salt induced hypertension. 4033027: [Risk factors in the development of steroid-induced hypertension in patients with nephritis]. 5634507: Steroid-induced hypertension in the rat. 5749233: [On two cases of steroid induced hypertension]. 5773218: The pathogenesis of the glomerular changes in steroid-induced hypertension in the rat. 6027455: A study of the effects of renal artery constriction on hypertension caused by deoxycorticosterone. Steroid-induced hypertension in the rat. 6096893: The aim of this study was to determine the effect of ACTH-induced hypertension on the hemodynamic dose-response curves to intravenous infusion of prostacyclin (PGI2) in conscious sheep. PGI2 was infused for 10 minutes at doses of 0.05-0.50 micrograms/kg per min and hemodynamic dose-response curves were performed before, during and after ACTH-induced hypertension. These studies suggest that in this model of steroid-induced hypertension the resistance vessels are more sensitive to PGI2 and that the blood pressure response to PGI2 is regulated by different mechanisms to those seen prior to ACTH. 6321063: A hypothesis is proposed to explain how the 'hypertensinogenic' actions of a steroid may produce hypertension. 6513729: These results provide further evidence for our concept of a 'hypertensinogenic' class of steroid activity and are the first demonstration of specific antagonism of steroid induced hypertension. 7050977: We conclude that alternate day steroid therapy is indicated in adult renal transplant recipients to treat steroid-induced diabetes, hypertension and minor prednisone side effects, but is not useful for obesity. 7471521: A model of adrenocortical steroid-induced hypertension based on the effects of ACTH administration has been developed in sheep. 7917157: The hypothesis that cortisol-induced hypertension might be secondary to steroid-induced hyperinsulinemia was examined by determining whether reversal of hyperinsulinemia by octreotide would reverse cortisol-induced hypertension. Thus, octreotide was effective in lowering plasma insulin concentrations but di not lower blood pressure in normal subjects with cortisol-induced hypertension. These data do not support the notion that steroid-induced hyperinsulinemia is responsible for steroid-induced hypertension. 7951167: Here, we examined the relationship between steroid-induced hypertension and components of the renin-angiotensin system. Previous work has demonstrated contraceptive steroid-induced hypertension in rats. 8591894: On the basis of evidence suggesting the activation of the kallikrein-kinin system in steroid-induced hypertension, we considered the possibility that the angiotensin-converting enzyme inhibitor captopril would lower the arterial blood pressure in deoxycorticosterone acetate (DOCA)-salt hypertensive rats through kininase II inhibition. 870223: Multifactorial analysis of chronic hypertension induced by electrolyte-active steroids in trained, unanesthetized dogs. These results point to a primary role of arteriolar resistance in determining the initiation and maintenance of hypertension induced by electrolyte-active steroids. 8732997: The role of the extraadrenal synthesis of steroids raises new avenues for research into the causes of hypertension. 10472071: Elevated aortic stiffness induces high systolic blood pressure, augmented pulse pressure with increased ventricular afterload, reduced subendocardial blood flow and augmented pulsatile stress in the peripheral arteries. 10981158: ISH, by definition, is wide pulse pressure hypertension resulting largely from excessive large artery stiffness and representing an independent risk factor for cardiovascular disease in the older aged population. 11923811: Sustained hypertension may be due to increased aortic stiffness. 21284131: Residual stenosis of descending aorta (AoD) and stiffness in the precoarctation region supposedly lead to hypertension. 22416438: Such patients' postocclusive reactive hyperemia test demonstrates a significant decline of vasomotor endothelial function, 43% cases show an inertial type of the vasomotor reaction reflecting an important role of hormonal unbalance in AH progression primarily due to increased stiffness of the vascular wall and endothelial dysfunction. 24065014: FINDINGS: Hypertension in elderly people differs from that in younger people in that (1) hypertension is predominantly systolic because of vascular stiffness; (2) it is associated with reduced baroreflex sensitivity, which increases blood pressure variability and vulnerability to hypotension during common daily activities; (3) it is associated with cognitive and functional decline as well as adverse cardiovascular outcomes; and (4) hypertension may be beneficial in frail people older than 85 years. 27456526: These observations are consistent with higher vascular stiffness at an early stage in the pathogenesis of hypertension. 29449619: ETA receptor blockade may have therapeutic potential for improving peripheral vessel structure and function in the treatment of aortic stiffness-induced hypertension. 30590888: Stiffness of the arterial wall and predicted vascular age as a predictor of cardiovascular disease when stress-induced hypertension in the military personnel. 31625778: Vascular stiffness plays a key role in the pathogenesis of hypertension. 31655529: Role of aortic stiffness and inflammation in the etiology of young-onset hypertension. CONCLUSION: In this study, increased PWVs and the levels of inflammation markers were associated with aortic stiffness and inflammation in patients with young-onset hypertension, suggesting their role in the etiology of hypertension. We aimed to explore the relationship between inflammation and aortic stiffness and investigate their role in the etiology of young-onset hypertension. 31780955: Results: In agreement with our clinical diagnosis, the model showed that an increase of aortic stiffness followed by augmentation of peripheral resistance are the prime causes of realistic hypertension. 6106402: In aged people a differentiation has to be made between \arteriosklerotic hypertension\ due to increased stiffness of the aorta and true hypertension in older patients. 16873404: These results suggest that a physiological hyperosmotic stimulus produces sympathetically mediated hypertension in conscious rats. 1986980: The sympathetic nervous system but not vasopressin may play an important role in the chronic phase of central NaCl-induced hypertension. These results indicate that sustained sodium stimulus on the central nervous system causes mild hypertension and alters water and sodium balance. 21842150: In addition, stimulation of the CNS by some stimuli (e.g., angiotensin II) causes mild hypertension that may modulate peripheral immune responses leading to aggravation of blood pressure elevation. 230798: Studies using a precursor of DNA, namely [3H] thymidine, and autoradiography have shown that proliferation of SMC is an important and early response to atherogenic stimuli, such as cholesterol feeding, surgically induced hypertension or endothelial injury. 24605401: In addition, stimulation of the CNS by some stimuli (e.g. angiotensin II) causes mild hypertension that may modulate peripheral immune responses leading to aggravation of blood pressure elevation. 25244096: Here, we have described a pathway in which hypertensive stimuli promote dendritic cell (DC) activation of T cells, ultimately leading to hypertension. Oxidative damage and inflammation are both implicated in the genesis of hypertension; however, the mechanisms by which these stimuli promote hypertension are not fully understood. 25879533: We reported that continuous high glucose stimulus causes endothelial senescence more markedly than hypertension or dyslipidemia stimulus. 28912720: Activation of autonomic neural pathways by chronic hypertensive stimuli plays a significant role in pathogenesis of hypertension. 3032109: The hemodynamics prevailing in cancer tissue are known to be quite abnormal, at least in some cases, in that the tumor vessels are inert to vasoactive stimuli, a feature that has been exploited in the development of pharmacoangiography or induced hypertension chemotherapy. 3540271: Stimuli that trigger pulmonary hypertension cause hypoxia, suggesting the importance of hypoxic pulmonary vasoconstriction (HPV). 37549970: CONCLUSIONS: Memory gammadelta T cells develop in response to hypertensive stimuli, and contribute to the pathogenesis of hypertension. 3906628: Stranger evidence comes from studies of mice showing that symbolic stimuli in the form of disordered social relations lead to hypertension and increased heart size. 7640977: Any noxious stimuli below this level initiate reflex sympathetic activity resulting in life threatening hypertension uncontrollable by the feedback parasympathetic activity. 7691695: Pathophysiological conditions such as vasospasm, hypertension, cardiac arrhythmia and myocardial hypertrophy, and atherosclerosis, are also caused by abnormal biomechanical stimuli. 7857755: Afferent stimuli from the scarred or diseased kidneys into the central nervous system may activate the sympathetic nervous system and contribute to the genesis of hypertension in patients with chronic renal failure. 12956398: It also significantly prevented STZ-induced polydypsia, hyperphagia, hypertension, and bradycardia but not the loss of body weight. 1418828: STZ produced diabetes and hypertension within 1 to 2 weeks in all three groups of RRM rats but blood pressure was unaffected by 60% or 25% RRM alone. 151754: Hypertension induced by streptozotocin in the rat. 15200422: CONCLUSION: We conclude that the P2X(7) receptor is not expressed appreciably under normal conditions, but that following glomerular injury it is significantly up-regulated, mainly in podocytes, though also in endothelial and mesangial cells, of animals with STZ-induced diabetes mellitus or TGR hypertension. 153477: Chronic hypertension induced by streptozotocin in rats. 17272402: Administration of streptozotocin in conjunction with a high-fat diet induced systemic hypertension, diabetes, and renal damage in rats. 18425420: Chronic treatment with telmisartan significantly (P < 0.05) prevented STZ induced hypertension and elevated fasting glucose level with simultaneous increase in serum insulin levels. 19738487: Chronic treatment with spironolactone significantly prevented STZ-induced bradycardia, hypertension, and elevated fasting glucose level with simultaneous increase in serum insulin levels. 22001983: Chronic treatment with telmisartan significantly prevented STZ-induced hypertension and tachycardia and elevated fasting glucose and insulin levels. 22653691: STZ-induced hypertension and bradycardia were also prevented by perindopril treatment. 24026828: Chronic treatment with spironolactone prevented STZ-induced hypertension, tachycardia and elevated rate of pressure development and decay. 24965174: This study evaluated the effects of alagebrium (ALT-711), an AGE breaker, combined with nifedipine, a Ca(2+) channel blocker, in a rat model of streptozotocin-induced DH. 7881138: The present study was undertaken to investigate the combined effects of hypertension and streptozotocin-induced diabetes mellitus in the rat. 7946165: Recently, Hebden and colleagues demonstrated endothelial injury in a rat model with streptozotocin-induced diabetes mellitus and deoxycorticosterone acetate-induced hypertension. 20110613: In contrast, sporadic AD has been proposed to start with an insulin-resistant brain state (IRBS).We investigated the effect of IRBS induced by intracerebroventricularly (icv) administered streptozotocin (STZ) on behavior, glycogen synthase kinase-3 (GSK) alpha/beta content, and the formation of AD-like morphological hallmarks Abeta and tau protein in AbetaPP Tg2576 mice. 20683499: In the present study, the effect of crocins on sporadic Alzheimer's disease induced by intracerebroventricular (icv) streptozocin (STZ) in male rats was investigated. 21465495: These results suggest that antioxidant property is involved, at least in part, in the neuroprotective effect of (MeOPhSe)(2) on SDAT induced by STZ in mice. 21701788: Neuroprotective effect of cyclooxygenase inhibitors in ICV-STZ induced sporadic Alzheimer's disease in rats. 22886014: Streptozotocin-induced sporadic Alzheimer's disease: selection of appropriate dose. 22959057: Thus, the aim of the current study was to investigate the therapeutic effect of p,p'-methoxyl-diphenyl diselenide [(MeOPhSe)(2)], an organoselenium compound, against streptozotocin (STZ)-induced sporadic dementia of Alzheimer's type (SDAT) in rats. 23210085: Effect of Royal Jelly on spatial learning and memory in rat model of streptozotocin-induced sporadic Alzheimer's disease. 23351237: Role of testosterone in memory impairment of Alzheimer disease induced by Streptozotocin in male rats. 23457495: Selection of appropriate reference genes for RT-qPCR analysis in a streptozotocin-induced Alzheimer's disease model of cynomolgus monkeys (Macaca fascicularis). 23562514: Xanthoceraside attenuates learning and memory deficits via improving insulin signaling in STZ-induced AD rats. 23603201: Saxagliptin: a dipeptidyl peptidase-4 inhibitor ameliorates streptozotocin induced Alzheimer's disease. 23681104: Taurine ameliorates neurobehavioral, neurochemical and immunohistochemical changes in sporadic dementia of Alzheimer's type (SDAT) caused by intracerebroventricular streptozotocin in rats. 24117480: Vildagliptin: an anti-diabetes agent ameliorates cognitive deficits and pathology observed in streptozotocin-induced Alzheimer's disease. 24329968: Because geniposide is thought to act as a GLP-1 receptor agonist, we investigated the potential therapeutic effect of geniposide on STZ-induced AD model in rats. Geniposide ameliorates learning memory deficits, reduces tau phosphorylation and decreases apoptosis via GSK3beta pathway in streptozotocin-induced alzheimer rat model. 24503167: Acetylcholinesterase (AChE) activity was also significantly reduced by Rg5 whereas choline acetyltransferase (ChAT) activity was remarkably increased in the cortex and hippocampus of STZ-induced AD rats (P<0.05). Furthermore, it was observed that the expressions of COX-2 and iNOS were significantly up-regulated in STZ-induced AD rats and down-regulated strongly (P<0.05) by Rg5 compared with control rats. 24667360: Alzheimer's disease (AD), the most common form of dementia, is characterized by the loss of normal functions of brain cells and neuronal death, ultimately leading to memory loss. Dipeptidyl peptidase-4 inhibition by Pterocarpus marsupium and Eugenia jambolana ameliorates streptozotocin induced Alzheimer's disease. Therefore, PM and EJ extracts contain cognitive enhancers as well as neuroprotective agents against STZ induced AD. Therefore, in the present study, the neuroprotective roles of PM and EJ for ameliorating the streptozotocin (STZ) induced AD have been tested in rat model. 24719136: Agmatine improves cognitive dysfunction and prevents cell death in a streptozotocin-induced Alzheimer rat model. RESULTS: Agm suppressed the accumulation of amyloid beta and enhanced insulin signal transduction in STZ-induced Alzheimer rats [experimetal control (EC) group]. In this study, we investigated whether Agm treatment could attenuate apoptosis and improve cognitive decline in a STZ-induced Alzheimer rat model. MATERIALS AND METHODS: We studied the effect of Agm on AD pathology using a STZ-induced Alzheimer rat model. 24769303: Centrally administered streptozotocin (STZ), is known to cause Alzheimer's like memory deterioration. 24877042: The rat model of Alzheimer's disease was induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) using a stereotaxic instrument. Treadmill exercise alleviates impairment of spatial learning ability through enhancing cell proliferation in the streptozotocin-induced Alzheimer's disease rats. Decreased cell proliferation with decrement of BDNF and TrkB expressions in the hippocampus were observed in the STZ-induced Alzheimer's disease rats. 25096625: To determine whether mitochondrial perturbation is associated with the contribution of diabetes to AD progression, we characterized mouse models of streptozotocin (STZ)-induced type 1 diabetes and transgenic AD mouse models with diabetes. Diabetes is considered to be a risk factor in Alzheimer's disease (AD) pathogenesis. 25114075: AMPK activation ameliorates Alzheimer's disease-like pathology and spatial memory impairment in a streptozotocin-induced Alzheimer's disease model in rats. 25268773: Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model. Here, we found that the intraperitoneal administration of magnesium sulfate increased the brain magnesium levels and protected learning and memory capacities in streptozotocin-induced sporadic AD model rats. 25446674: Notably, saxagliptin (SAX), the DPP-4 inhibitor, recently showed efficacy in ameliorating streptozotocin-induced Alzheimer's disease; however, its effect on Parkinson's disease (PD) has not yet been elucidated. 25890375: Among these models, streptozotocin, PolyI:C-induced, and p25 neuroinflammation models are compatible with the inflammation hypothesis of Alzheimer's disease. 26330820: Streptozotocin induced Alzheimer's disease like changes and the underlying neural degeneration and regeneration mechanism. 26638997: Downstream modulation of extrinsic apoptotic pathway in streptozotocin-induced Alzheimer's dementia in rats: Erythropoietin versus curcumin. In conclusion, ICV-streptozotocin-induced Alzheimer's dementia activates hippocampal Fas ligand-mediated apoptosis, which could be reduced by erythropoietin and/or curcumin treatment. This study was designed to compare the beneficial effects of erythropoietin and/or curcumin in intracerebro-ventricular (ICV) streptozotocin-induced Alzheimer's like disease in rats. 27035793: The present study aimed to investigate the effect of luteolin, a flavonoid compound, on memory impairment in a streptozotocin (STZ)-induced Alzheimer's rat model. 27087133: Thus, the aim of the current study was to investigate the effect of NAC against streptozotocin (STZ) induced AD in mice. 27585561: This study investigates the streptozotocin (STZ)-induced AD model at three different times (2, 4 and 8 weeks afterwards) and in male and female rats, evaluating cognitive deficit, cholinergic neurotransmission, glucose uptake, glutathione content and specific glial markers (GFAP and S100B protein) in the hippocampus of the rat. 27746125: The present study aimed to investigate the effects of berberine (BRB) on spatial and learning memory, anxiety, acetylcholinesterase activity and cell death in an experimental model of intracerebroventricular streptozotocin (ICV-STZ) induced sporadic Alzheimer's-like dementia. 27913964: However, especially in mice, several characteristics involved in the streptozotocin (STZ)-induced AD pathology are not well known. 28106557: Blunted Respiratory Responses in the Streptozotocin-Induced Alzheimer's Disease Rat Model. 28188358: Protective effect of valproic acid in streptozotocin-induced sporadic Alzheimer's disease mouse model: possible involvement of the cholinergic system. 28299625: The effects of lipoic acid on redox status in brain regions and systemic circulation in streptozotocin-induced sporadic Alzheimer's disease model. 28342971: Here we show for the first time the potential neuroprotective effect of a novel dual GLP-1/GIP receptor agonist (DA-JC4) in the icv. streptozotocin (STZ)-induced AD rat model. 28382978: Long-term treatment with intranasal insulin ameliorates cognitive impairment, tau hyperphosphorylation, and microglial activation in a streptozotocin-induced Alzheimer's rat model. 28397428: Twelve rats with Alzheimer's disease, induced by STZ injection (3 mg/kg) into both lateral ventricles using a stereotaxic frame (bilaterally ICV-STZ), were divided into 2 groups 5 days after the STZ injection: one treated with rhEPO 5000 (IU/kg/day, i.p.) and the other with 0.9% NaCl (1 mL/kg/day, i.p.) for 2 weeks. 28480351: MATERIAL AND METHODS: AD was induced by administering streptozotocin i.e. 28687315: The main purpose of this study was to investigate the involvement of Nox2 in memory, in AD-related brain abnormalities, oxidative damage, inflammation and neuronal death in the hippocampus in the streptozotocin (STZ)-induced AD-like state by comparing the effects of that drug on mice lacking gp91phox-/- and wild-type (Wt) mice. 28702935: Vitamin D3 attenuates cognitive deficits and neuroinflammatory responses in ICV-STZ induced sporadic Alzheimer's disease. Therefore, the present study was aimed to investigate the neuroprotective effects of vitamin D3 on ICV-STZ induced sporadic AD. 28929339: Intranasal Insulin Ameliorates Cerebral Hypometabolism, Neuronal Loss, and Astrogliosis in Streptozotocin-Induced Alzheimer's Rat Model. 28987281: We found that STZ-induced AD impaired LTP in the dentate granule cells. 29126976: Involvement of glucose related energy crisis and endoplasmic reticulum stress: Insinuation of streptozotocin induced Alzheimer's like pathology. 29132093: Thus, we investigated the possible efficacy of the AChE inhibitor 2-[(6-Nitro-2-benzothiazolyl)amino]-2-oxoethyl4-[2-(N,N-dimethylamino)ethyl] piperazine-1 carbodithioate (BPCT) in a streptozotocin (STZ)-induced Alzheimer's disease model (SADM). 29133125: Very low doses of muscimol and baclofen ameliorate cognitive deficits and regulate protein expression in the brain of a rat model of streptozocin-induced Alzheimer's disease. The presented study demonstrated that in a rat model of STZ-induced AD both muscimol and baclofen at the tested doses exerted memory-enhancing and anti-inflammatory effects, as well as normalization of acetylcholine esterase and GABA expression. 29232315: PURPOSE: This study aimed to examine the effects of swimming exercise pretreatment on a streptozotocin (STZ)-induced sporadic Alzheimer's disease (AD) rat model and provide an initial understanding of related molecular mechanisms. 29501041: The animals were treated intracerebroventricularly with streptozotocin (STZ; 3 mg/kg) twice, on day 1 and 3, to induce AD-like condition, and the symptoms were evaluated after 14 days. 29587242: ANT treatment protected against the worsening of memory in STZ-induced SDAT. In conclusion, the present study showed that treatment with ANT attenuated memory deficits, protected against oxidative damage in the brain, and restored AChE and ion pump activity in an STZ-induced SDAT in rats. 29667108: 5-Hydroxytryptamine receptor 6 antagonist, SB258585 exerts neuroprotection in a rat model of Streptozotocin-induced Alzheimer's disease. 29765479: The present study was designed to investigate neuroprotective mechanism and therapeutic potential of evodiamine against intracerebroventricular streptozotocin (ICV-STZ)-induced experimental sporadic Alzheimer's disease in mice. 29782959: Moreover, prominent declines in oxidative stress, neuro-inflammation, and apoptotic parameters were recorded upon its injection in STZ-induced SAD mouse model. 29807069: Fasudil hydrochloride ameliorates memory deficits in rat model of streptozotocin-induced Alzheimer's disease: Involvement of PI3-kinase, eNOS and NFkappaB. 29927658: Injection of L-T4 (10 MUg/kg) alleviated memory deficits and also improved factors of oxidative stress and BDNF level in the STZ-induced AD rats. 30014576: Intracerebroventricular streptozotocin-induced Alzheimer's disease-like sleep disorders in rats: Role of the GABAergic system in the parabrachial complex. 30118774: The therapeutic effect of bergenin supplementation for 28 days, at three dose levels, was also evaluated in streptozotocin (3 mg/kg, ICV, unilateral) induced AD model in Wistar rats using Morris water maze and Y maze on 7th, 14th, 21st and 28th days. 30171934: The observations were further confirmed by in vivo therapeutic effects in streptozotocin (STZ)-induced SAD rats in the context of altered biochemical and behavioral features. 30333717: This study showed, for the first time, that the administration of an endocannabinoid can prevent AD-like effects induced by STZ, boosting further investigations about the modulation of endocannabinoid levels as a therapeutic approach for AD. 30359566: The results of this study document a region-specific impact of STZ-induced AD in respiratory brainstem nuclei. Impaired chemoreflex correlates with decreased c-Fos in respiratory brainstem centers of the streptozotocin-induced Alzheimer's disease rat model. 30481507: As cholesterol modifying agents have been supposed to alter AD like pathologies, the current study was designed to investigate the possible neuroprotective and therapeutic potential of ALN against ICV STZ induced experimental sporadic AD (SAD) in mice in a non-cholesterol dependent manner, using donepezil (5 mg/kg) as a reference standard. 30521994: The drug discovery to treat AD consists to develop compounds able to act in multiple molecular targets involved in the pathogenesis of the disease and the repositioning of old drugs for new application. The aim of the present study was to investigate whether ebselen (1-10 mg/kg), a multifunctional selenoorganic compound, ameliorates memory impairment, hippocampal oxidative stress, apoptosis and cell proliferation in a mouse model of sporadic AD induced by icv STZ (3 mg/kg, 1 MUl/min). In conclusion, the multifunctional selenoorganic compound ebselen was effective to reverse memory impairment, hippocampal oxidative stress and apoptosis in a mouse model of sporadic AD induced by icv STZ. 30641081: Twelve days after AD induction by streptozotocin (STZ), animals received either vehicle or MK-801 (NMDA receptor antagonist) in the hippocampus for 10 days. 30684605: This study aimed at investigating the protective effect of NAD-299 (the selective 5-HT1A receptor antagonist) and TCB-2 (the potent5-HT2A receptor agonist) on the hippocampal oxidative stress biomarkers and the number of intact neurons in streptozotocin (STZ)-induced Alzheimer's disease in rats. 30760053: Administration of hCG ameliorated the lowered density of hCG receptor-ir neurons in the cerebellum and prefrontal cortex in STZ-induced AD rats. We investigated the effects of different doses of hCG on hCG receptor density in the prefrontal cortex and cerebellum in a rat model of STZ-induced AD. AD was induced by intracerebroventricular injection of 3 mg/kg STZ. 31040784: Apelin-13 was found to significantly ameliorate STZ-induced AD-like phenotypes including congnitive deficit, cholinergic disfunction and the damage of neuron and synaptic plasticity. 31068802: Also, we evaluated the effect of edaravone, an antioxidant on diabetes-induced Alzheimer's-like complications and the additive effect of docosahexaenoic acid (DHA) on the efficacy of TPPU. Docosahexaenoic Acid Increases the Potency of Soluble Epoxide Hydrolase Inhibitor in Alleviating Streptozotocin-Induced Alzheimer's Disease-Like Complications of Diabetes. 31086208: To further our studies, the protective effect of QTC-4-MeOBnE (0.1 and 1 mg/kg for 20 days) on STZ-induced sporadic AD mice was determined. 31215291: Here, the possible protective effect of ABA was evaluated in streptozotocin (STZ)-induced AD rat model which were injected intracerebroventriculary (i.c.v.) with STZ (3 mg/kg). 31344367: In this study, the effects of yonk on cognitive behaviors as well as the pathological features in streptozotocin-induced SAD rat model were investigated. 31480727: beta-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer's Disease. 31595805: Effects of tannic acid in streptozotocin-induced sporadic Alzheimer's Disease: insights into memory, redox status, Na+, K+-ATPase and acetylcholinesterase activity. 31726088: Melatonin attenuates streptozotocin-induced Alzheimer-like features in hyperglycemic rats. 31834453: OBJECTIVE: The objective is to evaluate the effects of inosine on the behavioral and neurochemical parameters in a rat model of Alzheimer's disease (AD) induced by streptozotocin (STZ). 33448390: As glucose hypometabolism in the brain is an early sign of Alzheimer's dementia (AD), the diabetogenic drug streptozotocin (STZ) has been used to induce Alzheimer-like pathology in rat brain by intracereboventricular injection (icv-STZ). 34536437: Animals were subjected to treadmill exercise eight weeks before and four weeks after ALD induction by streptozocin (STZ). 34554409: STZ (3 mg/kg) was injected through an intracerebroventricular route to induce AD-like dementia. 10226862: In conclusion, treatment with trandolapril exerts beneficial antihypertensive actions in this model of induced hypertension, showing continuous control of blood pressure and prevention of structural and functional alteration of the aorta. 10454458: This novel hypertensive model may enable characterization of the functions of the renin-angiotensin system in the brain and determination of its role in the pathogenesis of hypertension. 10872564: We addressed the question whether the inherited defect in this model leads to salt-sensitive hypertension. 11356633: In this study, we propose a new biomechanical model for the wall adaptation to induced hypertension, including changes in VSM tone. 12385670: A bio-behavioral model of stress-induced hypertension is presented that explains how repeated exposure to stress in combination with genetic susceptibility might lead to the development of hypertension. 12747945: Isolation of male Sprague-Dawley rats provokes an increase in blood pressure, which has been proposed as a valid model of mild emotionally induced hypertension. 12768066: BACKGROUND: The remnant kidney model, usually involving sudden removal or ablation of 1- 1 / (2) to 1-5 / (6) of renal mass, results in compensatory hypertrophy followed by hypertension, proteinuria and declining glomerular filtration rate (GFR) associated with focal (FSG) and then global glomerulosclerosis (GS) and tubulointerstitial injury (TI). 1405318: Angiotensin converting enzyme inhibitors (ACEI) are believed to protect remnant kidney, but all previous studies used the ligation model which causes severe hypertension, and very few have compared drugs in rats having similar control of blood pressure (BP). We compared rats with uremia obtained by 70% excision of total renal mass, a model which causes mild, late hypertension. 15322681: This study was conducted to determine the effect of pregnanolone (PGN) on blood pressure of a rat model of stress-induced hypertension (SIH). 15343353: It is possible that earlier inconsistent results with these AGT polymorphisms with hypertension in African-derived populations may have resulted from an 'incomplete' model in the different study populations. 15815377: The authors investigated the effects of phenylephrine-induced hypertension on the development of cerebral edema and neuronal dysfunction during focal cerebral ischemia. The data indicate that, in this model, induced hypertension established soon after the onset of ischemia can serve to reduce the area of histochemically detectable neuronal dysfunction, and that not only is edema formation not aggravated, but it is actually reduced. The influence of phenylephrine-induced hypertension during focal cerebral ischemia on the formation of brain edema. 16046788: A gene-environment interaction model of stress-induced hypertension. The case for a gene-environment interaction model of stress-induced hypertension is detailed in this paper. 16278234: A loss of genome buffering capacity of Dahl salt-sensitive model to modulate blood pressure as a cause of hypertension. 1632999: In univariate analyses, variables significantly associated with better pharmacy compliance were perceived lifetime treatment of hypertension, greater than 5-year history of medication use, perceived cause of hypertension other than diet, use of more than one hypertension drug, lack of reported departure from the prescribed medication regimen, absence of drug abuse history, and race (Caucasian). In multivariate analyses, the best predictive model of pharmacy compliance included three variables: drug abuse history, perceived cause of hypertension, and pattern of medication use. 17316702: RESULTS: The data indicated an association between hypertension induced by the 2K/1C model and reduction of reproductive function, as demonstrated by an impairment of sexual behavior, higher plasma PRL and lower plasma testosterone and FSH. 18207159: We used the suprarenal abdominal aorta banding model to induce hypertension and hypertrophy. 18476427: METHODS: Rat myocardial (heart failure) model was established by anterio-descending coronary arterial ligation, and treated by nitric oxide synthase inhibitor 9-12 weeks after operation to induce hypertension and aggravate heart failure. 1928431: Dietary obesity and weight cycling in rats: a model of stress-induced hypertension? 1974541: To elucidate observed alterations in hypertensive subjects at both molecular and systemic levels in a comprehensive way, a model (a working hypothesis) for the molecular pathogenesis of hypertension is proposed. 20826133: We investigated the effects of the hydrogen sulfide (H2S)-releasing derivatives of aspirin (ACS14) and salicylic acid (ACS21) in a rat model of metabolic syndrome induced by glutathione (GSH) depletion, causing hypertension and other pathological cardiovascular alterations. 21207852: METHODS: The model of stress-induced hypertension (SIH) rat was established by electric-foot in company with noise, NADPH-d histochemistry technique was used to investigate the change of nitric oxide synthase (NOS) positive neurons. 2149566: To study the functional and metabolic correlates of left ventricular hypertrophy [LVH] in non-human primates, 7 hypertensive baboons [papio anubis] with 4.6 +/- 0.1 years of hypertension produced by a two-kidney one-clip model, and echocardiographically documented concentric LVH underwent serial phosphorus-31 [P-31] NMR Spectroscopy studies at rest and during inotropic cardiac stress produced by dobutamine infusion [5 micrograms/kg/minute]. 21528601: The model of stress-induced hypertension was established by foot-shock and noise stimulation in the other groups except group A. 22223042: In 2000, it was first reported that oxidative stress and arterial hypertension were produced in normal Sprague-Dawley rats by oral administration of buthionine sulfoximine (BSO), which induces glutathione (GSH) depletion, indicating that oxidative stress may induce hypertension. The contribution of several potential pathogenic factors has been evaluated in the BSO rat model, the prototype of oxidative stress-induced hypertension, including vascular reactivity, endothelium-derived factors, renin-angiotensin system activity, TXA(2)-PGH(2) production, sodium sensitivity, renal dopamine-induced natriuresis, and sympathetic tone. 22573528: The strategic plan should also expand education outreach efforts to high risk patient populations in using the lay health advisor model by focusing on prevention, early detection, and control strategies targeting obesity, genetic causes of CKD, diabetes, and hypertension. 23060473: In this model, the transgene prorenin was induced by indole-3-carbinol for 2 weeks allowing the induction of hypertension. 23157700: We employed the mouse model, which induced muscularization of pulmonary artery leading to hypertension by repeated intratracheal injection of Stachybotrys chartarum, a member of nonpathogenic and ubiquitous fungus in our envelopment. 23415204: CONCLUSIONS: Our results show evidence of one semantic model in regard to the causes of arterial hypertension and different from the biomedical cognitive pattern. 23774144: Intermittent hypoxia (IH) has been previously shown in a lean murine model to produce sustained hypertension and reverse the diurnal variation of blood glucose (BG). 2471889: From these results and those obtained in the experimental rat models of acquired hypertension, a model for the pathogenesis of the genetically determined hypertension is proposed in which a very early step in the development of hypertension is a genetically determined increase in renal alpha-adrenoceptors that causes enhanced sodium retention. A model for the pathogenesis of the genetically determined hypertension. 24719376: Two Kidney One Clip (2K1C) Goldblatt model was adopted to induce hypertension in rats. 25118666: The effects of hypotension and hypertension were simulated through boundary conditions by modulating the normotensive flow and pressure waveforms, in turn produced by a 1D systemic vascular model. 25298513: Thus, these results suggest that the mouse model of reduced uterine perfusion is applicable to facilitate novel mechanistic investigation into the etiology of hypertension that results from placental ischemia during pregnancy. 25395699: MATERIALS AND METHODS: Two Kidney One Clip (2K1C) model was adopted to induce hypertension in rats. 26597746: The high fructose diet is a well-studied model that induces hyperglycemia and hypertension in male rodents, but may not affect females. 27032687: In summary, we identified a naturally-developed hypertensive MetS NHP model, which is of great value in the studies on pathogenesis of MetS-associated hypertension and development of novel therapeutic strategies. 27498679: Hypertension leads to small vessel disease resulting in progressive damage to the white matter, cortex, and hippocampus. A few studies have been done with the two-clip, two-vessel occlusion renal model for induction of hypertension. 27570756: CONCLUSIONS: In summary, CKD induced by the 5/6 Nx model caused hypertension and increased serum levels of Cr, BUN, ALT, and AST. 27861631: We found that expression of a 15-kb human RENIN (hREN) transgene was aberrantly upregulated (>4.2-fold), while the endogenous mouse renin (mRen) gene was suppressed (>1.7-fold) in Tsukuba hypertensive mice (THM), a model for genetically induced hypertension. 28320306: In the current study, the RNA-Seq approach has been used to discover strain-specific SNPs in ISIAH (inherited stress-induced arterial hypertension) rats, which are known as a model of stress-induced arterial hypertension. 29615895: For the first model, 7-month-old Lanyu-miniature-pigs were given the abdominal aortic constriction operation to induce hypertension and their AD-related pathologies were assessed at 1, 2, and 3 months after the operation. 30005742: The lack of precise therapies for stress-induced hypertension highlights the need to explore the process of blood pressure changes. Here, as a model, we used rats with stress-induced hypertension, and found that a switch from an immunoregulatory (M2) to a pro-inflammatory (M1) dominant response occurred in microglia during development of stress-induced hypertension. 30385718: We modeled this effect in a KO rat model and showed that ALMS1 genetic deletion leads to hypertension. 30701746: Worksite hypertension as a model of stress-induced arterial hypertension. 30898984: Our studies show modest regulatory influence of moderate training on inflammatory markers in prehypertensive subjects and murine model of Ang II induced hypertension. 31326653: The Reduced Uterine Perfusion Pressure (RUPP) model results in hypertension and fetal growth restriction in a pregnant rat due to placental ischemia caused by mechanical obstruction of blood flow to uterus and placenta. We hypothesized that complement activation following placental ischemia stimulates the endothelin pathway to cause hypertension and impair fetal growth. 31707283: Contamination by BPA in this model caused hypertension and endothelial dysfunction and it was accompanied by a vascular ROS/NO imbalance, damage of endothelial layer and pro-apoptotic effects. 3337269: A novel model of nutritionally induced hypertension in the rat is described. 3371306: The borderline hypertensive rat: a model for studying the mechanisms of environmentally induced hypertension. 3436073: The BHR is discussed as a model for determining the triggers responsible for environmentally-induced hypertension. 4034262: The potential of this model for studies of the mechanisms by which environmental variables produce permanent hypertension is discussed. 6274915: Thus, the SHR PRA and aldosterone responses to sodium restriction and aldosterone response to A II were similar to that previously described in a subgroup of patients with essential hypertension suggesting that the SHR will serve as a model for exploring the mechanism(s) responsible for the hypertension in these patients. 6324224: This study investigated a model of psychosocial stress-induced hypertension in the rat, and examined effects of the prostaglandin E precursor, gamma-linolenic acid (GLA) on the development of hypertension during psychosocial stress. 7198098: The implications of using this model for the analysis of cardiovascular concomitants of stress-induced HT are discussed. 7329740: This underlying mechanism may be considered as a model of neural sensitization in the production of stress-induced limbic hypertension. 7498878: This model is comparable to hyperkinetic hypertension in hypertensive persons which, if it persists, will lead to established hypertension. 7541780: The two-kidney, one clip model was used to induce hypertension, and measurements were made 3 and 6 weeks after the left renal artery was clipped. 7788903: The model of hypertension consisted of silk tissue wrapping of the left kidney, which produced hypertension associated with perinephritis after 6 to 8 weeks. 7837830: The possibility of using the DOCA salt model of experimental hypertension in the guinea pig could help to elucidate the mechanisms responsible for hypertension and induced left ventricular hypertrophy, and thus improve prevention and treatment. 7840336: Rodents were assigned to the following groups: 1) normal control (NC); 2) abdominal aortic constriction (Abcon), a model that induces hypertension via renin-angiotensin II; 3) nephrectomy-deoxycorticosterone acetate treatment (DOCA), a model that induces hypertension through increased salt retention; 4) CR; 5) Abcon+CR; 6) DOCA+CR. 8472626: Our hypotheses were: (1) The condition of diabetes mellitus in a streptozocin animal model may show vascular changes similar to early pathology in macrovessels and (2) since the model is normotensive, inducing hypertension will result in early atherogenic pathology. 8496635: The tumor time-density curve following IP was characterized by a markedly delayed washout, with many hypovascular portions noted in the vascular model and a clear decrease in tumor vessels measuring 30 microns or less. in contrast, the peak value increased in the time-density curve and there was washout in the excretory phase following ATII induced hypertension. In view of the results, we suggest that a microcirculatory disorder resulting from IP administration could be improved under ATII induced hypertension. Following intraperitoneal(IP) administration of cis-diamminedichloroplatinum(CDDP), a dynamic study was conducted on rabbits in Angiotensin II(ATII) induced hypertension to investigate hemodynamic changes in VX2 ovarian tumors. 8585274: [Transgenic rats as a model for investigation of the pathogenesis of hypertension]. 8794817: Alterations in vascular reactivity in this model have not been extensively studied and could potentially be involved in the pathogenesis of L-NAME-induced hypertension. In vitro alteration of aortic vascular reactivity in hypertension induced by chronic NG-nitro-L-arginine methyl ester. 8804229: In general, these pheochromocytomas produce catecholamines that result in hypertension. Hypertension attributable to pheochromocytoma is a very attractive model for the elucidation of the pathogenesis of hypertension. 9336384: The SHR.BN-D1Mit3/Igf2 congenic strain represents an important new model for fine mapping and characterization of genes on chromosome 1 involved in the pathogenesis of spontaneous hypertension. 9675674: The model predicts that the geometric adaptation maintains the stress distribution in arterial wall to its control level, while the mechanical adaptation restores the normal arterial function under induced hypertension. 9779132: In the intact physiological model, induced hypertension by epinephrine and norepinephrine is not associated with global changes in CBF, ICP or COU which remain constant. 9797170: Administration of a low dose of adrenocorticotrophin to the rat is a suitable model for stress-induced hypertension. 11141480: The similar characteristics of microglia in the APP23 mice and in AD render the mouse model suitable to study the role of inflammatory processes during AD pathogenesis. 11193142: The APP23 line is a suitable model to analyze the contribution of APP, A beta, and amyloid to the pathogenesis of Alzheimer's disease. 14769913: These findings suggest a new model of AD pathogenesis in which a genomically orchestrated up-regulation of tumor suppressor-mediated differentiation and involution processes induces the spread of pathology along myelinated axons. 1497790: Mendelian genetics is a possible model for Alzheimer's disease etiology. 1741393: Ts 16 provides a model of spontaneous, genetically determined neurodegeneration that may be used to understand better the molecular pathogenesis of neuronal dysfunction in Alzheimer disease and Down syndrome. 18068305: The present study was designed to determine the time-course of the shift from neuronal to glial induction in the expression of these proteins in Down's syndrome, sometimes referred to as a human model of Alzheimer-like beta-amyloid (Abeta) deposition. 19096160: However, published data show that senescence-accelerated mouse (SAMP8), as a model of aging, display many features that are known to occur early in the pathogenesis of AD such as increased oxidative stress, amyloid-beta alterations, and tau phosphorylation. Here, the neurochemical, neuropathological, and behavioral alterations, characterized in SAMP8 mice are critically reviewed and discussed in relation to the potential use of this mouse model in the study of AD pathogenesis. 2039382: The proposed model postulates a role for environmental agents in the pathogenesis of Alzheimer's disease and accounts for families that show an aggregation of cases but no apparent pattern of inheritance. 20682182: We propose an integrative model on the pathogenesis of AD that includes several damage signals such as Abeta oligomers, oxygen free radicals, iron overload, homocysteine, cholesterol and LDL species. 21471644: The findings demonstrate that the effect of icv-STZ is regionally specific, lending further support for the method as a model of AD pathogenesis. 22112803: We have proposed a model which is consistent with most of the published data and current notions of AD pathogenesis and can serve as a hypothesis which can be tested. 22203915: Together, these data support a model of AD pathogenesis in which soluble Abeta initiates synaptic dysfunction and loss, as well as pathological changes in tau, which contribute to both synaptic and neuronal loss. 22459153: This model will allow the study of AD pathogenesis and testing of therapeutic strategies in a more relevant environment without experimental artifacts due to the overexpression of a single-mutant AbetaPP isoform using exogenous promoters. 22523954: This model allowed us to study the role of amyloid-beta25-35 in the pathogenesis of Alzheimer's disease and to test anti-amyloid substances. 22723178: So it might not be suitable to utilize the knockout murine model to explore biological function of Calhm1 in the pathogenesis of AD. 22735677: We integrate biomarker findings into a comprehensive model of AD pathogenesis from healthy aging to cognitive decline, the resilience to cerebral amyloid load (RECAL) matrix. 22785400: Amyloid-beta and tau pathology of Alzheimer's disease induced by diabetes in a rabbit animal model. AD-type pathology demonstrated in genetically unmodified rabbits calls attention to the considerable potential of the model for investigation of AD pathogenesis, diagnostics, and therapeutics. 22874668: Since in the brain and other tissues of these mice, wild-type human AbetaPP mRNA and protein levels are comparable to those of endogenous AbetaPP, this model may allow studies about the role of AbetaPP isoforms in the pathogenesis of AD. 23011729: The significance of this data and accompanying model pertains to the role transport plays in neuronal function, connectivity, and survival, and has implications in the pathogenesis of neurological disorders, such as Alzheimer's, Huntington and Parkinson's diseases. 23276384: The 3xTgAD mouse model was used to test the hypothesis that a ketone ester-based diet can ameliorate AD pathogenesis. 23383380: In this review we analyze the current situation in the use of zebrafish as a model for AD, discussing the reasons to use this experimental paradigm in CNS investigation and analyzing the several strategies adopted to induce an AD-like pathology in zebrafish. 23419876: The expression of GxxxG motifs on either reactant under consideration is in line with this model of Alzheimer's disease pathogenesis, which clearly differs from the amyloid Abeta cascade theory, and which can, furthermore, be understood as a basic model for apoptosis induction. 24150111: Consequently, 3xTg-AD mice may be a useful model in elucidating the role of immune system in the etiology of AD. 24239247: The aim of this study is to develop a predictive model using proton magnetic resonance spectroscopy (1H-MRS), a noninvasive technique that evaluates brain chemistry in vivo, for monitoring the clinical outcome of carriers of a fully penetrant mutation that causes AD. 24346216: We present a new model for etiology of Alzheimer's disease (AD) which postulates early involvement of specialized neuroprotective mechanisms in the pathology of AD. 24910393: A hypothetical model for the role of sleep and the Abeta diurnal pattern in AD pathogenesis is proposed. 25008180: In this study, we investigated the interrelation between AD and diabetes using a high-fat diet (HFD) in a mouse model of genetically induced AD-like neuropathology (3xTg-AD). 25131634: The results of this single-population gene expression analysis at the time of septohippocampal deficits in a trisomic mouse model shed light on a vulnerable circuit that may cause the AD-like pathology invariably seen in DS that could help to identify mechanisms of degeneration, and provide novel gene targets for therapeutic interventions. 2519521: The association of antibodies to cholinergic neurons with cognitive deficits in this rat model suggests that such antibodies may be involved in the pathogenesis of AD. 25213090: Furthermore, our study identifies a number of genes already known to be altered in human AD, thus confirming the use of the 5XFAD strain as a valid model for understanding AD pathogenesis and for screening potential therapeutic molecules. 25297091: Thus, generation of a macaque model of AD that links Abeta oligomers to tau and synaptic pathology has the potential to greatly advance our understanding of mechanisms centrally implicated in AD pathogenesis. 25310732: The 'amyloid cascade hypothesis' (ACH) is the most influential model of the pathogenesis of Alzheimer's disease (AD). 25754641: RESULTS: Here, using a Drosophila model of AD, we provide evidence suggesting that changes in neuronal excitability underlie the effects of sleep loss on AD pathogenesis. beta-amyloid (Abeta) accumulation leads to reduced and fragmented sleep, while chronic sleep deprivation increases Abeta burden. 25864576: Based on the schema of a well-received model of biomarker dynamics in AD pathogenesis, it has been postulated that SCD symptoms may result from compensatory changes in response to beta-amyloid accumulation and neurodegeneration. 26295040: We used a mouse model of amyloid beta- (Abeta-) induced AD, which is characterized by reactive gliosis and neuroinflammation in the brain, and we evaluated the effect of pentamidine on the main S100B-mediated events. 26461298: Similar results were obtained by using a C.elegans model of Amyloid beta (Alphabeta) -induced toxicity mimicking Alzheimer's disease. 26696886: Connectivity of Pathology: The Olfactory System as a Model for Network-Driven Mechanisms of Alzheimer's Disease Pathogenesis. 26759118: With this strategy, we identified a sequence of early events likely to account for disease onset and described a model that may facilitate efforts to decipher the factors triggering AD and to evaluate early neuroprotective strategies. 26918610: By using a new model of SCCH, our study unravels new insights into the implication of severe chronic cerebral hypoperfusion in AD pathogenesis, mainly by altering microglial cell activity and consequently Abeta clearance. 26959388: To establish a new mouse AD model that takes advantage of this benefit, we produced transgenic mice expressing amyloid-beta (Abeta), a causative element for AD, in their auditory hair cells. 27121378: METHODS: Wild-type (WT), TRPA1(-/-), amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic (APP/PS1 Tg) mice, the mouse model of AD, and APP/PS1 Tg/TRPA1(-/-) mice were used to examine the role of TRPA1 in pathogenesis of AD. 27569580: Collectively, our data show that the tTa:APPsi model is characterized by a lack of sex-related differences in APP expression, making this model useful in deciphering the mechanisms of sex differences in AD pathogenesis. 28186729: Although the amyloid (abeta peptide, Abeta) hypothesis is 25 years old, is the dominant model of Alzheimer's disease (AD) pathogenesis, and guides the development of potential treatments, it is still controversial. 28413635: The amyloid hypothesis has become the dominant model of AD pathogenesis; however, the details of the hypothesis are changing over time. 28459436: The findings in these index cases support a model in which early development of occult hippocampal hyperexcitability may contribute to the pathogenesis of AD. 28707174: The Puri-Li kinetic model is explored here to study the contribution of microglia and astroglia during the pathogenesis of Alzheimer's disease (AD). 29338754: Because the ADLPAPT mouse model recapitulates the main features of AD pathogenesis, the proteomic data derived from its hippocampus has significant utility as a novel resource for the research on the Abeta-tau axis and pathophysiological changes in vivo. 2934737: This possibility suggests a model for the pathogenesis of Alzheimer disease involving beta protein. 29615895: For the first model, 7-month-old Lanyu-miniature-pigs were given the abdominal aortic constriction operation to induce hypertension and their AD-related pathologies were assessed at 1, 2, and 3 months after the operation. 29754213: The Puri-Li kinetic model is modified to include neuronal calcium ion homeostasis to study the effect of calcium ions on the production of amyloid-beta peptides (Abeta), microglia, and astroglia during the pathogenesis of Alzheimer's disease (AD). 30043649: CONCLUSION: Our study on Drosophila model suggests that dysregulation of gut microbiota may participate in AD pathogenesis by influencing SCFA level. 30149447: The icv injection of STZ model and STZ exposed Neuro-2a cells may be potential experimental models for assessing molecules related to the pathogenesis of sAD. 30220236: By affirming markers of abnormal Abeta and tau proteins as the essential pathobiological signature of Alzheimer's disease, the Framework tacitly reinforces the amyloid (Abeta) cascade as the leading theory of Alzheimer pathogenesis. In light of recent evidence that the cascade is driven by the misfolding and templated aggregation of Abeta and tau, we believe that an empirically grounded Standard Model of Alzheimer's pathogenesis is within reach. 30557391: We show that mini-brains obtained from a non-AD control cell line are responsive to chemical compound induction, producing a shift of physiological Abeta concentrations, suggesting that this model can be used to identify environmental agents that may initiate the cascade of events ultimately leading to sporadic AD. 30837279: The senescence-accelerated mouse-prone 8 (SAMP8) model has been used to study age-related neurodegenerative changes associated with aging and the pathogenesis of AD. 30982098: In addition, on the basis of the new genetic landscape, resulting from the recent high-throughput genomic approaches and emerging neurobiological information, we propose an over-arching model in which the focal adhesion pathway and the related cell signalling are key elements in AD pathogenesis. 31342431: In this chapter, we demonstrate the use of all-atom molecular dynamics simulations to model the self-aggregation of a six-residue amyloidogenic peptide derived from amyloid beta, a 39-43 residue-long peptide associated with the pathogenesis of Alzheimer's disease. 31421155: In conclusion, we suggest that cerebral organoids are a suitable AD model for scientific study, and that will provide us a novel insight into the understanding of the pathogenesis of AD. 31450503: Blood platelets frequently serve as peripheral model for studying AD pathogenesis and might represent a reasonable biomarker source. 31551757: Studies on these biological mechanisms together with the use of the AOF model have the potential to shed light on key molecular pathways underlying AD pathogenesis for the development of precision medicine approaches that take sex and hormonal status into account. 31608251: This study assessed the effects of probiotic supplementation on spatial learning and memory, long-term potentiation (LTP), paired-pulse facilitation (PPF) ratios, nitric oxide (NO) concentrations, and lipid profiles in a rat model of amyloid beta (Abeta)(1-42)-induced Alzheimer's disease (AD). 34473990: This study establishes an excellent model to investigate the mechanism of activity-dependent hTau release and to better understand the role of phosphorylated tau release in the pathogenesis of AD since it relates to alterations in the early stage of neurodegeneration associated with increased neuronal activity. 34585626: An AD-like homocysteine (Hcy) rat model was established to evaluate the effects of miR-132-3p on AD pathogenesis in vivo . 7739409: A model is proposed to explain the aetiology of Alzheimer's disease. 8450928: Here we review current evidence in support of the cortical disconnection/cortical connectivity model of Alzheimer disease (AD) pathogenesis, a model which predicts that one of the first events in AD is damage to the entorhinal cortex and/or subiculum resulting in the disconnection of the hippocampal formation and neocortex, and the subsequent progression of the disease in a stepwise fashion along cortico-cortical connections. 9115271: This model provides important clues to the potential functions of different parts of the presenilin molecule and how these might relate to the pathogenesis of Alzheimer's disease. 9126173: The proposed mouse model may explain familial resistance to AD in man, provide extremely valuable insights into the etiology of AD, and suggest means for its prevention. 9330979: Requiring urgent resolution is whether cellular changes seen in brains of aging normals represent merely the earliest phase of typical AD (and therefore a good model for Alzheimer pathogenesis), or rather reflect a totally different aging syndrome distinct from AD. 10628927: Several reports have indicated that genes of these substances are crucial in the pathogenesis of hypertension. 12746271: Since the discovery of renin as a pressor substance in 1898, the renin-angiotensin (RAS) system has been extensively studied because it remains a prime candidate as a causative factor in the development and maintenance of hypertension. 14646690: Inter-individual differences in the action of these substances might be important in the pathogenesis of cardiovascular diseases such as acute myocardial infarction (AMI) and hypertension. 1513020: [Drugs and other substances inducing hypertension]. 1530375: It is suggested that endothelium-dependent relaxations are impaired in two-kidney, one-clip hypertension because of a cyclooxygenase-dependent substance interfering with the release and/or action of endothelium-dependent relaxing factor. 1531789: The role of the rate of increase in hematocrit (Hct) and changes in vasoactive substances as a cause of hypertension induced by the administration of recombinant erythropoietin (r-EPO) were examined in 20 stable hemodialysis (HD) patients. 1651964: Endogenous digital-like substance (DLS) is increased in patients with essential hypertension and is hypothesized to play a role in the pathogenesis of high blood pressure. 16886775: These results indicate that CES isolated from the shrimp eyestalk produces hypertension and tachycardia mediated by adrenergic receptors in association to calcium channels activation. 1776509: Following admission, brain protective substances (500 ml mannitol, 500 mg vitamin E, 500 mg phenytoin) and dextran, were administered to the patients, and induced hypertension was also performed. 19377226: Vascular endothelium dysfunction and increased endogenous vasoactive substances have been postulated in the pathogenesis of hypertension following multiple blood transfusions. 19871002: The reasons against accepting renin as the pressor substance responsible for the hypertension of renal ischemia may be summed up as follows:- 1. 20994298: Significance of basic argyrophil substance in the pathogenesis of hypertension. 2196126: To determine the role of an endogenous Na,K pump inhibitor/digoxin-like substance (DLS) in the pathogenesis of hypertension in acromegaly 76 subjects: 28 with acromegaly, 20 with essential hypertension and 28 healthy controls were studied. 2556303: These results suggest that Na+-K+ ATPase may play an important role in the maintenance of blood pressure through sodium efflux and that ouabain, Na+-K+ ATPase inhibitor, may change the renal sodium excretion and vascular responsiveness to endogenous pressor substances, leading to higher blood pressure after the administration of sodium and mineralocorticoid. 26673314: In a correspondence spanning 3 years, from January 1933 to April 1936, Cushing and Page collaborated to discover a substance responsible for hypertension. 3599802: It is now accepted that there is an endogenous digitalis-like substance (EDLS), previously called natriuretic factor, present in different mammalian species which participates to the regulation of the sodium balance and at least in some situations, to the genesis of hypertension. 6285109: In an attempt to evaluate the role of endogenous digitalis-like substance in the genesis of deoxycorticosterone (DOCA) -salt hypertension, the effects of intravenous anti-digoxin antibody on the blood pressure response were observed in male Wistar rats that underwent heminephrectomy followed by treatment with DOCA and saline. Involvement of endogenous digitalis-like substance in genesis of deoxycorticosterone-salt hypertension. Thus, it seems that endogenous digitalis-like substance plays an important role in the genesis of DOCA-salt hypertension. 7398346: Although angiotensin II has powerful vasoconstrictor properties, it is doubtful that any substance can produce sustained hypertension solely by increasing total peripheral resistance. The results of these studies clearly demonstrate that angiotensin has a powerful direct antinatriuretic effect, the magnitude of which is sufficient to cause marked hypertension at angiotensin concentrations well within the pathophysiological range. 7975661: As a vasoactive substance, DLF can participate in the regulation of blood pressure and play a role in the pathogenesis of arterial hypertension. 8215782: Moreover, genetic vascular changes affecting the structure of the vessels, the sensitivity to vasoactive substances or the geometry of the vascular system can also induce hypertension. 10608475: OBJECTIVE: In a model of hypertriglyceridemia and hypertension in rats (HTG), induced by adding refined sugar to the animals' drinking water, we investigated the response to an acute stress, such as ischemia and reperfusion. 12069355: We evaluated the myocardial function of rats with sugar-induced hypertriglyceridemia (HTG) and hypertension, and the effect of serum on myocardial performance in the isolated heart preparation. 1575950: Commentary on Reaven and Ho's \Sugar-induced hypertension in Sprague-Dawley rats\. 18374418: Although the exact pathological mechanisms behind sugar-induced hypertension are uncertain and may be multiple, disturbances in the renin-angiotensin system (RAS) manifested by elevated circulating levels of angiotensin-2 may be involved. Our data suggest that the RAS plays a significant role in sugar-induced hypertension and that NBC lowers SBP, at least in part, via actions on the RAS. 1873016: Sugar-induced hypertension in Sprague-Dawley rats. 19239143: Perinatal taurine depletion increases susceptibility to adult sugar-induced hypertension in rats. 20193752: The aim of this study was to evaluate the protective effect of Allanblackia floribunda aqueous extract on alcohol- and sugar-induced hypertension in rats. CONCLUSION: These results demonstrate that the aqueous extract of Allanblackia floribunda can prevent alcohol- and sugar-induced hypertension and oxidative stress in rats. 25484552: In conclusion, the data suggest that added sugars induce atherosclerosis, hypertension, peripheral vascular disease, coronary artery disease, cardiomyopathy, heart failure, and cardiac arrhythmias and that these effects of added sugars are mediated through ROS. The mechanism by which ROS induce the development of atherosclerosis, hypertension, peripheral vascular disease, coronary artery disease, cardiomyopathy, heart failure, and cardiac arrhythmias have been discussed in detail. 28373112: The present review article suggests that the consumption of a high-salt diet is not the cause of hypertension and that there are other factors, such as added sugars, which are causative for inducing hypertension and cardiovascular disease. For decades the notion that an excessive consumption of salt (NaCl) leads to hypertension has persisted. 28894625: Vascular reactivity experiments were conducted in rat aortic rings obtained from rats with and without sugar-induced hypertension, a model widely used to study such effects with cardiovascular agents. Dose-response curves to cumulative concentrations of all the extracts promote vascular relaxation in precontracted aortas from rats with and without sugar-induced hypertension. 8157859: The effects of high sugar diets on SBP were not due to angiotensin II inhibition, however, decreased availability of vasodilatory prostaglandins may play a role in the renal events and sugar-induced hypertension in SHR. OBJECTIVE: We examined whether sugar-induced systolic blood pressure (SBP) elevations in rats may develop, in part, through a mechanism common to salt-induced hypertension, i.e., renal retention of water and salt. CONCLUSIONS: Salt and water retention occur early during sugar-induced hypertension due to reduced renal excretion, consistent with some part in the pathogenesis. 8556833: Effects of chromium and guar on sugar-induced hypertension in rats. 9322992: In vivo plasma lipid oxidation in sugar-induced rat hypertriglyceridemia and hypertension. 10491314: These data support the suggestion that ROS and RNS, including superoxide radicals and nitric oxide, may play an important role in development of stress-induced hypertension in ISIAH rats. Manifestation of oxidative stress in the pathogenesis of arterial hypertension in ISIAH rats. 11688356: Cyclosporin-induced hypertension and endothelial dysfunction have been attributed to the effects of cyclosporin on factors controlling vasomotor tone. In transplanted patients with cyclosporin-induced hypertension, we have recently demonstrated upregulation of the NO system and superoxide and free radical overproduction, which, by increasing NO metabolism, could induce hypertension, vascular remodeling and chronic rejection. 11882628: The present experiments indicate that an increase in superoxide concentration within the renal medulla selectively reduces medullary blood flow resulting in chronic hypertension. 15103025: Imbalance between production and scavenging of superoxide anion results in hypertension by the inactivation of nitric oxide, and the increased oxidative stress from the resultant peroxynitrite that is produced promotes inflammatory processes such as atherosclerosis. 16106039: This study was performed to examine the role of superoxide formation in the regulation of renal hemodynamic and excretory function and to assess its contribution in the pathogenesis of ANG II-dependent hypertension. 18211830: One important example of the interaction between NO and ROS is the reaction of NO with superoxide to yield peroxynitrite, which may contribute to the pathogenesis of hypertension. 18650132: The involvement of reactive oxygen species such as superoxide is implicated in the pathogenesis of hypertension. 20053589: The findings indicate that dietary salt potentiates Ang-II-derived superoxide formation in the RVLM, resulting in a more severe hypertension. 23533693: The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. CONCLUSION: Glucocorticoid-induced hypertension in rats is prevented by alpha-lipoic acid via mechanisms other than mitochondrial superoxide reduction. AIMS: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition. 28590009: Moreover, rMnSOD prevents the nephrotoxicity induced by OTA probably restoring the balance between superoxide and NO that is most probably the cause of hypertension and renal functional alterations through the inhibition of NO synthase. 4053309: Following hypertension, the sustained vasodilation caused by acute hypertension was inhibited significantly by topical application of superoxide dismutase and catalase, showing that it was due in part to superoxide and other radicals derived from it. The appearance of superoxide anion radical in cerebral extracellular space during and after acute hypertension induced by intravenous norepinephrine was investigated in anesthetized cats equipped with cranial windows. The results show that superoxide and other radicals generated after acute hypertension interfere with acetylcholine-induced endothelium-dependent vasodilation, probably because they destroy the endothelium-derived relaxant factor. 8817404: Increased superoxide anion production in humans: a possible mechanism for the pathogenesis of hypertension. 8978321: Recent studies suggest that superoxide production by the NADPH/NADH oxidase may be involved in smooth muscle cell growth and the pathogenesis of hypertension. These findings suggest that Ang II-induced hypertension activates the NADPH/NADH oxidase system by upregulating mRNA levels of one or several components of this oxidase system, including the p22phox, and that the NADPH/NADH oxidase system is associated with the pathology of hypertension in vivo. 12735271: Seventy-one percent and 62% of patients were aware that stroke and heart attack respectively are possible consequences of high blood pressure. Forty-five percent attributed a variety of symptoms to their high blood pressure while 55% believed that stress was a cause of their high blood pressure. 17041804: In the following article we discuss the historical trends in terminology and epidemiology, clinical symptoms, and possible causes for therapy-resistant hypertension. 1828881: The diagnosis is not so easy and includes the usual history, physical examination (signs and symptoms of coarctation of the isthmic or abdominal aorta or of an abdominal mass or of one of the adrenal causes of hypertension), laboratory studies, abdominal ultrasound study and chest x-ray. 20203454: These factors may include BP measurement issues, poor adherence to antihypertensive medications, therapeutic inertia on the part of clinicians, lifestyle changes, secondary causes of hypertension, or ingestion of substances that interfere with BP control. Patients who demonstrate a deterioration in BP control should be questioned about adherence, recent changes to diet and lifestyle, signs and symptoms of secondary causes of hypertension, and use of any concomitant medications or other substances that may be known to increase BP or interfere with antihypertensive therapy. 20439562: The therapeutic goal is to improve postural symptoms, standing time, and function rather than to achieve upright normotension, which can lead to supine hypertension. 25864373: MATERIAL AND METHODS: We retrospectively reviewed data obtained from the medical records of 712 patients with no known diagnosis of hypertension who presented to a polyclinic due to symptoms related to elevated blood pressure (BP) and were screened for MHT. 28197344: Her initial presentation in hypertensive crisis with other symptoms led to diagnostic workup for secondary causes of hypertension and led to eventual diagnosis of paraganglioma. 30701375: Obesity, hypertension, heart disease, and diabetes can result from the symptoms of mental illness, the side effects from psychotropic medications, as well as disparities associated with being mentally ill. 33187680: Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms. 34075013: CASE REPORT A 58-year-old man with history including diabetes mellitus type 2, hypertension, and schizoaffective disorder was dismissed early from work due to symptoms of severe weakness, confusion, diaphoresis, dizziness, shortness of breath, palpitations, and a sensation of feeling hot. 34146434: The level in maternal circulation correlates with severity of hypertension and supports the involvement of STBEVs in causing maternal symptoms in PE. 37829494: A 45-year-old male with diabetes, hypertension and hyperlipidemia was referred to urology due to persistent symptoms of urinary frequency, urgency, nocturia, erectile dysfunction, and constant pain localized to the bladder, pelvis, and perineal area, 3-4 months after SARS-CoV-2 infection. 38107474: The present study describes the case of a 78-year-old patient with a medical history of high blood pressure, non-insulin-dependent diabetes mellitus, dyslipidemia, moderate aortic stenosis, chronic kidney disease and sarcoidosis under pharmacological treatment who attended the emergency department due to symptoms of neck pain, an increase in soft tissue, and dyspnea on moderate exertion with an evolution leading to respiratory failure. 8606221: RESULTS: Seven patients had precipitating events within 24 h of onset of symptoms that may have been causative of dissection and five had hypertension. 10464574: This paper provides a brief overview of the symptoms, progression, and etiology of AD, as well as of the prevalence and incidence of the disease. 10862215: OBJECTIVES: To determine the accuracy of the MMSE in predicting emergent AD in a sample of patients who were referred because of symptoms suggestive of memory problems and to determine whether an abbreviated version of the MMSE could be developed that would be as accurate as the full MMSE in predicting emergent AD. 16627930: Neurofibrillary degeneration characterized by abnormal hyperphosphorylation and aggregation of tau in affected neurons is directly associated with dementia symptoms and plays a pivotal role in the pathogenesis of Alzheimer disease (AD) and related tauopathies. 23634965: Specifically, since MCI coincides with the onset of clinical symptoms and brain atrophy, and LC pathology is already present at this early stage of AD pathogenesis, MCI may offer a critical window of time to initiate novel noradrenergic-based therapies aimed at the secondary wave of events that lead to progressive neurodegeneration. 25077345: Nutritional status of patients with certain neurological diseases such as stroke, Alzheimer's disease, Parkinson's disease, Epilepsy and Multiple Sclerosis can be altered because of symptoms associated with disease course, including certain micronutrient deficiency (folic acid, zinc, vitamin B6 and B12, vitamin D, vitamin E and vitamin C), changes in energy expenditure, intake decreased, gastrointestinal disorders and dysfunction of the bone mass. 26582973: Alterations in synaptic/neuronal activity and brain metabolism are considered among the earliest symptoms linked to the progression of AD, and lead to a central question in AD research: what is the role played by synaptic activity in AD pathogenesis? 27247784: The main of present paper was to investigate symptoms and causes of alzheimer disease from the view point of Iranian traditional medicine. 29051137: Although AD symptoms (83/271, 30.6%), causes of AD (80/271, 29.5%), and treatment (76/271, 28.0%) were commonly addressed, quality of life of people with AD (34/271, 12.5%) had more views than those more commonly-covered content areas. 29384656: Novel Multitarget-Directed Ligands Aiming at Symptoms and Causes of Alzheimer's Disease. 29865070: These results suggest that HKL has therapeutic potential for delaying the onset of AD symptoms by alleviating mitochondrial impairment and increasing hyperactivation of SIRT3 in the pathogenesis of preclinical AD. 30620503: If the somatic symptoms caused by adverse effects appear as a lack of animation or irritation, the changes due to adverse effects will be likely misunderstood as symptoms caused by progression of AD, behavioral and psychological symptoms. 31699319: Therefore, MALDI IMS taking account of the brain's functional connectivity and the spread of AD symptoms should be a powerful strategy for uncovering molecular signatures related to the AD trigger(s). 31771066: BACKGROUND: Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are often misdiagnosed with each other because of similar symptoms including progressive memory loss. 32827867: In particular, defects in cerebral glucose metabolism, which have been often noted even before the occurrence of clinical symptoms and histopathological lesions, are now regarded as critical contributors to the pathogenesis of AD. 33092411: Multidirectional in vitro and in cellulo studies as a tool for identification of multi-target-directed ligands aiming at symptoms and causes of Alzheimer's disease. 34420966: BACKGROUND: The differentiation of idiopathic normal pressure hydrocephalus (iNPH) from neurodegenerative diseases such as Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is often challenging because of their non-specific symptoms. 37922187: Frontotemporal dementia (FTD) is frequently misdiagnosed as Alzheimer's disease (AD) due to similar clinical symptoms. 37988777: However, it is still a grand challenge to accurately diagnose AD at its early stage because of the indiscernible early symptoms and the lack of sensitive detection tools. 10070030: Hereditary salt-losing syndromes have been ascribed to loss of function mutations in the alpha-, beta-, or gamma-ENaC subunit genes, whereas gain of function mutations (located in the COOH terminus of the beta- or gamma-subunit) result in hypertension due to Na+ retention (Liddle's syndrome). 10394240: Prevention of this syndrome, which represents the first secondary cause of hypertension, is until now disappointing. 10642293: Of these, the most successful have been studies that identified rare mendelian syndromes in which a single gene mutation causes high blood pressure. 11566956: In essential hypertension, a polygenic and multifactorial syndrome, several genes interact with the environment to produce high blood pressure. 136892: Variations in the mineralocorticoid hypertensive syndrome or, more aptly, the steroid hypertensive syndrome could account for the hypertension in a substantial portion of patients with reduced plasma renin activity. 17190991: She had been treated for cardiac failure and severe hypertension due to midaortic syndrome until she suffered seizure and repeated cerebral ischemic attack. 17521877: Mid-aortic syndrome remains an uncommon cause of hypertension in the pediatric population. 1951912: Two patients sustained spinal cord ischemia, and two developed hypertension due to \pseudo-coarctation\ syndrome. 2044434: A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. 21245605: This syndrome has multiple etiologies, most of which cause acute hypertension. 21318458: Nutcracker syndrome (NS) refers to compression of the left renal vein between the aorta and the superior mesenteric artery which results in left renal venous hypertension. 22318132: The PRES is typically associated with bilateral parieto-occipital T2 and FLAIR hyperintense MRI lesions and observed in various etiologic conditions leading to acute arterial hypertension. 22595392: This causes excess cortisol, simulating syndrome of apparent mineralocorticoid excess (AME), thus resulting in hypertension, hypokalemia and metabolic alkalosis. 23217201: CONCLUSIONS: PRES might be due to lupus per se besides other traditional causative factors such as hypertension. 23336180: Mutations in the novel serine/threonine WNK [With No lysine (=K)] kinases WNK1 and WNK4 cause PHAII (pseudohypoaldosteronism type II or Gordon's syndrome), a rare monogenic syndrome which causes hypertension and hyperkalaemia on a background of a normal glomerular filtration rate. 24365121: Posterior reversible encephalopathy syndrome from induced hypertension during endovascular thoracoabdominal aortic aneurysm repair. 24429046: Her young age and significant family history immediately prioritises secondary causes including phaeochromocytoma and familial syndromes causing hypertension. 25370165: CASE PRESENTATION: A 31-year-old woman presented with headache and poorly controlled hypertension due to severe MAS. 25680999: CONCLUSION: There are several reported examples of posterior reversible encephalopathy syndrome-induced licorice hypertension in adults, but none related to children. 26628389: Posterior Reversible Encephalopathy Syndrome as an Overlooked Complication of Induced Hypertension for Cerebral Vasospasm: Systematic Review and Illustrative Case. Furthermore, the electronic database MEDLINE was searched for additional data in published studies of PRES after induced hypertension. METHODS: We present an illustrative case of PRES in a patient with induced hypertension for SAH-related cerebral vasospasm and performed a systematic review. Posterior reversible encephalopathy syndrome (PRES) is a reversible intracranial complication that has rarely been reported in the setting of induced hypertension. Triple-H therapy, induced hypertension, hypervolemia, and hemodilution, is often used to treat cerebral vasospasm. 28697030: Severe Postpartum Headache and Hypertension Caused by Reversible Cerebral Vasoconstriction Syndrome: A Case Report. 29269696: This case is the first report of PRES without IVIg suggesting that Fisher syndrome induces hypertension and causes PRES. 29483232: Midaortic syndrome (MAS) is a rare cause of severe childhood hypertension characterized by narrowing of the abdominal aorta in children and is associated with extensive vascular disease. 30450431: NCS leads to LRV hypertension, resulting in left flank and abdominal pain, with or without haematuria and pelvic ureteral varices. 3067845: Glucocorticoid excess syndromes causing hypertension. 30866654: Important unmet needs in this field include the development of models that mimic the discrete hypertensive syndromes that now populate the clinic, resolution of ongoing controversies in the pathogenesis of hypertension, and the development of new avenues for preventing and treating hypertension and its complications. 31020259: Background: Severe forms of the midaortic syndrome cause persistent arterial hypertension and can lead to angina abdominalis. 31327271: Although maternal high-fructose intake induces cardiometabolic syndrome in adult offspring, whether it induces hypertension in successive multiple generations has not yet been studied. 31854150: Nutcracker syndrome (NCS) is a syndrome caused by compression of the left renal vein (LRV), between the abdominal aorta and the superior mesenteric artery, resulting in hypertension of the LRV and hematuria. 32210194: Therefore, treatment has better effects on hypertension produced by MS. 32326269: Supplementation with CSAT+ (r) prevented MetS-induced hypertension and decreased the vascular response of aortic rings to angiotensin II (AngII). 32516103: DISCUSSION AND CONCLUSIONS: In children and adolescents, vascular malformations like MAS must be considered as a possible cause of hypertension. 32544503: In conclusion, 2ME protects against MetS-induced hypertension and averts COMT inhibited expression and activity. 2-Methoxyestradiol ameliorates metabolic syndrome-induced hypertension and catechol-O-methyltransferase inhibited expression and activity in rats. The current study investigated the impact of 2ME on MetS-induced hypertension and the possible alterations in COMT expression and activity in rats. 32865201: CONCLUSIONS: The landscape of primary aldosteronism has evolved to recognize that it is a prevalent syndrome of renin-independent aldosterone production that contributes to the pathogenesis of hypertension and cardiovascular disease. 33478297: The mechanism by which hypertension is caused by NCP/NCS is rather complex and deserves further investigation. 33557413: TTh significantly improved MetS-induced hypertension, visceral adipose tissue accumulation, and glucose homeostasis derangements. 34643516: Since its identification, only forty years ago, definitions, diagnostic techniques have evolved, the consequences of this syndrome have been widely studied but establishing it as an independent cardiovascular (CV) risk factor has come up against the existence of many confounding factors, such as obesity, high blood pressure (hypertension)... 34760484: Mid-aortic syndrome is a rare cause of hypertension in the paediatric population. 35281112: By injecting pregnant mice with Ad-TAGLN2, we successfully generated a human PE-like syndrome that resulted in high blood pressure and some adverse pregnancy outcomes. 35818131: This case reports describe a rare disease, mid-aortic syndrome (MAS), that can cause severe heart failure and hypertension in infancy. 36017217: In this study, traditional Chinese medicine (TCM) syndrome of hypertension caused by high salt had been diagnosed and the pathogenesis of hypertension was explored from the perspective of intestinal microecology. Hypertension induced by a high salt diet belongs to liver-Yang hyperactivity syndrome. Rats in a high salt diet-induced hypertension group (CG) and normal group (CZ) were compared by 16S rRNA gene full-length sequencing and liquid chromatography and mass spectrometry to identify differences in the bacterial community structure, metabolites, and metabolic pathways. These findings suggest that a high salt diet induces hypertension of liver-Yang hyperactivity syndrome by mediating the microbiota associated with the glutamate/GABA-glutamine metabolic cycle via the gut-brain axis. 36968885: Mid-aortic syndrome, which results in the narrowing of thoracic or abdominal aorta, is a rare cause of hypertension, especially in newborns. 38344981: Despite the survival advantage, AA is associated with hypertension due to mineralocorticoid excess syndrome. 7138660: To make a more precise diagnosis, kidney biopsy was performed in 17 patients with a severe course of blood hypertension due to a mild urinary syndrome. 8048549: Second, low-renin syndrome defines the transition-to-establish phase in the pathogenesis of heart disease, diabetes mellitus, and hypertension in which the key feature is renin secretory hyporesponsivity. 8416084: This syndrome causes episodic hypertension in quadriplegic patients from excess sympathetic activity reflexly activated by bowel or bladder distention. 8564448: This syndrome is the third single-gene cause of human hypertension to be characterized, with glucocorticoid remediable aldosteronism (1992) and Liddle's syndrome (1994). 9175399: Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidaemia and atherosclerosis. 11792648: Reduced endothelial NO-cGMP vascular relaxation pathway during TNF-alpha-induced hypertension in pregnant rats. 11863253: Tumor necrosis factor-alpha-induced hypertension in pregnant rats results in decreased renal neuronal nitric oxide synthase expression. 15928030: The purpose of this study was to determine the role of endothlelin in mediating TNF-alpha-induced hypertension in pregnant rats. Recently, our laboratory reported that a 2-fold increase in plasma TNF-alpha produces hypertension in pregnant rats. 17954370: BACKGROUND: We previously showed that the infusion of tumor necrosis factor alpha (TNF-alpha) induces hypertension and vascular dysfunction in late pregnant but not virgin rats. 18852381: Moreover, TNF-alpha-induced hypertension (97+/-2 to 112+/-2 mm Hg; P<0.05) in pregnant rats was associated with AT1-AA production (TNF-alpha rats 9.2+/-2.3 U versus NP rats 1.0+/-0.8 U; P<0.05). 19745821: TNF-alpha-induced hypertension was associated with significant increases in renal and placental ET-1. Administration of 17-OHP attenuated TNF-alpha-induced hypertension and decreased renal ET-1. CONCLUSION: Progesterone directly abolished TNF-alpha-stimulated ET-1 and attenuated TNF-alpha-induced hypertension, possibly via suppression of the renal ET-1 system. 20431529: RESULTS: In response to TNF-alpha-induced hypertension, sFlt-1 increased from 180 +/- 5 to 2,907 +/- 412 pg/ml. Circulating sFlt-1 increased from 245 +/- 38 to 3,920 +/- 798 pg/ml in response to AT1-AA induced hypertension. 24005958: Tumour necrosis factor-alpha (TNF-alpha) is an important mediator in the pathogenesis of rheumatoid arthritis (RA) and hypertension. 31666827: Tumor necrosis factor-alpha (TNF-alpha) plays a vital role in the pathogenesis of hypertension. 36111265: In order to explore the changes and clinical significance of serum TNF- alpha and IL-6 and ET levels in the pathogenesis of hypertensive disorders of pregnancy (HDIP), echocardiography, and serum IL-6 and TNF- alpha changes in pregnant women with a hypertensive disorder, a clinical analysis method was proposed. 10630811: Both drugs are equally nephrotoxic, but tacrolimus induces less hypertension and less pronounced hyperlipidaemia. 10884522: Cyclosporin-A and tacrolimus can cause hypertension and renal failure through endothelin receptors. 11028414: [Cyclosporine- and tacrolimus-induced hypertension]. 11369839: Cyclosporin and tacrolimus also induce arterial hypertension. 11585243: Although cyclosporine has been influential in the improvement of transplant outcome, it has emerged as a major cause of hypertension after organ transplantation. There is evidence to suggest that the use of tacrolimus-based immunosuppression induces less hypertension compared with cyclosporine. 15701425: In particular, the lesser propensity of tacrolimus to cause hypertension and hyperlipidemia potentially offers decreased cardiovascular risk for heart and lung transplant recipients. 15919493: Cyclosporine (CsA) and less frequently tacrolimus (Tc) may cause hyperlipidemia and hypertension. 18370695: Corticosteroids can induce glucose intolerance, hypertension, hyperlipidemia, and weight gain. Cyclosporine and tacrolimus can induce glucose intolerance, hypertension, and hyperlipidemia. 21383022: FK506 [tacrolimus; hexadecahydro-5,19-dihydroxy-3-[2-(4-hydroxy-3-methoxycyclohexyl)-1-methylethenyl]-14,16-dimethoxy-4,10,12,18-tetramethyl-8-(2-propenyl)-15,19-epoxy-3H-pyrido[2,1-c][1,4]oxa-azacyclotricosine-1,7,20,21(4H,23H)-tetrone] is used clinically to reduce the incidence of allograft rejection; however, chronic administration leads to endothelial dysfunction and hypertension. 21518963: These data suggest that tacrolimus, through its activation of transforming growth factor-beta receptors in endothelial and hematopoietic cells, may cause endothelial dysfunction and hypertension by activating endothelial cells, reducing regulatory T cells, and increasing T-helper 17 cell polarization and inflammation. 21518964: Tacrolimus-induced hypertension: what's endothelial and hematopoietic FKBP12 got to do with it? 21963515: Together, these findings indicate that tacrolimus-induced chronic hypertension is mediated largely by NCC activation, and suggest that inexpensive and well-tolerated thiazide diuretics may be especially effective in preventing the complications of CNI treatment. In wild-type mice, the CNI tacrolimus caused salt-sensitive hypertension and increased the abundance of phosphorylated NCC and the NCC-regulatory kinases WNK3, WNK4 and SPAK. Moreover, hydrochlorothiazide, an NCC-blocking drug, reversed tacrolimus-induced hypertension. We hypothesized that CNIs induce hypertension by stimulating NCC. 23331314: Its etiology has been attributed to renal failure, immunosuppressive drugs such as cyclosporine and tacrolimus, and other potential entities leading to acute hypertension. 24718302: Tacrolimus-induced hypertension and nephrotoxicity in Fawn-Hooded rats are attenuated by dual inhibition of renin-angiotensin system. 25316243: Third, the activation of with-no-K(Lys) kinases/STE20/SPS1-related proline/alanine-rich kinase/thiazide-sensitive sodium chloride co-transporter (WNKs/SPAK/NCC) pathway has a central role in tacrolimus-induced hypertension. 26336164: Our results are consistent with the hypothesis that NCC activation plays a major role in tacrolimus-induced hypertension. Evidence in rodents suggests that tacrolimus-induced posttransplant hypertension is due to upregulation of the thiazide-sensitive Na+-Cl- cotransporter NCC. 26432904: However, it was unclear if tacrolimus-induced hypertension resulted from tacrolimus effects in renal epithelial cells directly or in extrarenal tissues, and whether inhibition of calcineurin was required. Together, these results suggest that tacrolimus causes hypertension predominantly by inhibiting calcineurin directly in cells expressing NCC, indicating thiazide diuretics may be particularly effective for lowering BP in tacrolimus-treated patients with hypertension. 28584011: Regulatory T-Cell Augmentation or Interleukin-17 Inhibition Prevents Calcineurin Inhibitor-Induced Hypertension in Mice. The immunosuppressive calcineurin inhibitors cyclosporine A and tacrolimus alter T-cell subsets and can cause hypertension, vascular dysfunction, and renal toxicity. Daily treatment of mice with cyclosporine A or tacrolimus for 1 week significantly decreased CD4+/FoxP3+ regulatory T cells in the spleen and lymph nodes, as well as induced hypertension, vascular injury and dysfunction, and glomerular mesangial expansion in mice. 29851248: CONCLUSION: LC40 treatment prevents hypertension and endothelial dysfunction induced by tacrolimus by inhibiting gut dysbiosis. SCOPE: The aim is to analyze whether the probiotic Lactobacillus fermentum CECT5716 (LC40) can prevent endothelial dysfunction and hypertension induced by tacrolimus in mice. Lactobacillus fermentum Improves Tacrolimus-Induced Hypertension by Restoring Vascular Redox State and Improving eNOS Coupling. 14024854: Primary arteritis of aorta causing renal artery stenosis and hypertension. 15190410: Proximal renal artery stenosis, in association with stenoses and/or aneurysms of aorta and its branches, suggests a Takayasu's disease and is an important, treatable cause of hypertension in young people. 1673862: Six children presented with severe hypertension caused by Takayasu's arteritis (TA), of whom four had bilateral renal artery narrowing and two coarctation syndrome. Angiotensin-converting-enzyme inhibitors should be used with caution in treating the hypertension caused by TA, since bilateral renal arterial narrowing is common and their administration may result in renal insufficiency. 1679002: Role of aorto-angioplasty in hypertension caused by Takayasu's arteritis. 20842956: The authors discuss the diagnostic and therapeutic implication regarding the clinical case of a young woman with hypertension due to atypical coarctation type Takayasu arteritis with impressive stenosis of renal arteries, of the proximal segment of celiac tripod and of superior mesenteric artery. 21724214: Although MAS is uncommon (0.5-2%), it is an important cause of hypertension in children and adolescents. 22290282: Takayasu arteritis as a cause of arterial hypertension. 23194278: This case depicts an atypical presentation of this disease where the girl visited many physicians for controlling the level of hypertension and put a diagnostic dilemma about the underlying etiology of young hypertension. CONCLUSION: Takayasu's Arteritis should also be kept in mind while searching for the cause of uncontrolled hypertension in the young age group. 23512530: In patients with TA, middle aortic syndrome with aortic and renal artery involvement causes severe hypertension that does not respond well to medical therapy. 23533898: Here we describe the case of a 4-year-old girl who presented with NF1 and hypertension due to atypical coarctation of the thoracic aorta. 25953247: The management of hypertension secondary to MAS frequently requires several anti-hypertensive medications along with endovascular and often surgical intervention. CASE-DIAGNOSIS/TREATMENT: A 9-year-old boy presented with headaches and vomiting and was diagnosed with severe hypertension secondary to idiopathic MAS affecting a long segment of the abdominal aorta and left renal artery stenosis. BACKGROUND: Middle aortic syndrome (MAS) is an uncommon cause of hypertension in children. 28202738: OBJECTIVE: Takayasu arteritis (TA) involving the renal artery can result in hypertension (HTN), renal dysfunction, and premature death. 29238882: The pathogenesis of hypertension due to TA is very complex and multifactorial. The objective of this study was to explore the presentation and management of hypertension secondary to Takayasu arteritis (TA) in a large cohort, single center in China. 29274: Takayasu arteritis is an important cause of severe persistent hypertension in nonwhite children. Takayasu arteritis with renal artery involvement was the cause of severe persistent hypertension in eight children under 12 years of age. 29373648: BACKGROUND: Renal artery stenosis (RAS) in isolation or in conjunction with middle aortic syndrome (MAS) are important vascular causes of childhood hypertension. 29531207: Middle-aortic syndrome is a surgically curable cause of childhood hypertension. 31616707: We aimed to demonstrate five young female patients who presented with a history of hypertension due to Takayasu arteritis. CASE SUMMARY: From April 2017 to October 2018, five female patients were diagnosed with hypertension due to Takayasu arteritis by computed tomography angiography (CTA) and laboratory tests. 5665686: Renal artery stenosis with hypertension due to primary aortic arteritis in a young girl. 5890903: [A case of hypertension caused by atypical coarctation of the thoracic aorta]. 8097612: Percutaneous transluminal renal angioplasty was performed in 54 consecutive patients with hypertension and renal artery stenosis caused by Takayasu's arteritis. 9142719: Middle aortic syndrome is increasingly recognized as a cause of hypertension in adolescents and young adults. 9868955: A 39-year-old woman was diagnosed by means of angiography as Takayasu arteritis complicated with severe systemic hypertension due to atypical coarctation of the aorta. 9922353: PATIENTS: Five patients, aged 4 to 17 years (mean 11.4 years), with upper limb hypertension due to middle aortic syndrome. 10523385: This study determined whether the androgen receptor plays a role in hypertension in male SHR and whether testosterone alone can cause the hypertension or whether conversion to dihydrotestosterone is necessary. 11904523: It is suggested that the enhanced hindlimb endothelial function represents a compensatory mechanism for testosterone-induced hypertension. 1655649: Chronic treatment of rats with the naturally occurring androgen, testosterone, leads to hypertension and cardiovascular disease. Expression of adrenal cytochromes P-450 in testosterone-induced hypertension. 21537151: CONCLUSIONS: In salt-loaded rats, testosterone seems to activate the renin-angiotensin system, resulting in sodium retention, higher BP and renal injury. 24855104: The results demonstrate that elevated testosterone during gestation induces hypertension in pregnant rats via heightened angiotensin II type 1 receptor-mediated signaling, providing a molecular mechanism linking elevated maternal testosterone levels with gestational hypertension. 25832114: Prenatal testosterone treatment also leads to fetal growth retardation, insulin resistance, and hypertension. 4392222: Testosterone-induced hypertension in the rat. 4645782: Prevention of methylandrostenediol, methyltestosterone and testosterone-induced hypertension in the rat by hypophysectomy. 6526083: Therefore, we studied the differences in the pressor mechanisms and the changes in urinary prostaglandin E (PGE) and kinin excretions among deoxycorticosterone acetate (DOCA)-salt hypertension, 19-OH-AD induced hypertension, and testosterone induced hypertension. 7087483: The present experiment compared the ability of testosterone and 19-nortestosterone to cause hypertension in rats. Both steriods caused adrenal atrophy, nephromegaly, relative hypoproteinemia and increased hematocrit, but only testosterone provoked saline polydipsia, hypernatremia, hypertension, cardiomegaly and vascular lesions. 1012116: The prevalence of hypertension was lower than that reported from Albury in 1971, Brunswick in 1972 or Busselton in 1969, but the difference from the latter is likely to be due to a higher treatment rate in Queenscliff. 10146863: Depletion of iron stores, hypertension, increased blood coagulability and reduced dialyser efficiency resulting from epoetin treatment may all add a small additional component to the true cost. 10485340: Thus, treatment with Dex altered the levels of these proteases which might have a role in the pathogenesis of hypertension and in altered blood coagulation. This study was designed to investigate the alterations in the levels of various proteases such as angiotensin converting enzyme (ACE), kallikrein, aminopeptidases, urokinase and plasmin in serum-heart and kidney and to find out whether the changes in the levels of these enzymes could explain the pathogeneses of hypertension induced by Dexamethasone (Dex). 10678593: Direct costs amount to more than 50% of the total costs of hypertension, and almost 70% of these are attributable to drug treatment. 10744360: L-NAME treatment induced arterial hypertension, in vitro aortic hyperresponsiveness to phenylephrine, impaired vasodilatory response to acetylcholine and no significant change in response to sodium nitroprusside. 10860767: AST causes hypertension, left ventricle (LV) hypertrophy and decreases plasma corticosterone level. 10904027: The effects of BSO were mitigated by concomitant antioxidant therapy despite GSH depletion, which supports the notion that oxidative stress was involved in the pathogenesis of hypertension in this model. Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. 10954000: METHODS: Hypertension, in Sprague-Dawley rats was induced by the oral administration of the arginine analog N(omega)-nitro-L-arginine methyl ester (L-NAME) in their drinking tap water for a period of 4 weeks. Enhanced expression of Gi proteins in non-hypertrophic hearts from rats with hypertension-induced by L-NAME treatment. 10976302: OBJECTIVE: To characterize clinical and clinicopathologic findings, response to treatment, and causes of systemic hypertension in cats with hypertensive retinopathy. 11073071: All treatments produced an initial hypertension within 2 min of drug administration followed by a significant decrease in arterial blood pressure (ABP) in horses administered 3 to 7.5 microg/kg medetomidine and 1 mg/kg xylazine. 11095160: The role of ovarian hormones and their withdrawal in the pathogenesis of hypertension and related target organ damage is considered, as are the results of drug treatment of high blood pressure in women. 11179079: We concluded that peripheral administration of losartan as well as embusartan can cause sufficient central effects to prevent the sympathetic hyperactivity and hypertension induced by chronic peripheral ouabain and central sodium. Sympathetic hyperactivity and hypertension caused by chronic treatment with ouabain or sodium-rich artificial cerebrospinal fluid (aCSF) can be prevented by central administration of an angiotensin type 1 (AT(1)) receptor blocker. 11196457: Difficulties with suppressive therapy resulted in severe hypertension. 11399644: Recent studies have suggested that subtle microvascular and tubulointerstitial injury in the kidney can cause salt-sensitive hypertension. To test this hypothesis, we determined whether the mild renal disease induced by transient blockade of nitric oxide (NO) synthesis would result in salt-sensitive hypertension and whether prevention of the renal injury by coadministration of the immunosuppressive agent mycophenolate mofetil (MMF) would block the development of salt sensitivity. Mycophenolate mofetil prevents salt-sensitive hypertension resulting from nitric oxide synthesis inhibition. L-NAME treatment resulted in acute hypertension and the development of mild renal injury. 11416417: Hypertension in the Elderly: An Update on Treatment Results and Recommendations - A Position Paper From the Council on Geriatric Cardiology. 11416595: This review summarizes the clinical profile of hypertension in women, the rationale for treatment, and the consequences of therapy, with an emphasis on age and gender biased risk assessment. 11549291: Possible mechanism(s) responsible for hypertension caused by treatment of mice with MC is also discussed. 11564974: CONCLUSIONS: Early fructose dietary treatment results in moderate hypertension and glucose intolerance, which is prevented by a single neonatal treatment with AT1R-AS. 1157222: It is concluded that significant alterations in ion transport by vascular smooth muscle occur before and during the development of hypertension induced by treatment with DOCA plus saline. 11669463: Cortical infarct volume was not significantly modified by either 2-week or 6-week L-NAME treatment, despite induced hypertension, whereas it was significantly higher in SHRs than in normotensive rats. 11673173: GDC treatment did not attenuate mean intraaneurysmal pressures, but both dampened the pressure amplitude and delayed pressure increases during locally induced hypertension. 11791005: Treatment with L-NAME induced marked arterial hypertension and cardiomyocyte hypertrophy, both of which were significantly reduced by propranolol and atenolol. The effects of propranolol and atenolol were investigated on arterial hypertension, cardiomyocyte hypertrophy, and ventricular ischaemic lesions induced by an 8-week treatment with the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 20 mg/rat per day) in Wistar rats. Our study demonstrates that propranolol and atenolol reduce arterial hypertension, cardiomyocyte hypertrophy and myocardial fibrosis induced by L-NAME, suggesting that beta-blockers are of beneficial value in treatment of vascular and cardiac alterations caused by chronic nitric oxide deficiency. 11821012: Effects of angiotensin blockade in the rostral ventrolateral medulla on maintenance of hypertension induced by chronic L-NAME treatment. 11906319: (1) Salt sensitive hypertension, which occurs as a result of treatment with nitric oxide synthase inhibitors, is associated with a loss of the usual down-regulatory effect of dietary sodium on angiotensin II (Ang II) synthesis. 11985539: Another model of hypertension was induced by treatment with an inhibitor of nitric oxide synthesis, namely NG-nitro-L-arginine methyl ester (L-NAME). 12083596: Impaired memory (14%), confusion (6%), and hypertension (6%) represented the most commonly reported negative reactions secondary to the treatment. 1218518: The authors examined the changes in arterial blood pressure and the content of Noradrenaline in the myocardium, brain and aorta of rats with hypertension due to nephrectomy and treatment with desoxycorticosterone and NaCl, and after a chronic 6-month treatment of hypertension with various antihypertensive means. 12384457: Thus aldosterone and salt treatment in uninephrectomized rats led to severe hypertension and the development of a vascular inflammatory phenotype in the heart, which may represent one mechanism by which aldosterone contributes to myocardial disease. Aldosterone induced severe hypertension at 4 wk [systolic blood pressure (SBP), 210 +/- 3 mmHg vs. vehicle, 131 +/- 2 mmHg, P < 0.001], which was partially attenuated by eplerenone (SBP, 180 +/- 7 mmHg; P < 0.001 vs. aldosterone alone and vehicle). 12386513: The mainstays of treatment are careful maintenance of fluid balance, induced hypervolemia and hypertension, calcium antagonists, balloon or chemical angioplasty, and, in some centers, cisternal fibrinolytic drugs. 1248484: The high blood pressure fell significantly due to treatment with adelphan. 12577670: The diagnosis of hypertension in patients on chronic haemodialysis is not easy because the blood pressure changes as a consequence of therapy (haemodialysis) and attenuated circadian rhythm of blood pressure is often present. 13351978: [Effect of serpasil on arterial hypertension, review of results of treatment of 32 cases]. 13903847: Macromolecular hypertension and associated pathologic changes resulting from treatment with polyvinyl alcohol. 14757146: We compared the effects of 4 weeks treatment of the vasopeptidase inhibitor omapatrilat and the angiotensin converting enzyme inhibitor enalapril on the degree of fibrosis and the concentration of VIP in the heart in salt sensitive hypertension induced by treatment with L-nitro-omega-methylarginine (L-NAME). 1477292: Treatment with deoxycorticosterone acetate (DOCA) and salt for 12 weeks consistently induced hypertension in rats. 15126644: We investigated cardiac gene expression in response to acute (24 h) and chronic (14 day) infusion of ANG II in mice; 24-h treatment induces hypertension, and 14-day treatment induces hypertension and extensive cardiac hypertrophy and necrosis. Exposure of experimental animals to increased angiotensin II (ANG II) induces hypertension associated with cardiac hypertrophy, inflammation, and myocardial necrosis and fibrosis. 15193992: The chronic treatment of rats with N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) biosynthesis, results in hypertension. 15728783: Recombinant human erythropoietin therapy frequently causes hypertension in humans and animals with chronic renal failure. 1578515: Effect of high calcium diet on the formation of hypertension induced by chronic cadmium chloride (CdCl2) treatment was investigated in Wistar rats. 1630679: The authors examine the most recent findings on arterial hypertension with particular emphasis to morphological changes of the arterial wall and to the results of nicardipine treatment in spontaneous hypertensive rats (SHR). 1632999: In univariate analyses, variables significantly associated with better pharmacy compliance were perceived lifetime treatment of hypertension, greater than 5-year history of medication use, perceived cause of hypertension other than diet, use of more than one hypertension drug, lack of reported departure from the prescribed medication regimen, absence of drug abuse history, and race (Caucasian). In multivariate analyses, the best predictive model of pharmacy compliance included three variables: drug abuse history, perceived cause of hypertension, and pattern of medication use. 1655649: Chronic treatment of rats with the naturally occurring androgen, testosterone, leads to hypertension and cardiovascular disease. Expression of adrenal cytochromes P-450 in testosterone-induced hypertension. 16597192: CONCLUSION: Naturopathic medicine as a whole medical system supplies evidence-based lifestyle recommendations as suggested in management guidelines for diabetes, hypertension, and hyperlipidemia set forth by the respective national organizations - the American Diabetes Association (ADA), the Joint National Committee on Hypertension (JNC-7), and the National Cholesterol Education Program results of the third Adult Treatment Panel (NCEP ATP-III). 16691532: The rat model of hypertension induced by prolonged treatment with Nomega-nitro-L-arginine methyl ester (L-NAME) has been extensively used. Macrophage populations and cardiac sympathetic denervation during L-NAME-induced hypertension in rats. 16710099: CONCLUSIONS: L-NAME treatment leads to hypertension, proteinuria and renal fibrosis. METHODS: 36 Sprague-Dawley rats were divided into a control group and an experimental group, in which hypertension was induced by oral administration of L-NAME (100 mg/kg/day). 16714158: Treatment of resistant hypertension is predicated upon identification and reversal of secondary causes of hypertension, as possible, and effective use of multidrug regimens. 16716361: Chronic ouabain treatment produces hypertension acting on the central nervous system and at vascular levels. Ouabain-induced hypertension enhances left ventricular contractility in rats. Ouabain induces hypertension but not myocardial hypertrophy. 1687447: We are less able to rely on young age and resistance to treatment as indications for more extensive evaluation of secondary causes of hypertension; thus, greater reliance on history, physical examination, and clinical judgment is required if we are to identify potentially treatable causes. 16915305: Run training prevented the arterial hypertension induced by L-NAME treatment (LN-SD: 135+/-2 and 141+/-2 mm Hg for both doses of L-NAME) compared to LN-SD groups (154+/-1 and 175+/-2 mm Hg, for 2 and 10 mg of L-NAME, respectively). 16942669: The treatment offered depends on the cause of the hypertension and the underlying health of the liver. 17212192: BMI was in correlation with severity of hypertension as well as with obtained treatment result. 17215651: Treatment of resistant hypertension requires confirmation of true resistance, diagnosis and treatment of secondary causes of hypertension, adoption of appropriate lifestyle modifications, and effective use of multidrug antihypertensive regimens. 17261647: Chronic treatment with the immunosuppressive drug rapamycin leads to hypertension; however, the mechanisms are unknown. 17324744: Folic acid, but not BH(4), prevented the development of hypertension caused by ACTH and Dex treatment. 17436021: Chronic treatment of rats with N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) biosynthesis, results in hypertension mediated partly by enhanced angiotensin-I-converting enzyme (ACE) activity. 17519555: CONCLUSION: Hypertension caused by chronic ethanol treatment as well as L-NAME administration could be associated with the reduction of APN and APA activity. 17582440: Although there has not been a large, randomized clinical trial of this treatment, the available clinical data suggests that induced hypertension can result in at least short-term neurological improvement, with an acceptable degree of safety. 17679034: CONCLUSIONS: These results indicate that gamma-MSH deficiency is a consequence of the bromocriptine treatment responsible for the salt-sensitive hypertension, and these results also identify the time course during which this hypertension develops. 17679742: Non-compliance to anti-hypertensive therapy remains the most common cause of resistant hypertension. 17972502: Hypertension secondary to anti-angiogenic therapy: experience with bevacizumab. 1815311: [A case from practice (234). Torsades de pointes under quinidine therapy and diuretic-induced hypokalemia. 2. Hypertension and coronary heart disease - tachycardia with atrial flutter - biventricular heart insufficiency - sick-sinus syndrome - 3. Arterial hypertension. 4. chronic bilateral venous insufficiency]. 18286835: Other first-tier options include induced hypocapnea (hyperventilation; paCO2 < 35 mmHg), hyperosmolar therapy (mannitol, hypertonic saline) and induced arterial hypertension (CPP concept). 18391085: Successful treatment requires identification and reversal of lifestyle factors contributing to treatment resistance; diagnosis and appropriate treatment of secondary causes of hypertension; and use of effective multidrug regimens. 1854087: Mean arterial pressure was significantly reduced for various periods with all treatments; however, IV administration of 0.02 mg of detomidine/kg caused hypertension initially. 18551923: Besides effective and prompt treatment, it is mandatory to screen for secondary causes of the hypertension. 18572415: Hypertension was induced by 4-weeks treatment with N(omega)-nitro-l-arginine-methyl ester (l-NAME). 18574054: Successful treatment requires identification and reversal of lifestyle factors contributing to treatment resistance; diagnosis and appropriate treatment of secondary causes of hypertension; and use of effective multidrug regimens. 1888244: STUDY OBJECTIVE: --To determine the prevalence of resistant hypertension in a tertiary care facility, the frequency of its various causes, and the results of treatment. 18959838: Successful treatment of resistant hypertension is predicated on improvement of lifestyle factors; accurate diagnosis and treatment of secondary causes of hypertension; and use of effective multidrug regimens. 19043981: These results indicate that hypertension induced by chronic ouabain treatment is accompanied by increased endothelial nitric oxide participation and impaired endothelium-dependent hyperpolarizing factor contribution in acetylcholine-induced relaxation. 1915722: Ultrastructural changes in the blood-brain barrier after nimodipine treatment and induced hypertension. 19332223: The mechanism for anti-VEGF therapy-induced hypertension is not well understood; however, nitric oxide pathway inhibition, rarefaction, and oxidative stress may be important in its pathogenesis. 19372677: Arterial hypertension caused by sunitinib therapy was effectively controlled by the use of an angiotensin-converting-enzyme inhibitor. 19373508: Treatment for IAH/ACS should be selected on the basis of the severity of symptoms and the cause of IAH. 19462818: Since these alterations suggested the presence of vasogenic edema induced by hypertension, we diagnosed him as having reversible posterior leukoencephalopathy syndrome (RPLS) induced by hypertension. Therefore, we considered that hypertension was induced by oral CBZ therapy. 19623085: Outcomes are improved by prompt diagnosis and treatment of hypertension, preventing hypertensive end-organ damage, choice of an appropriate first line antihypertensive treatment, and not subjecting children to invasive investigations looking for an alternative secondary cause of hypertension. 19626329: We propose that the ouabain-induced reduction of the renal dopamine D(1) receptor function serves as a mechanism responsible for sodium retention, and this contributes to the hypertension induced by chronic ouabain treatment. 19889865: Therefore, the present study was undertaken in conscious rats in which hypertension was induced by treatment with l-NAME over the course of either 2 or 14 days. The role played by the sympathetic drive in the development of N(G)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension is not firmly established. In conclusion, the evaluation of the sympathetic drive in conscious rats demonstrated that the arterial hypertension induced by l-NAME treatment over the course of 2 and 14 days does not show sympathetic overactivity. 19918172: Malingering hypertension is clinically suspected when there is a potential external secondary gain, absence of patient cooperation during diagnostic evaluation and a lack of response to antihypertensive treatment. 19918475: Once a diagnosis of tuberculosis autonephrectomy is made the next decision is whether any further investigations and treatment is necessary as the condition has been reported to be a cause of hypertension and reactivation of tuberculosis is also possible. 1997896: Thirty anesthetized cats were randomly assigned to one of three groups of 10 cats each: nimodipine treatment, nimodipine treatment combined with induced hypertension, or a control group. 20041987: Chronic L-NAME treatment induced hypertension, elevated the oxidative load and inhibited NOS activity. To elucidate the possible role of the nitric oxide (NO) pathway in the hemodynamic actions of melatonin, the effects of this indolamine on vascular function during hypertension induced by the NO-synthase (NOS) inhibitor, N(omega)-nitro-L-arginine-methyl ester (L-NAME) were investigated. Melatonin interactions with blood pressure and vascular function during L-NAME-induced hypertension. 2024530: After successful treatment of the condition leading to hypertension, circadian periodicity returned in some patients. 20661669: Treatment of resistant hypertension is aimed at reversing lifestyle factors contributing to treatment resistance, accurately diagnosing and appropriately treating secondary causes of hypertension, and effectively using multidrug regimens. 20823711: RESULTS: The continuous light and L-NAME treatment led to hypertension, left ventricular hypertrophy (LVH) and fibrosis. 20842251: OBJECT: The purpose was to highlight the diagnosis and treatment of extra-adrenal para-gangliomas, which often causes catecholamine hypersecretion and hypertension. 21146124: However, VEGF-targeted therapies cause hypertension in 30% to 80% of patients. In this article, we review current understanding of the mechanisms of VEGF-targeted therapy-induced hypertension, discuss similarities with preeclampsia, review implications for therapy of this increasingly common clinical problem, and discuss the potential use of blood pressure increase as a biomarker for proper drug dosing and effective VEGF pathway inhibition. 21263123: Treatment resulted in mild hypertension, a blunting of weight gain, gross polydipsia, polyuria, and sodium intake, alterations in urinary sodium and potassium turnover, and serum sodium retention. 21273786: CONCLUSION: Although ouabain treatment induced hypertension in all groups, a larger noradrenaline induced contraction was observed over 20 weeks of treatment. 21327576: RESULTS: We identified three patients (two female and one male), ranged in age from 62 to 70 years who developed PRES after treatment with induced or permissive arterial hypertension. 21461391: Successful treatment requires identification and reversal of lifestyle factors or drugs contributing to treatment resistance, diagnosis and appropriate treatment of secondary causes of hypertension, use of effective multidrug regimens and optimization of diuretic therapy. 21527770: In a Cox proportional hazards model using HTN as a time-dependent covariate, PFS (HR of disease progression or death = .603, 95% CI = .451 to .805; P < .001) and OS (HR of death = .332, 95% CI = .252 to .436; P < .001) were improved in patients with treatment-induced HTN defined by maximum SBP; OS (HR of death = .585, 95% CI = .463 to .740; P < .001) was improved in patients with treatment-induced HTN defined by maximum DBP, but PFS was not. 21822477: This special issue of the journal expoars a whole spectrum of topics related to resistant hypertension: several articles address pathophysiolog and secondary causes of resistant hypertension and modern approaches to therapy. 21968750: Recognition and treatment of secondary causes of hypertension among patients with resistant hypertension may help to control blood pressure and reduce cardiovascular risk. 22051897: Taken together, these results demonstrated that the sap of Acer okamotoanum ameliorated high BP induced by L-NAME treatment in a rat model. 22222493: We discuss the similarity between preeclampsia and VEGF-targeted therapy-induced hypertension. Antiangiogenic-induced hypertension: the molecular basis of signaling network. 22240443: Hypertension can lead to erectile dysfunction as a consequence of high blood pressure (BP) or due to antihypertensive treatment. 22258333: BACKGROUND: We have shown that the ouabain-sensitive alpha2 Na,K-ATPase is required for adrenocorticotropic hormone (ACTH)-induced hypertension and gestational blood pressure regulation. These findings indicate that the underlying mechanisms of hypertension induced by DOCA-salt treatment are different from those of ACTH-induced hypertension. 2232308: Among the risk factors, hypertension has gradually decreased due to treatment and lower intake salt in Japan. 22730391: Recently, angiotensin II (ANG II) chronic treatment, which induces hypertension, was shown to generate nitrosative stress in addition to oxidative stress. 22785409: Recent evidence implicates nitric oxide (NO) suppression and endothelin-1 (ET-1) stimulation as potential mechanisms leading to antiangiogenic therapy-induced hypertension. 22851729: Management of antiangiogenic therapy-induced hypertension. 22871654: A poor response to therapy should trigger a search for a secondary cause of hypertension. 22895622: In conclusion, GSPE antagonized ouabain-induced hypertension and vascular remodeling and is recommended as a potential anti-hypertensive agent for patients with hypertensive vascular diseases. Recent studies indicate that chronic ouabain treatment leads to hypertension and hypertensive vascular remodeling. 22980569: Renal artery aneurysm: an endovascular treatment for a rare cause of hypertension. 23024265: This study tests the hypothesis that activation of the NK-1Rs by SP occurs during hypertension induced by deoxycorticosterone (DOCA)-salt treatment, which contributes to renal injury in this model. 23033370: We sought to identify the key chemokine receptors associated with macrophage infiltration into the vascular wall during deoxycorticosterone acetate (DOCA)/salt-induced hypertension in mice and to evaluate the impact of pharmacological inhibition of these receptors on blood pressure and leukocyte accumulation. Intervention with a CCR2 antagonist, INCB3344 (30 mg/kg per day, IP), 10 days after the induction of hypertension with DOCA/salt treatment, reduced the aortic expression of CCR2 mRNA and completely reversed the DOCA/salt-induced influx of macrophages. 23084334: Recurrence of acute severe hypertension, nephrotic state (edema/ hypoalbuminemia), and renal insufficiency may lead to recurrent PRES and thus early treatment of trigger factors, especially of hypertension, is important to reduce the episodes of PRES. 23128822: The degree of BP reduction after 8 weeks of spironolactone treatment did not differ significantly between the three tertiles of baseline systolic BP and patients with and without a secondary cause of hypertension. 2327189: The lesions caused by these experimentally established pathological conditions were analysed by the following criteria, after treatment with a Ca-blocking agent (Nitrendipine, Bayer, Leverkusen): Changes in systematic blood pressure; Histochemical detectability of myocardial and vascular lesions as a consequence of artificially induced hypertension and hypoxaemia; Assessment by means of the tracer technique (Ferrlecit, Nattermann, Cologne) of alterations to vascular permeability in small cardiac vessels of rats treated and not treated with the Ca-blocking agent; Detection of lesions in small vessels of other organs, such as intestine, mesentery, and pancreas, in rats treated and not treated with the Ca-blocking agent. 23339959: Treatment led to an increase in systolic arterial pressure by >20 mm Hg in 14 applications (n=7 patients) resulting in severe hypertension (>180 mm Hg) in 4 applications (n=3). 23537524: Hypertension caused by anti-VEGF therapy can be effectively treated; progression of proteinuria and/or renal dysfunction may require tapering, or even withdrawal of anti-VEGF treatment. 23606891: Currently, there is a growing interest in the traditional Chinese medicine (TCM) for patients with hypertension mainly due to the personalized therapy of TCM in many countries. 2385317: On the other hand, treatment with induced hypertension is a widely accepted measure to reverse ischemic deficits caused by vasospasm. 23860374: Treatment with the synthesized TNF-alpha inhibitor 3,6-dithiothalidomide reversed pathologic vessel wall alterations after induced hypertension and hemodynamic stress. 2406101: The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. 24119421: We considered as an adapted justification: a white coat effect demonstrated by ambulatory blood pressure monitoring (ABPM) or home blood pressure monitoring; scheduled reassessment of the BP by ABPM; recent change in antihypertensive treatment (less than 4 weeks); hospitalization needed for complete evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage in patients with grade 1 or 2 hypertension. 24323051: Prompt recognition of DCI and immediate treatment by means of induced hypertension and balloon or pharmacological angioplasty are considered important by many physicians, although the evidence to support such approaches is limited. 24403467: Hypertension induced by bevacizumab predicted therapy efficacy. 24468640: [Hypertension secondary to treatment with latanoprost]. 24611002: PURPOSE: The World Health Organization (WHO) concluded that poor adherence to treatment is the most important cause of uncontrolled high blood pressure, with approximately 75% of patients not achieving optimum blood pressure control. 24640584: CONCLUSION: Relaxin's removal during the treatment may intervene in the pathogenesis of intradialytic hypertension. 24694383: CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone. 24695748: Aldosterone-salt treatment induces not only hypertension but also extensive inflammation that contributes to fibrosis in the rat kidney. 24791187: Successful treatment requires identification and reversal of life-style factors contributing to treatment resistant and diagnosis and appropriate treatment of causes of hypertension. 24942010: Changes in adrenoceptors and G-protein-coupled receptor kinase 2 in L-NAME-induced hypertension compared to spontaneous hypertension in rats. This work compares the expression of adrenoceptors (ARs) and G-protein-coupled receptor kinase (GRK) 2 (RT-PCR and immunoblotting) and functional responses in conductance (aorta) and resistance vessels (mesenteric resistance arteries; MRA) in two different models of rat hypertension: hypertension induced by chronic treatment with L-NAME (N(G)-nitro-L-arginine methyl-ester) (L-NAME-treated rats; LNHR), and genetically induced hypertension (spontaneously hypertensive rats; SHR). 25076181: These findings represent a new approach to the development of therapeutic protocols for the treatment of Pb-induced hypertension. 25234339: Treatment with the vitamin C and polyphenol combination resulted in higher BP variation: the rate of night-time systolic BP variation (P= 0.022) and pulse pressure variation (P= 0.0036) were higher and the rate of daytime systolic BP variation was higher (P= 0.056). 25369256: Anti-vascular endothelial growth factor (VEGF) therapy has been shown to disrupt the normal nitric oxide signaling pathway, producing systemic arterial hypertension following systemically administered anti-VEGF in oncology by exactly that mechanism. 25405823: SUMMARY: Vascular intervention remains important for the treatment of stenosed and occluded arteries leading to organ ischaemia or hypertension, and for aneurysmal disease. 2544114: Although tail-cuff measurements of arterial pressure indicated that the ACTH treatment produced hypertension, this was not confirmed by direct 24-h measurements of mean arterial pressure. ACTH-induced hypertension in rats: fact or artifact? 25468878: According to current practice guidelines, treatment consisted of induced hypertension. 25531211: It should be encouraged for detecting high BP or proteinuria, especially if antiangiogenic therapies are envisaged because of the supplementary risk of hypertension and proteinuria induced by these treatments. 25557543: Patients were classified as normotensive or hypertensive depending on whether hypertension developed that was attributable to therapy. Bevacizumab-induced hypertension is a predictive marker for improved outcomes in patients with recurrent glioblastoma treated with bevacizumab. Bevacizumab-induced hypertension is a well-documented side effect, and some reports have suggested this occurrence to be related to treatment outcome in other cancers. Bevacizumab-induced hypertension may be a physiologic marker of outcome in patients with recurrent GBM. 25683700: Because the majority of hypertensive patients were under corticosteroid treatment, the iatrogenic cause of hypertension cannot be excluded. 25719927: Although studied extensively through experimental and clinical trials, current treatment guidelines to prevent delayed cerebral ischemia is limited to oral nimodipine, maintenance of euvolemia, induction of hypertension if ischemic signs occur and endovascular therapy for patients with continued ischemia after induced hypertension. 25820137: Treatment with either indomethacin (to inhibit cyclooxygenase-dependent eicosanoid production) or varespladib (which inhibited eicosanoid production) triggered acute hypertension in Mmp2(-/-) mice, revealing their reliance on eicosanoids for blood pressure homeostasis. 25832114: Prenatal testosterone treatment also leads to fetal growth retardation, insulin resistance, and hypertension. 26007281: Successful treatment requires identification and reversal of lifestyle factors contributing to treatment resistance; diagnosis and appropriate treatment of secondary causes of hypertension; and use of effective multi drug regimens. 26068063: Cardiac-specific overexpression of metallothionein attenuates myocardial remodeling and contractile dysfunction in l-NAME-induced experimental hypertension: Role of autophagy regulation. Our results revealed that l-NAME treatment (14 days) led to hypertension and myocardial anomalies evidenced by interstitial fibrosis, cardiomyocyte hypertrophy, increased LV end systolic and diastolic diameters (LVESD and LVEDD) along with suppressed fractional shortening. l-NAME compromised cardiomyocyte contractile and intracellular Ca(2+) properties manifested as depressed peak shortening, maximal velocity of shortening/relengthening, electrically-stimulated rise in intracellular Ca(2+), elevated baseline and peak intracellular Ca(2+). This study was designed to examine the effect of cardiac-specific overexpression of metallothionein, a cysteine-rich antioxidant, on myocardial contractile and intracellular Ca(2+) anomalies in N(G)-nitro-l-arginine methyl ester (l-NAME)-induced experimental hypertension and the mechanism involved with a focus on autophagy. 26081815: BACKGROUND: Treatment-induced hypertension might correlate with antiangiogenesis treatment efficacy. 2632718: The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. 26379557: Furthermore, starting at 6 weeks after the induction of 2K1C hypertension, oral treatment with the HEX (10 mg/Kg/day) for 7 days reduced blood pressure in hypertensive animals (134 +/- 6 vs. 170 +/- 4 mmHg, respectively). 26559126: Here, the role of NO-GC1 in hypertension provoked by contractile agonists angiotensin II (Ang II) and norepinephrine (NE) was evaluated in NO-GC1-deficient mice. Hypertension induced by chronic Ang II treatment did not differ between wild-type (WT) and NO-GC1 knockout mice (KO). Angiotensin II-Induced Hypertension Is Attenuated by Reduction of Sympathetic Output in NO-Sensitive Guanylyl Cyclase 1 Knockout Mice. 26628389: Posterior Reversible Encephalopathy Syndrome as an Overlooked Complication of Induced Hypertension for Cerebral Vasospasm: Systematic Review and Illustrative Case. Furthermore, the electronic database MEDLINE was searched for additional data in published studies of PRES after induced hypertension. METHODS: We present an illustrative case of PRES in a patient with induced hypertension for SAH-related cerebral vasospasm and performed a systematic review. Posterior reversible encephalopathy syndrome (PRES) is a reversible intracranial complication that has rarely been reported in the setting of induced hypertension. Triple-H therapy, induced hypertension, hypervolemia, and hemodilution, is often used to treat cerebral vasospasm. 26711739: Role of the Gut Microbiome in Obstructive Sleep Apnea-Induced Hypertension. These studies demonstrate a causal relationship between gut dysbiosis and hypertension, and suggest that manipulation of the microbiota may be a viable treatment for OSA-induced, and possibly other forms of, hypertension. 26721259: CONCLUSIONS: Our data indicate that initiation of therapy with high-dose simvastatin does not alter baseline CBF or response to induced hypertension. 26919165: In addition, cancer treatment may be associated with other cardiac events, such as severe treatment-induced hypertension and vasospastic and thromboembolic ischemia, as well as rhythm disturbances, including QTc prolongation, that may be rarely life-threatening. 26931476: Our aim is to provide an overview of the latest Federal Drug Administration (FDA) approved VEGF inhibitors and TKI's causing hypertension so that others managing patients on these treatments may easily recognize hypertension attributable to these agents and feel comfortable and confident in providing appropriate management and treatment of this side effect. Update of Targeted Therapy-Induced Hypertension: Basics for Non-Oncology Providers. This manuscript focuses on hypertension induced by vascular endothelial growth factor (VEGF) inhibitors and tyrosine kinase inhibitors (TKI). 27035988: Prolonged treatment with the low-dose VEGF blockade caused hypertension and significantly decreased circulating levels of thyroid hormone free-T3 and -T4, leading to functional impairment of thyroid. 27151061: After 14 days of pre-treatment, the animals were induced with hypertension by oral administration of l-NAME (40 mg/kg/day). 27164264: Sensitive markers for sunitinib therapy include KDR positivity and early-developed treatment-induced hypertension. 27187011: METHODS: We investigated diameter, tone, and mechanics of intramural coronaries taken from ovariectomized female rats (n = 11) that received chronic AII treatment to induce hypertension, and compared the results with those found in female rats that were also given estrogen therapy (n = 11). The aim of this study was to analyze the effects of ovariectomy and estrogen therapy in a rat model of menopausal hypertension induced by angiotensin II (AII). 27211205: Recognition, diagnosis and treatment of secondary causes of hypertension lead to good clinical outcomes and the possible reversal of end-organ damage, in addition to blood pressure control. 27251093: Maternal suramin treatment induced programmed hypertension in male offspring, which was prevented by maternal NAC therapy. We examined whether maternal N-acetylcysteine (NAC) therapy prevented maternal suramin treatment-induced programmed hypertension in offspring and explored the effects of this therapy on NO, H2S, and RAS pathways in the kidneys. 27334059: The DOCA-salt treatment induced hypertension in both genotypes, as observed by increases in systolic blood pressure. In conclusion, the results of this study suggest that the presence of KLF5 in postn-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension. 27379932: However, from data obtained during the last few years, we know that surgical causes of hypertension are unusual: less than 10% of the patients in a reference centre. Arterial hypertension is a very common disease, and one of the main causes of death in our countries. The first step of treatment must be the research for curable causes of hypertension. 27596834: Altogether, angiotensin II-induced hypertension not only exacerbated Alzheimer's disease-like pathological changes such as impairment of cerebral blood flow, functional connectivity, and cognition only in Alzheimer's disease model mice, but it also induced decreased functional connectivity in wild-type mice. Elevated angiotensin II causes hypertension and contributes to Alzheimer's disease by affecting cerebral blood flow. We studied effects of two months of angiotensin II-induced hypertension on systolic blood pressure, and treatment with the angiotensin II receptor blockers, eprosartan mesylate, after one month of induced hypertension in wild-type C57bl/6j and AbetaPPswe/PS1DeltaE9 (AbetaPP/PS1/Alzheimer's disease) mice. 2790213: Vascular changes associated with deoxycorticosterone-NaCl-induced hypertension. Alterations were observed in the arteries, some of which were related to hypertension, but not to treatment, and some were due to treatment alone. 28002425: Our results suggest that inclusion of culturally relevant stress measures, like unfair treatment in African Americans, may reveal new genes and biological pathways relevant to the etiology of hypertension, and may also improve our understanding of the complexity of gene-environment interactions that underlie complex diseases. 28082452: METHODS AND RESULTS: Angiotensin-II (AngII) treatment resulted in high blood pressure (BP) associated to increased plasma S1P and circulating T-cell counts. Sphingosine-1-phosphate signalling-a key player in the pathogenesis of Angiotensin II-induced hypertension. 28089721: There was a significant difference between patients with treatment-induced HTN (n = 110) versus patients with no treatment-induced HTN (n = 193) for PFS (15.6 vs. 6.4 months, respectively; P < .001) and OS (34.9 vs. 13.9 months, respectively; P < .001). BACKGROUND: Research suggests that baseline use of angiotensin system inhibitors (ASIs) improves outcome in patients with metastatic renal cell carcinoma (mRCC), but it remains unknown whether the type of antihypertensive medication used to initiate management at onset of treatment-induced hypertension (HTN) is associated with outcome. 28100919: The HFD treatment caused mild obesity and hypertension in the normotensive rats, while rats receiving both ELE and the HFD had significantly lower body weights, less visceral and perirenal fat, lower blood pressure and thinner aortic media than the control rats receiving the HFD only. 28152482: Quantitative RT-PCR was employed to evaluate the mRNA levels of the three alpha1-ARs (alpha1A, alpha1B, alpha1D) in HPMC isolated from normotensive and hypertensive patients, and also in tissues from two animal models of hypertension: spontaneously hypertensive rats (SHR) and hypertension induced by chronic treatment with L-NAME. 28584011: Regulatory T-Cell Augmentation or Interleukin-17 Inhibition Prevents Calcineurin Inhibitor-Induced Hypertension in Mice. The immunosuppressive calcineurin inhibitors cyclosporine A and tacrolimus alter T-cell subsets and can cause hypertension, vascular dysfunction, and renal toxicity. Daily treatment of mice with cyclosporine A or tacrolimus for 1 week significantly decreased CD4+/FoxP3+ regulatory T cells in the spleen and lymph nodes, as well as induced hypertension, vascular injury and dysfunction, and glomerular mesangial expansion in mice. 2877043: Finger plethysmography made it possible to show and quantify the peripheral vascular repercussions of hypertension on the digital artery and evaluate the changes induced by treatments. 28882537: In this review, we outline research efforts to understand the mechanisms and pathophysiology of hypertension resulting from bevacizumab treatment. Bevacizumab-induced hypertension: Clinical presentation and molecular understanding. Moreover, we highlight current knowledge of the pharmacogenetics of bevacizumab-induced hypertension, which may be used to develop strategies to prevent or minimize this toxicity. 28915536: In addition, hypertension with hypercholesterolemia-induced increases in tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1beta (IL-1beta) levels in renal tissues were inhibited by treatment with EGb761. 28919617: This study assessing the response & side effects of intravenous antihypertensive drug in the treatment of pregnancy induced severe hypertension shows that Labetalol fulfils the criteria of an antihypertensive drug for this purpose. The study was performed to assess the response & side effects of injectable Labetalol in the treatment of pregnancy induced severe hypertension. 28962478: After 14 days of pre-treatment, the animals were induced with hypertension by oral administration of L-NAME (40 mg/kg/day). 29145955: Newly developed targeted therapy can exert off-target effects causing hypertension, thromboembolism, QT prolongation, and atrial fibrillation. 29278541: PURPOSE OF REVIEW: For decades, it has been widely accepted that initiation of salt-induced hypertension involves a type of kidney dysfunction (natriuretic handicap), which causes salt-sensitive subjects to initially excrete less of a sodium load than normal subjects and undergo abnormal increases in cardiac output, and therefore blood pressure. SUMMARY: To advance discovery, prevention, and treatment of primary abnormalities causing salt-induced hypertension, greater research emphasis should be placed on identifying mechanisms mediating subnormal renal vasodilation and abnormally increased renal vascular resistance in response to high-salt diets. Mounting evidence indicates that in most salt-sensitive subjects, renal vasodysfunction, defined as impaired renal vasodilation and abnormally increased renal vascular resistance in response to increased salt intake, in the absence of greater sodium retention than in salt-loaded normal subjects, is involved in initiation of salt-induced hypertension. Here we discuss emerging views that renal vasodysfunction, not natriuretic dysfunction (subnormal sodium excretion), is usually a critical factor initiating salt-induced hypertension. The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced hypertension. 29311252: Results are compatible with a significant role of reduced renal medullary NO bioavailability in VEGF inhibitor-induced hypertension. The present study was designed to test the hypothesis that VEGF receptor inhibitor treatment leads to hypertension through decreased renal medullary formation of NO and endothelin-1. In the renal medulla, inhibition of NO formation by local L-NAME or by impaired endothelin-1 leads to hypertension. 29463871: However, 15 days after initiation of treatment, the blood pressure of the clonidine only-treated DM mice began to increase and resulted in a high final blood pressure. 29483228: Although VEGF (vascular endothelial growth factor) inhibitors (VEGFIs), are effective anticancer therapies, they cause hypertension through unknown mechanisms. 2964946: Twelve minutes of hypoxia were imposed on isolated isovolumic (balloon-in-left-ventricle) buffer-perfused hearts from 14 rats with pressure-overload hypertrophy (LVH; LV/body wt ratio = 3.43 +/- 17) secondary to hypertension induced by uninephrectomy plus deoxycorticosterone and salt treatment and from 17 age-matched controls (LV/body wt ratio = 2.22 +/- 0.12, p less than 0.001). 29755695: On the other hand, hypertension is a long-term consequence of antineoplastic treatment, including both chemotherapy and targeted agents. 29801906: The paradigm for first line therapy in patients with vasospasm of induced hypertension, hypervolemia, and hemodilution has recently been challenged. 29959593: Management of VEGF-Targeted Therapy-Induced Hypertension. 30005742: The lack of precise therapies for stress-induced hypertension highlights the need to explore the process of blood pressure changes. Here, as a model, we used rats with stress-induced hypertension, and found that a switch from an immunoregulatory (M2) to a pro-inflammatory (M1) dominant response occurred in microglia during development of stress-induced hypertension. 30054426: Treatment with AAA was started either simultaneously with induction of hypertension or 10 days later, during established hypertension. 3022512: Finger and calf arteries contribute to the decrease of the total peripheral vascular resistance during treatment with enalapril; thus, ACE inhibition is capable of correcting the increased peripheral resistance which often is the main cause of arterial hypertension. 31495277: Although nonadherence to treatment contributes to uncontrolled hypertension, it is likely that not all the pathophysiological mechanisms are neutralized by the various classes of antihypertensive treatment currently available, and, the counter-regulatory mechanisms triggered by these treatments may decrease their blood pressure-lowering effect. 3172908: [Arterial hypertension secondary to Guillain-Barre syndrome. Treatment with a labetalol and chlorpromazine combination. Apropos of a case]. 32309607: However, other therapies (such as hormonal therapy, tyrosine kinase inhibitors, anti-VEGF drugs etc.) can also affect the cardiovascular system and lead to ischemia, hypertension or vascular thromboembolism. 33081013: Conventional chemotherapy, adjunct treatments, and novel targeted therapies collectively caused new onset hypertension in 33-68% of treated patients. 33309195: Both treatments caused hypertension which was more profound with thiafentanil (mean overall MAP = 140 +/- 14 mmHg; p < 0.001). 3497281: Because of the well-recognized increased incidence of hypertension in black patients, and its role as a major risk factor in coronary heart disease, the sequelae of hypertension were considered in relation to results of surgical therapy.The study population included 93 men (57 percent) and 70 women (43 percent); mean age was 59 years (fourth to ninth decade). 3517664: If vasospasm and ischemia do develop, energetic treatment with hypervolemia and induced hypertension can be started without fear of rebleeding. 36233717: The omittance of invasive endovascular rescue therapies in SAH patients with CVS, additional to induced hypertension, does not lead to a higher rate of DCI. 3698472: Treatment of rats with a flavonoid-type drug (anthocyanosides of Vaccinium myrtillus) for 12 days before the induction of hypertension kept the blood-brain barrier permeability normal and limited the increase in vascular permeability in the skin and the aorta wall. 37486: Despite the very spectacular results of medical treatment, it remains essential to seek a renal cause for hypertension, since many renal conditions which require specific treatment present with hypertension alone. 38063016: BACKGROUND: Therapeutic-induced hypertension treatment (iHTN) is helpful for alleviating early neurological deterioration (END) in acute small vessel occlusive stroke. 3828503: Hormonal treatment did not change the reactivity of rats with hereditary stress-induced arterial hypertension to both stress factors employed, enhanced it by intracerebral norepinephrine injection but decreased it by carbocholine intracerebroventricular injection. 38391284: Several cancer therapies cause hypertension which has resulted in a growing and vulnerable population of patients with difficult to control hypertension which has significant downstream effects. 38559889: We aim to provide a current review of the mechanisms by which these therapies induce hypertension, the risk factors and predictors of the development of hypertension, and management strategies to minimize the risk of cardiovascular complications in patients receiving vascular endothelial growth factor inhibition as part of cancer treatment. 3952624: Treatment with induced arterial hypertension with phenylephrine was instituted. 4040123: When combined, the two treatments resulted in hypertension more severe than that produced by either stress or ethanol consumption alone. 4085929: [Hypertension in rats caused by metyrapone and heat-stress treatment]. 422935: Young female rats were given a regimen of intraperitoneal cadmium treatments reported to cause hypertension reliably within a month. The suggestion that cadmium-induced hypertension in rats might be due to renal sodium retention, known to result from Cd treatment, was examined. 466431: No significant changes in DA content were observed in any region of the brain following induction of hypertension by the three different methods. NA content increased significantly in various areas: the increase of NA in the pons-medulla was common to all procedures inducing hypertension. In two substrains, selected from the Hebrew University strain, for their respective sensitivity (H) or immunity (N) to hypertension induced by DOCA--salt treatment, there were no significant increases in NA or DA in any part of the brain following DOCA--salt treatment. Noradrenaline (NA) and dopamine (DA) distribution in different brain areas was assayed following induction of hypertension. 4764584: Treatment of chronic gangrenous skin lesions with measures increasing distal blood pressure with special regard to induced moderate hypertension. 5425276: It is concluded that experimental hypertension of renal origin or induced by DCA treatment can develop even though most of the sympathetic nervous system has been destroyed. Experimental hypertension in the rat, induced either by renal artery stenosis or by treatment with deoxycorticosterone acetate (DCA) developed maximally over a period of 8 weeks. 6085384: Chronic treatment with nitrendipine prevents spontaneous (Okamoto rats) and salt-induced (Dahl rats) hypertension and cardiac hypertrophy. 616936: [Chronic arterial hypertension in children (pathogenic mechanisms and treatment of the main causes of chronic arterial hypertension in children)]. 6203489: At this time the ITC therapy is used in combination with induced-hypertension-chemotherapy (IHC therapy). 6243503: Pain sensitivity was studied in renal and DOCA-salt hypertensive rats, and in two strains of rats derived from the same parental strain for their sensitivity (H) or immunity (N) to hypertension induced by DOCA-salt treatment. 6252632: The small number of hypertensions really induced by oral contraceptives is opposed with the great number of hypertension (essential or not) revealed by oral contraceptives. Careful investigation of these patients revealed that only in some had hypertension been caused by OC treatment, which goes against the commonly held opinion that arterial hypertension in OC patients is always caused by hormonal treatment. Three conditions have to be satisfied in order to incriminate with certainty the responsibility of oral contraceptives inducing hypertension : normal blood pressure before therapy (included pregnancies), normalization of blood pressure in a delay of three months at most after the discontinuation, no other etiology of hypertension. 6270798: This study leads to point out some peculiar characteristics: virilization of external genitalia in girls is most usually important; arterial hypertension is delayed, usually after some years; plasma androgens and desoxycortisol are highly elevated; plasma 17-hydroxyprogesterone is slightly elevated and this may be misleading; good results of treatment which must preferably use hydrocortisone since plasma cortisol is sometimes low; long-term risks in treated children include chronic hypertension in both sexes, advanced puberty in girls and pubertal gynecomastia in boys. 6279507: In hypertension induced by deoxycorticosterone acetate (DOCA)-salt treatment, as in Dahl genetic hypertension, there was also no difference in membrane potential (Em) between hypertensive and normotensive rats. 6344619: Although these results are consistent with a volume-vasoconstrictor analysis of hypertension, the results of therapy could not have been prejudged from renin profile or responsivity. 646259: When hypertension fails to respond to medical treatment there is usually another explanation, such as poor patient compliance, excessive salt ingestion, drug interactions, spuriously high office readings, or an unsuspected secondary cause for the hypertension. 6471775: In our patient there was in particular a lack of hypertension in spite of proven hypercatecholaminemia, an initially good effect of the post-operative aggressive chemotherapy according to the neuroblastoma study NBL 79 (4b) resulting in a transient reduction of the pulmonary metastases, furthermore a diminuation of the total tumour mass induced by the last applied treatment with the radiopharmaceutical 131I-metaidiobenzylguanidine. 6543221: Also strips from regular normotensive Wistar rats (NWR) which failed to develop hypertension after deoxycorticosterone (DOC)-salt treatment (DNR) were compared to those from NWR with DOC-salt induced hypertension (DHR). 6697561: On ceasing treatment, blood pressure returns rapidly to pretreatment values suggesting that the original cause of the hypertension is still present. 6774065: This therapy resulted in substantially higher blood pressure, cerebral perfusion pressure, blood flow, and oxidative metabolism than those of a group of monkeys that had been treated similarly with mannitol, and than those of an untreated group. 6805590: Thirty-seven reports of the treatment of hypertension by non-pharmacological means were compared with the results of treatment by standard drug regimens. 6881029: Treatment with atropine regularly eliminated the reflex bradycardia and caused the hypertension to appear soon (average of 6 seconds to maximal level). 7093050: [Late treatment results in arterial hypertension due to renal artery lesion in nonspecific aortoarteritis]. 7284193: [Evaluation of treatments results in arterial hypertension obtained at 2 levels of intervention: the specialist center and basic medicine]. 7389263: Parathyroid hormone- and deoxycorticosterone acetate-induced hypertension in the rat. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 7671060: Thereafter i.v. continuous administration or oral treatment may be necessary, depending on the cause of hypertension. 7810723: Myocardial fibrosis has been investigated in 3-, 16-, and 24-mo-old normal rats and also in 24-mo-old rats subjected to deoxycorticosterone acetate (DOCA)-salt treatment-induced-hypertension. 8021005: This treatment induced arterial hypertension, a moderate left ventricular hypertrophy, and a decrease in plasma thyroxine. 8105829: INTERVENTIONS: Treatment with fenoldopam or placebo was initiated immediately after other causes of hypertension had been ruled out. 8134804: The major thrust of treatment must, in the first instance, be aimed at the condition causing the hypertension. 8220662: Prolonged, 28 days treatment with lysine vasopressin (1 U/kg/day ip) induced hypertension and modified the dose-response curve for tremorine. 8282355: We determined the status of vascular kallikrein in rats with severe hypertension caused by treatment with deoxycorticosterone acetate (DOCA) and drinking of 1% NaCl for 6 weeks. 8389819: Treatment-induced hypertension requiring pharmacological intervention was seen in four patients. 8394783: Cyclosporine therapy after cardiac transplantation causes hypertension and renal vasoconstriction without sympathetic activation. 8485634: In conclusion, calcium supplementation clearly attenuated the development of hypertension, cardiac hypertrophy, and sodium retention induced by the DOC-NaCI treatment. 8586809: CONCLUSION: The present data strongly suggest that endogenous glucocorticoid in the central nervous system may not have a role in the regulation of systemic haemodynamics and hormones under resting conditions, but does play an important part during the glucocorticoid excess state, for example glucocorticoid hypertension caused by oral treatment with dexamethasone. OBJECTIVE: To determine whether the central nervous system has a pressor or a depressor role in glucocorticoid-induced hypertension. 8621212: Low-dose L-NAME treatment induced hypertension only when associated with sodium overload. 8808210: DOCA-NaCl treatment causes hypertension, accelerates development of proteinuria, and leads to glomerulosclerosis in rats with autoimmune Heymann nephritis. Thus in autoimmune Heymann nephritis, DOCA-NaCl treatment causes hypertension and increased renal mass together with upregulation of local cytokine and growth factor production, which may further aggravate hypertension and accelerate progression of renal damage. To study the mechanisms of kidney injury induced by renal haemodynamic load in chronic nephritis, we studied by immunohistochemistry the local expression of various cytokines, growth factors and adhesion molecules in the kidneys of Heymann nephritic rats with or without DOCA-NaCl-induced hypertension. 8831080: UNLABELLED: To assess the role of dexamethasone treatment as a cause of systemic hypertension and associated complications, blood pressure was registered prospectively before, during and after a 4-week dexamethasone course in 22 neonates with chronic lung disease. CONCLUSION: Dexamethasone induced hypertension is transient, even after a 4-week course, and is not associated with hypertensive complications, so treatment is not necessary. 8842431: In conclusion, in rats with hypertension due to 7 days treatment with the P1-purinoceptor antagonist, DPSPX, there is an increase in sensory-motor vasodilatation of the mesenteric arterial bed. 8867715: Although high dose epinephrine treatment led to a significantly higher blood pressure during early reperfusion, rapidly changing heterogeneities of early brain recovery were observed in both groups. 8934362: L-NAME treatment resulted in higher blood pressure and increased severity of conduit artery hypertrophy, but reduced cardiac and small artery hypertrophy, and enhanced aortic endothelin-1 mRNA. 8980890: Acutely exacerbated hypertension and increased inflammatory signs due to radiation treatment for metastatic pheochromocytoma. 9029741: Although several studies have produced promising results, nephrotoxicity and hypertension can result from CyA treatment, and their development must be understood in order to facilitate patient management. 9116920: The present study aimed to evaluate whether elevated blood pressure and insulin resistance coexist during CsA therapy to prove the similarity between essential hypertension and CsA induced hypertension. OBJECTIVES: Essential hypertension and insulin resistance frequently coexist; cyclosporine A (CsA) is known to induce hypertension which has been used as a model for essential hypertension. CONCLUSIONS: CsA therapy induces elevated blood pressure and insulin resistance as seen in patients with essential hypertension, thus CsA induced hypertension is considered to have pathophysiological similarities to essential hypertension. 9158213: This effect of hypertension was mostly caused by the associated antihypertensive treatment because untreated hypertensive patients had survival rates equal to normotensive patients (RR, 0.87; P = 0.70). 9280208: CONCLUSION: That Ang II levels are elevated in sucrose-induced hypertension and decreased after vanadium therapy suggests that the renin-angiotensin system plays a role in the induction of hypertension in this model. 9299205: Treatment of rats with amlodipine in diabetic and diabetic-hypertensive animals significantly prevented STZ-induced loss of body weight, hypertension and bradycardia. 9315348: Chronic treatment of normotensive SD rats with the NO synthesis inhibitor, N omega-nitro-L-arginine (L-NNA; 0.5 g.L-1 in drinking water for 2 weeks), resulted in sustained hypertension. 9350067: Polycythaemia and hypertension induced by chronic rHuEPO therapy were associated with increased urinary NO2- and NO3- (NOx-) excretion, while co-administration of L-NAME, but not aminoguanidine, reduced NOx- excretion. 9369284: Four-week DOCA-salt treatment induced hypertension associated with cardiac hypertrophy. 9370381: Our findings clearly show that FHL rats are more susceptible to developing renal damage after induction of hypertension by chronic L-NAME treatment. Difference in susceptibility of developing renal damage in normotensive fawn-hooded (FHL) and August x Copenhagen Irish (ACI) rats after N(omega)-nitro-L-arginine methyl ester induced hypertension. This was further investigated by comparing the effects of N(omega)-nitro-L-arginine methyl ester (L-NAME) induced hypertension on functional and structural renal damage in two normotensive strains, the resistant August x Copenhagen Irish rat (ACI) and the normotensive fawn-hooded (FHL) rat, which also appears to carry a susceptibility locus for renal failure. 9439971: Before treatment and 4, 10 and 15 days after induction of hypertension, we evaluated histological retinal damage and NGF levels in aqueous humor using an immunoenzymatic assay. 9458851: L-NAME treatment induced hypertension that was associated with increased plasma renin activity. 9486087: Maternal carbenoxolone treatment lowers birthweight and induces hypertension in the offspring of rats fed a protein-replete diet. 9488223: RESULTS: L-NAME treatment induced hypertension (systolic blood pressure control 129.2+/-2.7 mmHg and SBP L-NAME treatment 176.3+/-5.2 mmHg, P< 0.001). 9555685: More data on the consequences of treatment of women with hypertension are needed, particularly longterm studies to assess the impact of treatment on mortality. 9567746: Treatment of rats with spirapril in diabetic and diabetic with hypertensive animals significantly prevented STZ-induced loss of body weight, hypertension, and bradycardia. 9617750: Role of endothelin ET(A) receptors in the hypertension produced by 4-day L-nitroarginine methyl ester and cyclosporine treatment. 9869498: This treatment induced arterial hypertension (+35%) and moderate LV hypertrophy (LVH; +60%) without right ventricular (RV) hypertrophy. 10412794: A discussion of target therapy based on the proposed pathogenesis of AD is also briefly reviewed. 10764737: Caffeine treatment sensitizes neurons expressing mutant PS1 to apoptosis induced by amyloid beta-peptide, a neurotic peptide linked to the pathogenesis of AD. Many cases of early-onset inherited Alzheimer's disease (AD) are caused by mutations in the presenilin-1 (PS1) gene. 11193790: A brief discussion of target therapy based on the proposed pathogenesis of AD is also reviewed. 12861345: Potential therapeutic strategies for AD treatment include palliative treatment with nonspecific neuroprotecting agents, symptomatic treatment with psychotropic drugs for noncognitive symptoms, cognitive treatment with cognition enhancers, substitutive treatment with cholinergic enhancers to improve memory deficits, multifactorial treatment using several drugs in combination and etiopathogenic treatment designed to regulate molecular factors potentially associated with AD pathogenesis. In our opinion, the pharmacological treatment of AD should rely on a better understanding of AD etiopathogenesis in order to use current drugs that protect the AD brain against deleterious events and/or to develop new drugs specifically designed to inhibit and/or regulate those factors responsible for premature neuronal death in AD. 16472958: The implication of PPAR-gamma in the control of Abeta-induced inflammation suggests a new target for AD therapy and emphasize the contribution of neuroinflammatory mechanisms to the pathogenesis of AD. 17084014: This review will demonstrate data from humans and animals which promote NGF as a potential therapeutic target by (1) outlining the hypothesis behind using NGF for the treatment of AD, (2) reviewing both the normal and AD altered signaling pathways and effects of NGF in the central nervous system (CNS), and (3) examining the results of NGF treatment obtained from animal models of AD and AD patients. 18542908: New treatment strategies have developed since publication in 1991 of the amyloid hypothesis on the pathogenesis of Alzheimer's disease. 19585951: Many of these new therapies are based on our best current understanding of the pathogenesis of Alzheimer's disease, and are designed to try to either slow or halt the progression of the disease. 20119496: MAIN METHODS: Here, we have explored the anti-amyloid properties of these SMAbetaBA's in mice doubly transgenic for human prensenilin-1 (PS1) and APP gene mutations that cause early-onset AD. AIMS: One promising approach for treatment of Alzheimer's disease (AD) is use of anti-amyloid therapies, based on the hypothesis that increases in amyloid-beta (Abeta) deposits in brain are a major cause of AD. 22382658: Molecular approaches to the treatment, prophylaxis, and diagnosis of Alzheimer's disease: endoplasmic reticulum stress and immunological stress in pathogenesis of Alzheimer's disease. 22531418: Amyloid-beta (Abeta) producing enzymes are key targets for disease-modifying Alzheimer's disease (AD) therapies since Abeta trafficking is at the core of AD pathogenesis. 23474291: Lowering the production and accumulation of Abeta has been explored as treatment for Alzheimer's disease (AD), because Abeta is postulated to play an important role in the pathogenesis of AD. 23954180: However, no cure or disease-modifying treatments are currently available, and the molecular and cellular mechanisms responsible for the etiology of AD remain under debate. 24040810: Thus Alzheimer disease (AD) treatment strategies based solely on the amyloid-beta clearance should be re-examined in light of the vast accumulating evidence that increased oxidative stress in the human brains is the key causative factor for AD. 24365186: Treatments for T2DM and AD attempt to slow cognitive decline, and recent investigations have focused on agents that may alter pathways common to AD and T2DM pathogenesis. 24599114: Our results indicate that by interacting with Abeta42 soluble species, delaying Abeta plaque formation, protecting against neuronal death and dendritic spine loss and preventing AD cognitive deficits, the Reelin pathway deserves consideration as a therapeutic target for the treatment of AD pathogenesis. 25027006: FAD hiPSCs harboring disease properties can be used as humanized models to test novel diagnostic methods and therapies and explore novel hypotheses for AD pathogenesis. 2755560: 3) While there is still a search for a symptomatic treatment for AD, the path to find a treatment for the Alzheimer disease process must first pass through a phase of basic research to find the cause of Alzheimer's disease. 27693185: A major obstacle to presymptomatic diagnosis and disease-modifying therapy for Alzheimer's disease (AD) is inadequate understanding of molecular mechanisms of AD pathogenesis. 28385651: Moreover, treatment with drugs that block AT1R (AT1R blockers, ARBs) ameliorates most of the clinical risk factors leading to AD. 28709498: Identifying specific signaling pathways involving Abeta has allowed for the development of more precise therapeutic interventions targeting the most relevant molecular mechanisms leading to AD. 29248451: Single modality of \One-molecule-one-target\ strategy for treating AD has failed and so future therapies on \Combination-drugs-multi-targets\ strategy (CDMT) will need to address multiple aspects to block the progression of pathogenesis of AD. 29623038: In this review, we will describe how recent advances in stem cell technology have shed light on a novel treatment strategy and revolutionized the mechanistic investigation of AD pathogenesis. 30059692: Thus, there are urgent needs for the development of new therapies that target on the proximal cause of AD. 30227819: The lack of effective treatments for AD stems mainly from the incomplete understanding of causes of AD. 31818365: Currently available therapeutic agents for AD provide only symptomatic treatments, mainly because the complete mechanism of the AD pathogenesis is still unclear. 31824296: Therapeutic interventions aiming to restore mitophagy functions can be used as a strategy for ameliorating AD pathogenesis. 31960800: In order to find disease-modifying therapies to confront this challenge, a more complete understanding of the pathogenesis of Alzheimer's disease is necessary. 32898852: Systems-based proteomics to resolve the biology of Alzheimer's disease beyond amyloid and tau.The repeated failures of amyloid-targeting therapies have challenged our narrow understanding of Alzheimer's disease (AD) pathogenesis and inspired wide-ranging investigations into the underlying mechanisms of disease. 33188924: This review questions the major assumptions about Abeta on which therapies for AD were premised, and invites renewed interrogation into AD pathogenesis. 33417222: Therapeutic interventions aiming to restore mitophagy functions can be used as a strategy for ameliorating AD pathogenesis. 34160781: The Tg2576 is frequently used in AD research to test therapeutic interventions targeting cellular mechanisms contributing to the genesis of AD. 36561895: There are just a few FDA-approved treatments without side effects in the market, and their efficacy is restricted due to their narrow target in the etiology of AD. 37186274: This study sheds light on apoptotic pathways that are cardinal for neuronal survival and perform crucial role in the occurrence of AD along with the trends in therapeutics targeting apoptosis induced AD. 37833948: However, as reviewed in this article, results from the numerous clinical trials that have tested anti-Abeta therapies to date indicate that this peptide plays a minor role in the pathogenesis of AD. 3789676: These results indicate that cholinergic muscarinic binding by peripheral blood lymphocytes may be useful in the study of alterations associated with aging and SDAT, as well as in evaluating changes induced by certain cholinergic drug treatments. 38003477: By providing an integrative perspective, we anticipate paving the way for future research and treatments focused on exploiting the BBB's role in AD pathogenesis and therapy. 12567393: Within the pediatric age group, chylothorax is rare and has been reported almost exclusively in the setting of thoracic surgical procedures or central venous hypertension secondary to central venous catheter thrombosis. 13074027: [Obstruction of the terminal portion of the aortic arch treated by aortectomy with bilateral lumbar gangliectomy; surprising amelioration of peripheral circulatory disorders, but in a few months, appearance of a fatal arterial hypertension caused by ascending thrombosis]. 13119435: [Permanent arterial hypertension caused by ascending thrombosis in the bifurcation of the aorta: report of two personal cases]. 13165983: Sudden onset of hypertension caused by thrombosis of the renal arteries (Goldblatt phenomenon). 13502890: Hypertension due to thrombosis of the renal artery; a case report. 14316224: THROMBOSIS OF THE RENAL ARTERY AS A CAUSE OF CURABLE ARTERIAL HYPERTENSION (DESCRIPTION OF A CASE). 14418229: [A case of chronic pyelonephritis with vascular thrombosis causing arterial hypertension]. 14791178: [Hypertension following gunshot wound, caused by thrombosis of the abdominal aorta, occlusion of the ureter and hydronephrosis]. 14922505: Hypertension due to thrombosis of the renal artery: report of a case in which a cure was obtained by nephrectomy. 14939429: Hypertension due to thrombosis of the renal artery; report of a case in which a cure was obtained by nephrectomy. 19021758: The stable upregulation of the biosynthesis of the vascular protector, PGI(2), in cells is an ideal model for the prevention and treatment of thromboxane A(2) (TXA(2))-mediated thrombosis and vasoconstriction, both of which cause stroke, myocardial infarction, and hypertension. 2132037: Surgical repair is indicated in tight stenoses with impending thrombosis and in stenoses responsible for severe hypertension which does not respond to anti-hypertensive treatment. 26903742: High androgen level contributes to the development of atherosclerosis, thrombosis leading to hypertension and hypercholesterolemia. 28677005: Tumor thrombosis may be clinically relevant, causing splenoportomesenteric hypertension, possibly responsible for life-threatening upper gastrointestinal bleeding. 3329157: Twenty-two patients were cured of hypertension, four showed improvement and in three the transplanted kidneys failed to function due to vascular thrombosis postoperatively. 37427671: Notably, one patient had a past history of hypertension and coronary artery disease and was on postoperative low molecular heparin due to lower extremity venous thrombosis. 3880603: The hypertension was due to long-standing cirrhosis in 4 patients; the other 3 patients had prehepatic hypertension due to thrombosis involving the portal vein in 1 and the splenoportal confluence in 2. 5363710: [A case of hypertension due to unilateral obstructive thrombosis of the renal artery]. 11867385: UNLABELLED: Although the mechanism of tourniquet-induced hypertension is still unclear, plasma norepinephrine concentrations continuously increase in parallel to arterial blood pressure during tourniquet inflation. 15101858: Preoperative stellate ganglion blockade prevents tourniquet-induced hypertension during general anesthesia. 1515391: CONCLUSIONS: In this setting, tourniquet-induced hypertension is rare. 17294989: Magnesium and ketamine are equally effective in attenuating tourniquet-induced hypertension and spinal c-fos mRNA expression, suggesting that this effect may be due to reduced pain transmission. 2604159: [Effects of clonidine on tourniquet-induced systemic arterial hypertension in general anesthesia]. 2917909: Tourniquet-induced hypertension in a horse. 33431616: Femoral artery block (FAB) attenuates thigh tourniquet-induced hypertension: a prospective randomized, double-blind, placebo-controlled trial. 34784460: Background: This study assessed the effect of a single bolus administration of lidocaine on the prevention of tourniquet-induced hypertension (TIH) and compared the effect of lidocaine to that of ketamine in patients undergoing general anesthesia. 36326771: Femoral periarterial block (FAB) has been shown to attenuate tourniquet-induced hypertension in patients undergoing general anesthesia. 36549034: Combined femoral artery block and femoral nerve block reduces thigh tourniquet-induced hypertension. 6461346: Tourniquet-induced hypertension. 7628940: Tourniquet-induced hypertension in an ostrich. The tourniquet-induced hypertension in this ostrich was similar to that reported for human beings and horses. 9075039: Tourniquet-induced hypertension correlates with autonomic nervous system changes detected by power spectral heart rate analysis. Tourniquet-induced hypertension (T-HTN) defined at 30% increase above baseline. 11862037: Long-term use of cyclosporine A (CsA) is associated with deleterious effects such as nephrotoxicity and hypertension as a result of its toxicity on microvasculature. 12695417: Chronic use, however, has a destructive toxic effect on the kidney, resulting in hypertension. 17727353: Research examining the etiology of lead toxicity-induced hypertension reveals that the free radical production and lowering of inherent antioxidant reserves resulting from lead toxicity are directly related to vasoconstriction underlying lead-induced hypertension. 1782369: Although rehabilitation in this series was excellent, a significant percentage of cases have continuing problems with metabolic bone disease, hypertension and renal impairment, mainly due to cyclosporin toxicity. 19125641: NE can have direct cardiomyocyte toxicity and/or can stimulate myocardial remodeling secondary to the induction of hypertension. 22409470: Acrodynia and hypertension in a young girl secondary to elemental mercury toxicity acquired in the home. 23034493: We describe a 4-year-old boy who presents to the emergency department with lethargy, bradycardia, and initial hypertension followed by hypotension due to guanfacine toxicity after ingestion of standard doses of the extended release formulation. 28528304: Moreover, iAs and MMA may have higher toxicity and lead to both hypertension and skin lesions than to only hypertension. 29087545: In terms of maternal toxicity, prenatal cocaine exposure causes hypertension, placental abruption, spontaneous abortion, poor pregnancy weight gain, and undernutrition secondary to appetite suppression. 29395180: A 17-month-old child presented with hypertension, fussiness, constipation, and arthralgia due to mercury toxicity from a skin-lightening cosmetic used by her mother and grandmother. 29478133: PURPOSE OF REVIEW: Acute drug-induced hypertension, sympathomimetic toxicity, and other hyperadrenergic states can be caused by both xenobiotic toxicity and withdrawal. 33187680: Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms. 34386529: In this review, we provide a comprehensive overview of the effects of chemotherapeutic agents on vascular toxicity leading to hypertension, microvascular rarefaction thrombosis and atherosclerosis, and affecting drug delivery. 9668394: In terms of maternal toxicity, prenatal cocaine exposure causes hypertension, placental abruption, spontaneous abortion, poor pregnancy weight gain, and undernutrition secondary to appetite suppression. 1423339: An elderly woman developed an Alzheimer-like subacute dementia as a result of propranolol toxicity. 16866916: According to the amyloid cascade hypothesis, both familial and sporadic Alzheimer's disease (AD) is caused by the toxic effect of over-production and/or aggregation of beta-amyloid (Abeta). 17676931: Amyloid beta (Abeta) toxicity has been hypothesized to initiate the pathogenesis of Alzheimer's disease (AD). 17873593: Recent data also reveal that general anesthesia produces enduring cognitive impairment in aged but not young rodents and that halothane and isoflurane increase the generation and toxicity of amyloid beta, a protein strongly implicated in the pathogenesis of Alzheimer's disease. 18160097: Although neuronal apoptosis in Alzheimer's disease is generally interpreted as the consequence of the toxicity of extracellular beta-amyloid (Abeta) peptide aggregates, some experimental results provide evidence that the Abeta overproduction can be the result of a primary neuronal degeneration. 19765580: Recently, modulation of beta-amyloid (Abeta) toxicity, one of the major potential causes of Alzheimer's disease, has emerged as a possible therapeutic approach to control the onset of Alzheimer's disease. 19969390: Alternatively, our analysis of the specific effects of DR on neuronal toxicity downstream of Abeta and tau pathologies with negative results may simply confirm that the neuro-protective effects of DR are upstream of the initiating events involved in the pathogenesis of AD. 20159774: Since accumulation of DNA damage has been detected in the brains of AD patients, our results suggest that the DNA damage-activated kinases Chk1 and Chk2 may be involved in tau phosphorylation and toxicity in the pathogenesis of AD. 20466736: Our results demonstrate that tau phosphorylation at Ser262 is crucial for Abeta42-induced tau toxicity in vivo, and suggest a new model of AD progression in which activation of DNA repair pathways is protective against Abeta42 toxicity but may trigger tau phosphorylation and toxicity in AD pathogenesis. The amyloid-beta 42 (Abeta42) peptide has been suggested to promote tau phosphorylation and toxicity in Alzheimer's disease (AD) pathogenesis; however, the underlying mechanisms are not fully understood. 21876248: The entangled relationship of brain aging, mitochondrial dysfunction, and amyloid-beta peptide (Abeta42) toxicity occupies the center stage in the pathogenesis of Alzheimer's disease (AD). 22565015: Recently, it has been hypothesized that copper toxicity may be a contributory factor in the etiology of the neurodegenerative disease AD. 22903022: Together these experiments allowed the discrimination of the intermediate states more responsible of oligomer toxicity, providing new insights on the correlation between the aggregation process and the toxicity and confirming the peculiar role in the pathogenesis of Alzheimer disease of Abetapy3-42 peptide. 22947874: The amyloid-beta(25-35) peptide plays a key role in the etiology of Alzheimer's disease due to its extreme toxicity even in the absence of aging. 22952452: Our results suggest that loss of axonal mitochondria may play an important role in tau phosphorylation and toxicity in the pathogenesis of AD. Abnormal phosphorylation and toxicity of a microtubule-associated protein tau are involved in the pathogenesis of Alzheimer's disease (AD); however, what pathological conditions trigger tau abnormality in AD is not fully understood. 23160010: Our results imply that Abeta-DNA interaction needs to be considered as a significant cause of the toxicity in the pathogenesis of AD. 23550703: Since DNA damage is accumulated in diseased brains, Chk1 and Chk2 may be involved in tau phosphorylation and toxicity in AD pathogenesis. 23700270: In the present study, we showed neuroprotective effects of peptide derived from H. trimaculatus against amyloid-beta42 (Abeta42) toxicity which are central to the pathogenesis of Alzheimer's diseases (AD). 24710686: Mitochondrial toxic effects of Abeta through mitofusins in the early pathogenesis of Alzheimer's disease. 24796109: It is understood that molecules involved in this inflammation promote pathological processes leading to AD, whereas other molecules work to protect neuron/brain function from toxicity found in AD pathogenesis. 24820962: These results demonstrate the neuroprotective effects of CHD through inhibition of microglia-mediated neuroinflammation in in-vitro and in-vivo AD-like models induced by Abeta oligomer1-42 toxicity. 25187042: These results support a role of Abeta administration in inducing age-dependent cholinergic loss and neuroinflammation, and additionally provide evidence for a more age-appropriate model of adult-onset Abeta toxicity demonstrating pathological changes that reflect the early stages of AD pathogenesis including neuroinflammation, cholinergic loss and beginning stages of memory impairment. 25212543: Huperzine A is isolated from Huperzia serrata and is used for treatment of Alzheimer's disease, due to its low toxicity and long effective period. 25595891: Nonetheless, it now seems increasingly unlikely that amyloid toxicity is the cause of sporadic AD, which leads to cognitive decline. 25707809: Carbohydrates have been earlier used in the treatment of AD because of their low toxicity, high efficiency, good biocompatibility, and easy permeability through the blood-brain barrier. 25964177: Abeta (25-35) is the smallest peptide in the amyloid peptide family that retains the toxicity of a full length peptide responsible for Alzheimer's disease and is chosen here as the model solute. 27055069: In addition, all of the new BAMs were capable of protecting differentiated SH-SY5Y neuroblastoma cells from toxicity and concomitant oxidative stress induced by AD-related aggregated Abeta (1-42) peptides. 27240009: Recently, soluble AbetaOs have been regarded as reliable molecular biomarkers for the diagnosis of AD because of their high toxicity for neuronal synapse and high concentration levels in the brains of AD patients. 27662318: This concept is further strengthened by the protective effect of mitochondrial medicine on synaptic function against the toxicity of amyloid-beta, a key player in the pathogenesis of AD. 2900537: Glutamate toxicity may play a role in the pathogenesis of Alzheimer's disease. 29199234: However, the effects of EZJ on amyloid beta (Abeta) toxicity, which is a main cause of Alzheimer's disease (AD), remain to be elucidated. 29332042: The purpose of our article is to assess the current understanding of Indian spice, curcumin, against amyloid-beta (Abeta)-induced toxicity in Alzheimer's disease (AD) pathogenesis. 29736334: In this study, we tested hydroalcoholic extracts of S. scardica for their potential to counteract amyloid-beta toxicity and aggregation, which plays a crucial role in the pathogenesis of Alzheimer's disease. 29888266: Here we focus on what is known about the role of autophagy in amyloid toxicity in AD from mammalian models and how Drosophila models can be used to further investigate AD pathogenesis. Using Drosophila Models of Amyloid Toxicity to Study Autophagy in the Pathogenesis of Alzheimer's Disease. 30016667: However, other amyloid peptides are now gaining considerable attention as potential key participants in AD due to their proposed higher neuronal toxicity. 30935198: The aggregation of Abeta16-22 peptide, the smallest fragment of full-length Abeta1-42 with seven residues, plays a very crucial role in Abeta toxicity, hence causing Alzheimer's disease. 31183966: Taken together, this study revealed that Akt is involved in the aging process and Abeta toxicity, and manipulating Akt can restore both neuronal functions and improve behavioral activity during the processes of aging and AD pathogenesis. 31275419: The deposition of amyloid beta (Abeta) is the main hallmark of Alzheimer's disease (AD) and there is no effective drug to cure the progressive cognitive loss or memory deficits caused by the aggregative toxicity of Abeta protein. 31415717: BACKGROUND/AIMS: Amyloid plaques, generated during the progression of Alzheimer's disease, cause major neurological deficits due to substantial cell toxicity and death. 31926632: Natural products hold considerable interest for the development of preventive neuroprotectants to treat neurodegenerative disorders like AD, due to their low toxicity and general beneficial effects on human health with their anti-inflammatory and antioxidant features. 33081348: Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches. Several studies have indicated that oxidative stress plays a crucial role in the pathogenesis of AD. 33328884: How Microglia Manages Non-cell Autonomous Vicious Cycling of Abeta Toxicity in the Pathogenesis of AD. 33482095: gamma-secretase is a promising therapeutic target for Alzheimer's disease, but all inhibitors and modulators have failed due to toxicity or low efficacy. 33642992: Since hypothesis put forward by Arispe and collegues in 1993 that amyloid-beta makes ion-conducting channels and that Alzheimer's disease may be due to the toxic effect of these channels, many studies have confirmed that APs are formed by prefibrillar oligomers of amyloidogenic proteins and are a common source of cytotoxicity. 33806326: Recent evidence suggests that the formation of soluble amyloid beta (Abeta) aggregates with high toxicity, such as oligomers and protofibrils, is a key event that causes Alzheimer's disease (AD). 34886786: There is great popularity gained by natural supplements as the treatment for AD, due to the higher toxicities of synthetic drugs. 35006003: This study provides new molecular leads on altered protein dynamics relevant to neurodegeneration, neuroplasticity, and AD progression induced by Abeta42 toxicity. Production and deposition of beta-amyloid peptides (Abeta) are among the major hallmarks of the pathogenesis of Alzheimer's disease (AD). 3767535: The most common dementia diagnoses were Alzheimer's-type dementia (74.5%) and dementia due to toxic effects of drugs (9.5%). 38551492: Soluble amyloid-beta protein oligomers (AbetaO) (mainly AbetaO 42 ) that circulate in biological fluids have been recognized as a molecular biomarker and therapeutic target of AD due to their high toxicity, and they are correlated much more strongly with AD compared to the insoluble Abeta monomers. 8869917: The deficiency of selenium, which may act physiologically as an antagonist of tellurium, in the Alzheimer's disease brain would also be in keeping with the hypothesis of tellurium toxicity as a factor in the pathogenesis of Alzheimer's disease. 18670375: AIM: Transplant renal artery stenosis (TRAS) is the most frequent vascular complication following transplantation and is a potential curable cause of resistant hypertension, allograft dysfunction, and graft loss. 1992008: Hypertension induced by hypothalamic transplantation from genetically hypertensive to normotensive rats. 20061920: CONCLUSIONS: Liver transplantation and associated immunosuppression evidently cause hypertension, and possibly elicit diabetes in susceptible individuals. 2138422: We have previously shown that transplantation of kidneys from genetically hypertensive to normotensive rats result in hypertension in renal graft recipients. 2318524: Our data indicate that secondary damage to the renal grafts caused by high perfusion pressure before transplantation can induce hypertension in recipients of these kidneys. Hypertension in rats induced by renal grafts from renovascular hypertensive donors. 2669526: Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension. 27496479: The aim of this retrospective clinical study was to estimate the prevalence of arterial hypertension among patients after successful liver transplantation and the role of immunosuppressive drugs in the pathogenesis of hypertension in these patients. CONCLUSIONS: Based on study findings, the following conclusions were drawn: arterial hypertension occurs in more than 50% of patients after liver transplantation (significantly higher frequency than in the general population); calcineurin inhibitors may participate in the pathogenesis of arterial hypertension in patients after successful liver transplantation; and the clinical importance of these findings and the influence on cardiovascular outcome of the liver transplant recipients need further investigation. 31004464: In additional experiments, we used a design to determine whether blockade of B7-dependent costimulation with CTLA4-Ig or blockade of IL-17 with IL-17-neutralizing antibody could prevent hypertension caused by faecal microbiota transplantation (FMT) from SHR to WKY. 3296353: Administration of corticosteroids during the first three months after transplantation is implicated as a possible cause of persisting high blood pressure. 7788707: When the development of high SBP in PHR was prevented for 2 months after weaning by antihypertensive drugs, transplantation of one kidney from these rats to BNX PNR always induced a sustained hypertension in the recipient. 8279054: Evidence that simultaneous transplantation of a left kidney and adrenal gland may result in severe hypertension after clamp removal. 8309780: When the development of high BP in the PH rats was prevented for 2 months after weaning by antihypertensive drugs, transplantation of kidneys from these rats to bilaterally nephrectomised PN rats always induced a sustained hypertension in the recipient. 8665594: When the development of high SBP in PHR was prevented for 2 months after weaning by antihypertensive drugs, transplantation of one kidney from these rats to BNX PNR always induced a sustained hypertension in the recipient. 9346686: Long-term treatment with corticosteroids after orthotopic liver transplantation (OLT) may cause adverse effects, particularly hypertension, diabetes, and bone disease. 9719172: BACKGROUND: The unregulated renin release by native kidneys is one of the factors responsible for the high incidence of hypertension after renal transplantation but, even after three decades of transplantation, there is still a lack of a method to identify it as the major cause of hypertension. 10499440: Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta). 10937919: Considering the increase in the prevalence of both traumatic brain injury and AD in recent times, the possibility that brain trauma may provoke the early development of AD has important implications for health service planning, preventative efforts, and medico-legal compensation settlements. 11504565: BACKGROUND AND PURPOSE: The impact of traumatic brain injury (TBI) on the pathogenesis of Alzheimer disease (AD) is still controversial. 18492093: These findings fail to support the premise that progressive plaque pathology after TBI ultimately results in AD. Additionally, TBI induces AD-like amyloid beta (Abeta) plaque pathology within days of injury potentially resulting from massive accumulation of amyloid precursor protein (APP) in damaged axons. 19326964: Traumatic brain injury (TBI) induces the rapid formation of Alzheimer's disease (AD)-like amyloid-beta (AB) plaques in about 30% of patients. 25380674: Cognitive impairment represents a major debilitating feature of many neurodegenerative and psychiatric disorders, including Alzheimer's disease, mood disorders, schizophrenia and fragile X syndrome, as well as being a result of traumatic brain injury or cranial irradiation. 26176913: Thus, cis P-tau is a major early driver of disease after TBI and leads to tauopathy in chronic traumatic encephalopathy and Alzheimer's disease. 26899581: In addition, we discuss the evidence that supports the hypothesis that TBI may lead to AD. 27395469: [Late-onset Neurodegenerative Diseases Following Traumatic Brain Injury: Chronic Traumatic Encephalopathy (CTE) and Alzheimer's Disease Secondary to TBI (AD-TBI)]. 27654282: Although whether traumatic brain injury (TBI) could cause AD has not been established, CTE is shown to be associated with TBI. 27915236: We describe the common underlying neurobiology in alcohol and AD, and examine ways alcohol likely contributes to neuroinflammation directly via stimulation of Toll-like receptors and indirectly from small bowel changes, hepatic changes, withdrawal and traumatic brain injury to the pathogenesis of AD. 28776265: The present study intended to explore the effect of TBI on metabolism and its role in AD pathogenesis. 29318971: To address these issues, we have proposed the use of an animal model of concussion/TBI as a supplement to AD transgenic mice to provide an indication of an AD drug candidate's potential for preventing PPCD and resulting progression towards dementia in AD. 29933008: This review summarizes the current knowledge and concepts regarding the connection between long-term consequences of TBI and aging-associated neurodegenerative disorders including Alzheimer's disease (AD), chronic traumatic encephalopathy (CTE), and Parkinsonism, with implications for novel therapy targets. 30395237: The precise nature of how r-mTBI leads to, or precipitates, AD pathogenesis remains unclear. 30618712: However, the precise nature of how r-mTBI leads to or precipitates AD pathogenesis is currently not understood. 30837829: Investigation of secondary mechanisms triggered by aberrant downstream alterations in bioactive metabolites of these phospholipids, and their modulation at the appropriate time-windows of opportunity could help facilitate development of novel therapeutic strategies to ameliorate the neurodegenerative consequences of rmTBI or the potential triggering of AD pathogenesis by rmTBI. 30906371: Unusual FDG-PET Findings in Traumatic Brain Injury; Did Traumatic Brain Injury Provoke Rapid Progression of Alzheimer's Disease? 31778772: Knockout of AEP or C/EBPbeta diminishes TBI-induced AD-like pathology and cognitive impairment in the 3xTg AD mouse model. 31975836: DSM-5 recognizes the following etiologies for NCDs: NCD due to Alzheimer's disease, vascular NCD, NCD with Lewy bodies, frontotemporal NCD, substance-/medication-induced NCD, NCD due to traumatic brain injury, NCD due to Huntington's disease, NCD due to HIV infection, NCD due to prion disease, and NCD due to other medical conditions. 33171143: In the first part of this review, we analyze the experimental literatures on tau pathology in various TBI models and review the distribution, biological features and mechanisms of tau pathology following TBI with implications in AD pathogenesis. 34140411: Depletion of C/EBPbeta inhibits TBI-induced AD-like pathologies in these mice. 34539542: Various aspects of the mechanism of TBI-induced AD have been elucidated. However, there are also studies opposing the view that TBI is one of the causes of AD. 34831202: However, no effective therapies are currently available for TBI-induced AD-like disease. 35136958: Unfortunately, no effective therapies are currently available for prevention and treatment of the traumatic brain injury-induced Alzheimer's disease-like neurodegenerative disease. 36966972: Several lines of evidence indicate that pharmacological or genetic inactivation of MAGL, which boosts 2-AG levels and reduces its hydrolytic metabolites, resolves neuroinflammation, mitigates neuropathology, and improves synaptic and cognitive functions in animal models of neurodegenerative diseases, including Alzheimer's disease (AD), multiple sclerosis (MS), Parkinson's disease (PD), and traumatic brain injury (TBI)-induced neurodegenerative disease. 37205508: Traumatic brain injury in mice generates early-stage Alzheimer's disease related protein pathology that correlates with neurobehavioral deficits. 37284155: Next, a critical new study has identified that acetylated tau protein, which has been found to be increased in the brains of Alzheimer's disease and CTE patients, can be induced by TBI, is neurotoxic, and that its reduction via already-existent therapeutics is neuroprotective. 38261283: A comprehensive analysis of research results shows that the cascade of reactions triggered by TBI includes all the main elements of the pathogenesis of AD: disorders of energy metabolism, microcirculation and clearance of cerebral metabolic products. 38411868: Traumatic Brain Injury in Mice Generates Early-Stage Alzheimer's Disease Related Protein Pathology that Correlates with Neurobehavioral Deficits. 10226871: Dietary NaCl-induced hypertension in uninephrectomized Wistar-Kyoto rats: role of kidney function. This study tests the hypothesis that combination of unilateral nephrectomy and a high sodium chloride (NaCl) diet causes hypertension in otherwise normotensive Wistar-Kyoto (WKY) rats and that this hypertensive response is due to a deficit in the remaining kidney's function. These data suggest that the combination of unilateral nephrectomy and dietary NaCl excess causes hypertension in the normotensive WKY rats, but the hypertensive response is not likely due to a functional deficit in the remaining kidney. 1071596: Bilateral compression of adrenal glands combined with unilateral nephrectomy and followed by imposition of a high sodium chloride intake caused severe hypertension in all rats, accompanied by enlargement of the heart, kidneys and adrenal glands, atrophy of the thymus and severe nephrosclerosis. 1122560: The experimental hypertension was induced by unilateral nephrectomy, followed by the administration of DOCA and the elevated sodium diet. 13379210: [Healing evolutionary arterial hypertension secondary to surgical nephrostomy unilateral nephrectomy]. 18147353: Renal lesions in chronic hypertension induced by unilateral nephrectomy in the rat. 1896099: Over 40 years ago, Grollman reported that unilateral nephrectomy (UN) in rabbits precipitated hypertension and suggested that liberation of a pressor substance by an ischemic or damaged kidney could not be causative. 202775: Chronic administration of small doses of prostaglandin-synthesis inhibitor indometacin against the background of a salt load or unilateral nephrectomy induces the development of arterial hypertension in rats. 2304314: In young rats consuming 1% NaCl drinking solution, unilateral nephrectomy and bilateral adrenal enucleation caused a hypertension. 30334256: We used three hypertensive rat models: (1) rats with hypertension induced by chronic angiotensin II infusions (AngII model), (2) rats with hypertension induced by unilateral nephrectomy followed by high salt diet (HS/UNX), and (3) spontaneously hypertensive rats (SHR). 33651165: The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. 4084358: We have studied the effect of unilateral nephrectomy alone or in association with experimentally-induced (DOCA-salt treatment) or genetic (SHR) hypertension on the formation of lesions in the contralateral renal artery. 4321628: Changes in the enzymic capacity of the rat kidney and heart due to unilateral nephrectomy and deoxycorticosterone induced hypertension. 514639: Arterial lesions and hypertension induced by saline, unilateral nephrectomy, and deoxycorticosterone in spontaneously hypertensive SHR rats. 7919055: Hypertension and left ventricular hypertrophy was induced by unilateral nephrectomy plus wrapping of the contralateral kidney in cellophane. This study has shown that hypertension induced by perinephritis caused left ventricular hypertrophy which was associated with a prolongation in ventricular refractoriness in the rabbit. 858173: After lesioned rats had recovered normal drinking and blood pressure, unilateral nephrectomy with figure-of-eight wrapping of the remaining kidney failed to produce the hypertension and increased drinking observed after renal wrapping in shamlesioned rats. 950759: The administration of DOC to rats with unilateral nephrectomy resulted in more distinct hypertension than in those with both kidneys preserved. [Renal prostaglandins in DOCA-sodium chloride-induced hypertension in rats]. 1030172: Cardiovascular reactivity in hypertension due to unilateral renal artery stenosis before and after contralateral nephrectomy. 1032258: The role of some mechanisms in the development of hypertension due to unilateral renal artery stenosis is influenced by the presence or absence of the intact opposite kidney. 11390784: In hypertension caused by unilateral renal artery stenosis, the nonstenotic kidney becomes renin depleted but fails to prevent hypertension. 11956860: In patients with neurofibromatosis, hypertension is mainly caused by renovascular disease, whereas in tuberous sclerosis (TSC) reasons for hypertension are renoparenchymal lesions, such as angiomyolipoma or cysts. We report on a girl with TSC and hypertension due to unilateral renal artery stenosis associated with aneurysmatic changes of internal carotid artery. 14986083: We describe a newborn with severe hypertension and proteinuria secondary to unilateral renal artery stenosis. 1822252: The sympathetic nervous system in hypertension due to unilateral renal artery stenosis in man. 1839287: The authors present the clinical case of a 31 year female with systemic vascular hypertension secondary to a 65 percent unilateral fibromuscular renal artery stenosis. 30204997: We present a term newborn female, with arterial hypertension and an important congestive heart failure, caused by a unilateral renal artery stenosis, with functional abolition and atrophy of the affected kidney, which required an important inotropic and antihypertensive support during her first days of life, with significant clinical improvement subsequently. 4436891: Comparison of split function ratios with renal vein renin ratios in patients with curable hypertension caused by unilateral renal artery stenosis. 7019457: Renal autotransplantation was performed on 15 subjects with renovascular hypertensive disease owing to unilateral renal artery stenosis. 9709471: We measured blood ammonia in pre-angioplasty samples from the renal veins, aorta and inferior vena cava of 15 patients with hypertension due to unilateral renal artery stenosis confirmed by arteriography. 15660333: Experimental evidence suggests a complex but potentially direct causal role for uric acid in the pathogenesis of hypertension and atherosclerosis. 15840020: Thus, hyperuricemia induces endothelial dysfunction; this may provide insight into a pathogenic mechanism by which uric acid may induce hypertension and vascular disease. Furthermore, rat studies have shown that hyperuricemia-induced hypertension and vascular disease is at least partially reversed by the supplementation of the nitric oxide synthase (NOS) substrate, L-arginine. 16672142: Uric acid causes hypertension in a rat model through the activation of the renin-angiotensin system, downregulation of nitric oxide, and induction of endothelial dysfunction and vascular smooth muscle proliferation. 17060508: Experimental evidence supports a causative role for uric acid in the pathogenesis of hypertension. 18701632: Mild hyperuricemia induced by uricase inhibition causes intrarenal oxidative stress, which contributes to the development of the systemic hypertension and the renal abnormalities induced by increased uric acid. 19857674: Uric acid induces glomerular hypertension, microvascular disease, and renal interstitial fibrosis and is an independent risk factor for cardiovascular complications. 20885365: The results from animal studies and clinical observations support renal microvascular and tubulointerstitial injury being the key to uric acid-induced hypertension. The identification of conceivable biological mechanisms by which uric acid could cause high blood pressure has led to new insights about therapeutic modalities that may control high blood pressure and cardiovascular outcomes. Associations with other systemic derangements, including endothelial dysfunction, low-level systemic inflammation, sympathetic overactivity and insulin resistance, render uric acid to a complex but potentially direct causal role in the pathogenesis of hypertension. 21088389: After uric acid was recognized as the causative factor in gout, increased prevalence of renal disease and hypertension in this patient population caught the attention of the medical community. 21616780: Blood pressure was monitored by tail-cuff method, urinary and plasma uric acid was measured by autoanalyzer during the induction of hypertension in 1-, 2-, 3- and 4-week DOCA-salt-treated Sprague-Dawley rats. 22672087: Over time, uric acid uptake into vascular smooth muscle cells causes cellular proliferation and secondary arteriolosclerosis that impairs pressure natriuresis, causing sodium-sensitive hypertension. While more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early-onset hypertension. 23089272: Although more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early onset hypertension. 23736817: RECENT FINDINGS: The proposed mechanism of uric acid-induced hypertension is biphasic, with a reversible early phase, implying added significance for new-onset hypertension. 24419747: PURPOSE OF REVIEW: To discuss the evolving data regarding uric acid as a potential cause of hypertension and progressive renal dysfunction and its clinical and research implications. 24502620: In conclusion, the examination of the role of circulating purine nucleotides and uric acid in pathogenesis of hypertension and possible development of renal disease, together with XO role in ROS production, may help in modulating their liberation and ROS production in slowing progression from hypertension to renal failure. 27423331: Furthermore, we added an entirely new section on the role that simple carbohydrates (fructose in particular) and uric acid may play in the pathogenesis of hypertension in pediatric age. 29351480: Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress), and uric acid, and triggers hypertension. 31683330: CONCLUSION: In conclusion, urate-lowering therapy protects rats against fructose-induced obesity hypertension. Hyperuricemia Inhibition Protects SD Rats Against Fructose-Induced Obesity Hypertension Via Modulation of Inflammation and Renin-Angiotensin System in Adipose Tissue. OBJECTIVE: The present study was aimed to reveal the relationship between uric acid and fructose-induced obesity hypertension and its mechanisms. METHODS: A rat model with obesity hypertension was induced by a high-fructose diet. 8922344: In this study we evaluated the possible involvement of uric acid and xanthine oxidase in the pathogenesis of hypertension by examining their association with mean arterial pressure (MAP) and factors related to blood pressure. 14174370: [ON A CASE OF NEPHROGENIC HYPERTENSION DUE TO UNILATERAL OBSTRUCTIVE ANGIOPATHY (STENOSIS OF THE RIGHT RENAL ARTERY) SECONDARY TO CHRONIC INFLAMMATION OF PERIARTERIAL CELLULAR TISSUE]. 17691928: This review summarises the studies in man and animals that have investigated the potential role of vascular disorders in the aetiology of atherosclerosis and hypertension arising from early life nutritional deprivation or excess. 19003752: We report a 22-year-old female who developed nephrogenic arterial hypertension and intestinal ischemia due to congenital afibrinogenemia-associated angiopathy of large abdominal arteries. 36247997: The present study tries to explore not only the gender-specific association between H-type hypertension and SIVD but also the indirect effects of H-type hypertension on cognition through the ischemic brain injury caused by SIVD. 37215139: Hypoxic pulmonary hypertension (HPH) is a complicated vascular disorder characterized by diverse mechanisms that lead to elevated blood pressure in pulmonary circulation. 38109884: Renal artery stenosis is one of the common vascular diseases that cause hypertension in children. 38243321: OBJECTIVE: Hypertension caused by vascular Behcet's disease (BD) is an important prognostic factor of paediatric BD. 5358673: [Surgical therapy of hypertension, with special reference to hypertension caused by vascular diseases]. 5755365: [Surgical management of hypertension due to vascular disorders]. 9509227: Derangements in endothelial production of nitric oxide are implicated as both cause and consequence of vascular diseases, including hypertension, atherosclerosis, and coronary artery disease. 11772511: The results show that serum TNF-alpha was lower in mild-moderate AD compared to severe AD and dementias due to vascular disease, as well as the TNF-alpha/IL-1beta ratio. 15087585: In Alzheimer's disease (AD), white matter structural pathology is due to Wallerian degeneration and central angiopathy. 1781965: Results confirm the frequent association of white matter abnormalities in patients with DAT that are possibly caused by amyloid angiopathy and may contribute to cognitive impairments. 20608291: The atrophy of the brain with Alzheimer's disease is considered to be caused by the amyloid angiopathy of small blood vessels and the degeneration of capillaries and vascular feet. Based on this viewpoint, this review article emphasizes that the morphological changes to small blood vessels in the brain with Alzheimer's disease convey crucial information and clues for solving the underlying mechanism that causes the disease. 21575878: Risk of Alzheimer's disease incidence attributable to vascular disease in the population. 2377677: Despite the obviously more important degeneratively conditioned dementias, particularly of the Alzheimer-type, dementias due to vascular disorders are still of considerable relevance. 24084803: In the current review, the most common types of dementia, including Alzheimer disease, frontotemporal dementia, dementia due to vascular disease, and several others, are described. 28017827: Risk of incident clinical diagnosis of Alzheimer's disease-type dementia attributable to pathology-confirmed vascular disease. 34690734: Synaptic loss, senile plaques, and neurofibrillary tangles are the functional and diagnostic hallmarks of AD, but it is the structural changes as a consequence of vascular disease that reduce brain reserve and compensation, resulting in an earlier expression of the clinical dementia syndrome. 35578799: They had diagnoses of mild or major neurocognitive disorder due to suspected AD (N=20), mild or major neurocognitive disorder due to suspected VaD (N=44), or no neurocognitive diagnosis (i.e., healthy adult comparisons; HC, N=34). 37334605: Stroke prognosis impacts AD development due to vascular disease. 9823829: BACKGROUND: Recent studies suggest that vascular disease may contribute to the cause of Alzheimer disease (AD). 10101484: Also primary endothelial injury induces hypertension and atherogenesis. The main injury factor is hypertension, which provides to endothelium disfunction with vasopressors level growth which induces hypertension. 15792994: We hypothesized that insulin resistance may cause imbalance between endothelial vasodilators and vasoconstrictors (e.g., NO and ET-1), leading to hypertension. 18151410: Cerebral complications resulting from hypertension caused by vasopressor drugs in obstetrics. 19343267: BACKGROUND: Vasopressor-induced hypertension is routinely indicated for prevention and treatment of cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). Norepinephrine-induced hypertension dilates vasospastic basilar artery after subarachnoid haemorrhage in rabbits. CONCLUSION: This study demonstrated that NE-induced hypertension causes angiographic dilatation of the BA in the SAH rabbit model. The aim of this study was to evaluate angiographic effects of normovolaemic Norepinephrine (NE)-induced hypertension therapy on the rabbit basilar artery (BA) after SAH. Based on these observations, it can be hypothesised that clinical improvement during vasopressor-induced hypertension therapy after SAH might be explained with cerebral vasodilatation mechanisms that lead to improvement of cerebral blood flow. Mechanisms underlying patients' clinical improvement during vasopressor-induced hypertension remain incompletely understood. Five days later the animals underwent follow-up angiography prior to and during NE-induced hypertension. 19398663: Matrix metalloproteinase-7 and ADAM-12 (a disintegrin and metalloproteinase-12) define a signaling axis in agonist-induced hypertension and cardiac hypertrophy. In mice with angiotensin II-induced hypertension and cardiac hypertrophy, myocardial ADAM-12 and downstream hypertrophy marker genes were overexpressed. We observed that induction of acute hypertension by vasoconstrictors (ie, catecholamines, angiotensin II, and the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester) required the posttranscriptional activation of vascular MMP-7. 23737209: Endocrine and neuroendocrine vasopressor hormones such as the renin-angiotensin system (RAS), aldosterone, and catecholamines are important for regulation of blood pressure and pathogenesis of hypertension and target organ damage. 25792345: This approach includes the use of vasopressors to induce hypertension with the aim of improved cerebral blood flow. 26207606: OBJECT: Vasopressor-induced hypertension (VIH) is an established treatment for patients with aneurysmal subarachnoid hemorrhage (SAH) who develop vasospasm and delayed cerebral ischemia (DCI). The safety of vasopressor-induced hypertension in subarachnoid hemorrhage patients with coexisting unruptured, unprotected intracranial aneurysms. 27033710: Poor outcome is associated with less negative fluid balance in patients with aneurysmal subarachnoid hemorrhage treated with prophylactic vasopressor-induced hypertension. 2909538: Vasoconstrictors such as angiotensin II (Ang II) play an important role in the pathogenesis of hypertension. 30650118: Vasopressor induced acute hypertension did not compromise myocardial oxygenation in healthy hearts despite increased cardiac workload and O2 demand. 31874423: Any use of vasopressors for active induction of hypertension marked the end of data collection. 7856916: Therefore, we carried out a study to examine the role of vasopressor-induced hypertension. CONCLUSIONS: An equal degree of acute hypertension induced by these three different vasopressors may play a role in reducing the threshold (plasma and brain lidocaine concentrations) as well as the cumulative convulsant doses associated with lidocaine-induced convulsions. 9230324: We propose a common mechanism: the vasoconstrictors caused systemic hypertension, increased left ventricular afterload, decreased left ventricular compliance, and decreased cardiac output. 10371764: Diabetic nephropathy, a cause for renal fibrosis, results from glomerular haemodynamic abnormalities: intra-glomerular hypertension is provoked by pre-glomerular vasodilatation (a consequence of hyperglycaemia) facing to constitutive, post-glomerular, vascular resistances. 11212977: OBJECTIVE: To determine the effects on pre- and post-glomerular vascular resistance of adrenocorticotrophin (ACTH)-induced hypertension in rats, before and after blockade of nitric oxide formation. Glomerular hypertension and hyperfiltration in adrenocorticotrophin-induced hypertension in rats: the role of nitric oxide. CONCLUSIONS: ACTH-induced hypertension produced glomerular hypertension and hyperfiltration, which may be due to nitric oxide-related vasodilatation of the renal vasculature. 15703565: Ascites results from sinusoidal hypertension and sodium retention, which, in turn, is secondary to vasodilatation and activation of neurohumoral systems. 17023887: Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. 17023954: Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. 17031170: Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. 17033306: Ascites results from sinusoidal hypertension and sodium retention, which is in turn secondary to vasodilatation and activation of neurohumoral systems. 22941887: Liver disease and portal hypertension can be associated with pulmonary vascular complications, including portopulmonary hypertension (POPH), characterised by an elevated mean pulmonary artery pressure secondary to an increased pulmonary vascular resistance, and hepatopulmonary syndrome (HPS), characterised by hypoxaemia due to pulmonary vasodilatation and shunting. 3056448: Systemic hypertension is both the cause and the consequence of renal disease. In contrast, systemic hypertension with afferent arteriolar vasodilatation leads to glomerular hypertension and is associated with structural injury. 8282367: This may contribute (possibly via glomerular hypertension and hyperfiltration due to decreased postglomerular vasodilation) to progressive hypertensive renal damage, particularly in groups predisposed to dopamine deficiency, such as diabetics, blacks, and the elderly. 9120002: It can be caused by glomerular hypertension produced by capillary vasodilation, due to diabetes, against constitutional glomerular resistance. 9321742: These vasodilatory factors are important in blood pressure regulation and possibly in the etiology of hypertension. 12655379: All patients were treated by microsurgical technique and such treatment was completed by nimodipine, intensive care unit management and in some cases of postoperative suspected vasospasm, induced arterial hypertension was applied. 12702028: These included symptoms referable to the GI tract, elevated pancreatic enzymes and hypertension, presumed to be the result of vasoconstriction. 1277403: In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. 12874088: These data suggest that ROS generation induced by augmented Ang II levels contributes to the development of CysA-induced hypertension. Treatment with cyclosporine A (CysA), a potent immunosuppressive agent, is associated with systemic and renal vasoconstriction, leading to hypertension. 1308908: Proof of this is the hypertension as a consequence of vascular spasm and proteinuria due to glomerular injury. 14567598: A multivariate analysis showed that factors significantly associated with vasospasm were age 40 to 59 years, history of hypertension, worse neurological grade, thicker blood clot on the cranial computerized tomography (CT) scan obtained on hospital admission, larger aneurysm size, presence of intraventricular hemorrhage (IVH), prophylactic use of induced hypertension, and not participating in the first European tirilazad study. 15121411: By contrast, portopulmonary hypertension results from excessive pulmonary vasoconstriction and vascular remodelling that eventually leads to right-heart failure. 16636899: During hypertension, there is a shift in the cerebrovascular autoregulation to the right, in the direction of higher blood pressures, as a consequence of decreased cerebrovascular compliance resulting from vasoconstriction and pathological growth. 1784921: The most important of these side-effects are arterial hypertension and nephrotoxicity due to vasoconstriction of glomerular arteries. 18457270: The occurrence of hypertension due to systemic vasoconstriction in patients before, during, and after surgery is not uncommon and can have serious consequences with regard to outcomes. 19034231: Portopulmonary hypertension results from excessive pulmonary vasoconstriction and vascular remodeling that eventually leads to right-heart failure and death if left untreated. 19871088: The results do not lend support to the view that brief daily periods of renal ischemia from intrarenal vasospasm, or from any other cause, can produce persistent hypertension of renal origin. 21971491: Hypertensive encephalopathy should be considered in patients with unilateral or asymmetric vasospasm when neurological worsening occurs in the contralateral hemisphere during induced hypertension and/or the patient paradoxically worsens despite raising blood pressure. 23369639: Portopulmonary hypertension results from excessive vasoconstriction, vascular remodeling, and proliferative and thrombotic events within the pulmonary circulation that lead to progressive right ventricular failure and ultimately to death. 24647709: In preeclampsia (PE), maternal systemic and renal vasoconstriction leads to hypertension and modest reduction in GFR exceeding that of RPF. 24967414: Renal Resistive Index was found to be related with renal dysfunction, hypertension, and posttraumatic hemorrhagic shock, probably due to vasoconstriction. 27002212: PoPH results from excessive vasoconstriction, vascular remodeling, and proliferative and thrombotic events within the pulmonary circulation that lead to progressive right ventricular failure and ultimately to death. 27015528: Portopulmonary hypertension is caused by pulmonary vasoconstriction and increased pulmonary vascular resistance. 28583409: This review addresses the mechanisms underlying the development of vasoconstriction that leads to local vascular hypertension in the lung and in the kidney with the result of organ dysfunction. 29181390: CKD model induced by L-NAME is characterized by systemic vasoconstriction, resulting in severe hypertension, albuminuria, renal ischemia, glomerulosclerosis, interstitial expansion, and macrophage infiltration. 3336839: Currently, the most effective therapy for reversing neurological deficits secondary to vasospasm and for augmenting cerebral blood flow is induced hypertension and hypervolemia. 38351286: Excessive catecholamine release following amphetamine use causes vasoconstriction and vasospasms, over time leading to hypertension, endothelial dysfunction or even cardiotoxicity. 4047359: Although intravascular volume expansion and induced arterial hypertension have been shown to be effective in the reversal of neurological deficits secondary to vasospasm, a large proportion of patients remain refractory to these methods. 6716223: In only one infant was the structure of the intra-acinar precapillary arteries virtually normal, as would be expected if vasospasm alone had caused the hypertension. 6877556: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. 7133349: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. 7210750: The crisis of hypertension is always to be regarded as an emergency situation, since always irreversible lesions may be appear on the different organs as a sequel of the permanent vasoconstriction and ischaemia. 7305671: Hypomagnesemia and vasoconstriction: possible relationship to etiology of sudden death ischemic heart disease and hypertensive vascular diseases. 7476815: Treatment of ischemic deficits caused by vasospasm relies on enhancing cardiac output, inducing arterial hypertension, and expanding the intravascular volume in an attempt to improve CBF. 7791970: Despite hypervolemic hemodilution, arterial hypertension, and pharmacological therapy, morbidity and mortality due to vasospasm remain high. 8780224: SCY II caused an initial hypertension induced by a general vasoconstriction, followed eventually by an elevated flow in both gut arteries due to dilation of the vascular beds. 9154334: The use of the immunosuppressive drug cyclosporin A (CsA) is limited by two major side effects, nephrotoxicity and hypertension, which are caused by drug-induced local vasoconstriction. 9661539: IMPLICATIONS: Acute hypoxemia in pigs is responsible for pulmonary vasoconstriction-induced pulmonary hypertension (which is restricted by the right ventricular failure), as well as a PaO2-dependent decrease in left ventricular afterload. 11258753: The peripheral and central nervous system are harbouring herpes simplex virus type 1 (HSV-1) and this virus has been proposed to be implicated in the aetiology of Alzheimer's disease (AD). 12226537: The proposition that environmental agents, such as diet, aluminum, and viruses, are as important as genetic factors in the etiology of Alzheimer's disease (AD) was advanced by the authors at the Challenging Views of Alzheimer's Disease meeting held in Cincinnati on July 28 and 29, 2001. 15319093: Various infectious agents, and viruses in particular, have been proposed as potential causes of Alzheimer's disease. 19221424: Our previous studies have implicated herpes simplex virus type 1 (HSV1) as an etiological agent in AD, and so we investigated whether infection with this virus induces AD-like tau phosphorylation. 2443213: These results, although negative, do not totally exclude the possibility that conventional viruses may play a role in the aetiology and pathogenesis of AD. 25747044: AREAS COVERED: The various roles that LRP/LR plays in cancer, AD and infectious diseases caused by viruses and bacteria have been examined in detail and an overview of the current patented therapeutic strategies targeting this receptor is given. 25932012: Chronic infection by spirochetes, and co-infection with other bacteria and viruses should be included in our current view on the etiology of AD. 26444787: CONCLUSIONS: The lack of any relation between humoral immune response against HHV-6 and AD and aMCI seems to rule out a role for this virus in the pathogenesis of AD. 2840102: However, unconventional slow viral infections share some of these traits with AD and yet they are caused by retroviruses or suspected viruses. 30087609: However, the recent discovery that Abeta is an antimicrobial peptide (AMP) acting against bacteria, fungi, and viruses gives increased credence to an infection hypothesis in the etiology of AD. These findings led to the \beta-amyloid hypothesis\ that proposes that Abeta is the major cause of AD. 3024793: The concluding section, on parallels between AD and diseases of the brain caused by unconventional viruses, defines strategies for isolating genes related to pathology. 31093882: Binding between Prion Protein and Abeta Oligomers Contributes to the Pathogenesis of Alzheimer's Disease. In addition, we proposed a potential mechanism to explain why infectious agents, such as viruses, conduce AD pathogenesis. 31456237: Important new information was presented regarding: the mechanisms of chromosomal integration for HHV-6A and -6B; the biology of inherited chromosomally integrated HHV-6A and -6B; animal models for, and animal viruses with similarities to, HHV-6A, -6B, and -7; established and possible disease associations, including provocative new information suggesting these viruses may be one trigger of Alzheimer's disease, and new treatment strategies. 31526227: Furthermore, evidence suggests that traditional infectious agents, including certain viruses and bacteria, may trigger AD. However, amyloid beta (Abeta) or tau, which can act like infectious proteins, or prions, might induce Alzheimer's disease (AD). 34971176: Yet, it is possible that the viruses play a role in the pathogenesis of AD, perhaps in the early stages of this dementia. 37170683: Furthermore, we infected these microtissues with HSV-1 virus and determined the HSV-induced pathogenesis associated with Alzheimer's disease, including neuron loss and the expression of Abeta. 38249527: This paradigm shift is substantiated by an extensive body of scientific literature, which underscores the significant contributions of microorganisms, encompassing viruses and gut-derived bacteria, to the pathogenesis of AD. 21499117: Vitamin D deficiency-induced hypertension is associated with vascular oxidative stress and altered heart gene expression. 23349943: To clarify the role of vitamin D-deficiency in CVD in vivo, we generated mouse models of diet-induced vitamin D deficiency in two backgrounds (LDL receptor- and ApoE-null mice) that resemble humans with diet-induced hypertension and atherosclerosis. Vitamin D deficiency induces high blood pressure and accelerates atherosclerosis in mice. 23719723: Vitamin D deficiency in adulthood is linked to the etiology of hypertension and to a multitude of adverse cardiovascular outcomes. 24929953: Vitamin D deficiency in the pathogenesis of hypertension: still an unsettled question. 28357170: Does Vitamin D Deficiency Lead to Hypertension? 28951226: Deletion of JNK2 prevents vitamin-D-deficiency-induced hypertension and atherosclerosis in mice. These data suggest that JNK2 signaling activation is necessary for the atherosclerosis and hypertension induced by vitamin D deficiency. To determine whether deletion of JNK2 prevents high blood pressure and atherosclerosis known to be induced by vitamin D deficiency in mice, we generated mice with knockout of JNK2 in a background susceptible to diet-induced atherosclerosis (LDLR-/-). 29114197: Evident from recent research that Vit D deficiency may be the cause for hypertension, cardiac autonomic imbalance, vascular endothelial dysfunction, metabolic syndrome, and even diabetes. 30192652: Vitamin D deficiency can lead to high blood pressure. 31099039: HYPOTHESIS: This study aimed to evaluate the possible crosstalk between GM dysbiosis and vitamin D deficiency in the pathogenesis of HTN. 32456803: In this work, a review is presented of the main mechanisms involved in the development of hypertension due to vitamin D deficiency. 33337598: High blood pressure induced by vitamin D deficiency is associated with renal overexpression and hyperphosphorylation of Na+-K+-2Cl- cotransporter type 2. This study aimed to test the hypothesis that high BP induced by VDD is associated with altered expression and covalent modification of apical sodium transporters along the nephron. 35737199: PURPOSE OF THE REVIEW: Results from epidemiological studies suggest that vitamin D (VD) deficiency (VDD) may be a cause of hypertension (HTN). 37993482: Several studies have revealed that vitamin D deficiency can lead to chronic vascular inflammation, diabetes mellitus, hypertension, congestive left ventricular hypertrophy, and heart failure. 10995524: The associated dysfunction in water and salt handling often induces hypertension. 11439738: Water and sodium removal play an important role in the genesis of intradialytic cardiovascular instability or hypertension. 13202335: [Experimental studies on the role of the pituitary in intraocular hypertension produced by nicotine and water]. 157830: Replacement of clonidine by water induced hypertension and lability which led to death in hypertensive but not in normotensive rats. 22796734: There is a widely held belief that hypervolaemia due to excess intake or inadequate removal of salt and water is the principal cause of hypertension in dialysis patients. 26178554: Liddle's syndrome or pseudoaldosteronism is a rare autosomal dominant disease mimicking primary hyperaldosteronism, characterized by early-onset hypertension, hypokalemia and hypoaldosteronism, caused by excessive salt and water reabsorption in the distal nephron. 28031693: High intake of dietary salt and low intake of water increase extracellular osmolality resulting in hypertension, in particular in salt-sensitive individuals. 28337713: In rats fed with high-fructose water to induce mild hypertension, 4-week treatment with recombinant FGF21 led to normalization of systolic blood pressure and improved serum lipid profile. 29556197: Background: Corticosteroids are associated with reduced bone mineral density (BMD), as well as water and salt retention, leading to hypertension. 6344213: Thus, chronically fed cadmium can induce hypertension in rats, but conditions are important. Additional observations on cadmium-induced hypertension indicate that: (1) concentrations from 0.1 to 5 ppm cadmium in water are pressor; (2) sex, strain, and age of animals are apparently not limiting factors; (3) there is associated sodium retention; (4) there is a concomitant decrease in the high energy phosphate content of tissues. Using Schroeder's food and water, but a slightly less cadmium-free environment, we repeatedly induced mild hypertension with 5 ppm cadmium, mild because control pressures were higher not because cadmium-fed animals had lower pressures. Rats with cadmium-induced hypertension have renal cadmium concentrations which bracket those of the average environmentally exposed American or European. 6862570: Previous studies have shown that a combination of avoidance conditioning schedules and increased intake of salt and water results in progressive hypertension in dogs within 14 days. 7018807: Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 7915651: Norepinephrine (NE) infused at doses of 0.7, 2.2 and 6.7 micrograms/min/kg body weight into conscious, salt and water loaded ducks dose-dependently induced arterial hypertension, reflex bradycardia and diuresis/natriuresis at unchanged glomerular filtration and reduced renal blood flow. 9026743: The mineralocorticoid action of cortisol causes a drop in serum potassium and an increase in serum sodium concentration, together with a metabolic alkalosis, which in the patient described led to retention of water resulting in weight increase and hypertension. 1179571: Renal arterial thrombosis from blunt trauma causes delayed hypertension in many patients, but few reports have been well documented. 13464393: [Forms of hypertension caused by trauma]. 13788542: Hypertension due to trauma of the kidney. 14478521: [Considerations on arterial hypertension caused by renal trauma]. 16553344: We review the pathogenesis of headache and cerebral hemorrhage after spinal anesthesia and propose differential diagnosis between spontaneous rupture related to hypertension and cerebrospinal fluid hypotension syndrome caused by trauma from lumbar spinal puncture. 16647623: CONCLUSIONS: Renal trauma is a rare cause of hypertension, mostly in young men. BACKGROUND: Blunt renal trauma (RT) may cause hypertension. 19555351: Finally, resuscitation using HBOC-201, after trauma and haemorrhage, resulted in mild hypertension ( approximately 5-10 mmHg). 23518197: Renal artery pseudoaneurysms are rare and under-recognized complications of blunt abdominal or back trauma that can cause hypertension. 2904210: Microbial infection or trauma at cardiovascular representation area of medulla oblongata as some of the possible causes of hypertension or hypotension. 3595625: Therapeutic embolization of renal artery to control severe hypertension due to renal trauma. 3729693: Focal brain injury to centers of blood pressure regulation, high levels of circulating catecholamines from generalized trauma or intracranial lesions, increased intracranial pressure, pheochromocytomas unmasked after trauma, and occult spinal cord injury with hyperreflexia represent possible causes of hypertension after brain injury. 8145890: Thus, ESWL may cause renal trauma and such trauma may induce later hypertension. 12505647: Further research on the zinc paradox in AD is needed in order to elucidate the exact role zinc plays in AD pathogenesis. 18376063: Recent studies also point to redox active metals such as iron, copper and zinc in mediating oxidative stress in AD pathogenesis. 18603329: Zinc is also involved, in a sex-dependent manner, in the pathogenesis of Alzheimer's disease (AD), where substantial declines in plasticity may occur. 19276540: Although multiple studies have suggested a role for alterations of zinc (Zn) and zinc transport (ZnT) proteins in the pathogenesis of Alzheimer's disease, the exact role of this essential trace element in the progression of the disease remains unclear. 2025422: Hypothesis regarding amyloid and zinc in the pathogenesis of Alzheimer disease: potential for preventive intervention. 20730621: The aim of this review is to discuss the role of redox metals Fe and Cu and non-redox metal zinc (Zn) in oxidative stress-related etiology of AD and PD. 30598025: Moreover, it is already established that metals (particularly copper, zinc and iron) have a key role in the pathogenesis of AD. 8073293: Rapid induction of Alzheimer A beta amyloid formation by zinc. 9164672: This paper reviews current investigations that suggest a role of zinc in the etiology of Alzheimer's disease. 9334223: Zinc-induced Alzheimer's Abeta1-40 aggregation is mediated by conformational factors. 9358828: CONCLUSIONS: While earlier literature promoted the use of zinc in AD patients, a recent study has contradicted this and implicated zinc in the aetiology of Alzheimer's disease. 10583721: We have described the first known case of a patient with neurofibromatosis type 1 who developed hypertension due to an aldosterone-producing adenoma of the adrenal. 10720580: APA can be cured through removal of the adenoma, whereas IHA leads to hypertension that must be treated with medication. 11549664: An aldosterone-producing adenoma causes surgically correctable hypertension. 11881068: Hypertension due to a giant aldosterone-secreting adenoma. 17938379: Aldosterone-producing adenomas (APAs) are a common cause of arterial hypertension, but the underlying molecular mechanisms are unknown, although a transcriptional modulation of aldosterone synthase (CYP11B2) has been suggested. 1912162: [Arterial hypertension secondary to an aldosterone-producing adenoma (APA)]. 24082060: Ins and outs of aldosterone-producing adenomas of the adrenal: from channelopathy to common curable cause of hypertension. 24428543: Somatic gain-of-function mutations of the Na(+),K(+)-ATPase alpha1-subunit have been found in aldosterone-producing adenomas that are among the causes of hypertension. 24817817: The syndrome accounts for 10% of all cases of hypertension and is primarily caused by bilateral adrenal hyperplasia or aldosterone-producing adenoma. 24943299: Primary aldosteronism (PA) accounts for ~10% of hypertension, which is commonly caused by an aldosterone-producing adenoma (APA) or bilateral adrenal hyperplasia. 25276129: Arterial hypertension caused by paediatric adenomas or tumours of the adrenal cortex or medulla has been associated with various hypertension-related neurological manifestations. 25538205: Primary aldosteronism (PA) secondary to excessive and/or autonomous aldosterone secretion from the renin-angiotensin system accounts for ~10% of cases of hypertension and is primarily caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenomas (APAs). 26312884: BACKGROUND: Cell origin of aldosterone-producing adenomas, a major cause of hypertension, is unknown. 6375348: Hypertension caused by an aldosterone-secreting adenoma. 8600610: OBJECTIVE: To determine the characteristics of an aldosterone-producing adenoma (APA) as a cause of hypertension, its mode of presentation and investigation, as well as the outcome of surgical removal. 9118515: BACKGROUND: Since hyperaldosteronism has been experimentally related to myocardial interstitial fibrosis, we investigated the effects of hypertension and excess aldosterone due to aldosterone-producing adenomas (APAs) on the heart. 10513378: A case is presented in which an elderly patient with preexisting first degree atrioventricular (AV) block progressed to second degree Mobitz Type I AV block during spinal anesthesia and associated with hypertension induced by a pure alpha 1 agonist. 15358274: Recent studies in hypertensive animals have shown enhanced expression and activation of MMPs and EGF receptors, and their inhibition attenuates cardiac hypertrophy, vasoconstriction and hypertension induced by GPCR agonists such as angiotensin II, endothelin-1 and phenylepherine. 1683093: L-phenylephrine, an alpha-1 agonist, induced hypertension, bradycardia and a significant gastric relaxation. 17273114: Hypotension has also been reported as well as hypertension, the latter thought to be due to peripheral alpha2B agonism with peripheral vasoconstriction. 17330852: These results suggest that continuous neck exposure to 12 mT SMF for at least 2 weeks may depress or suppress sympathetic agonists-induced hypertension, hemodynamics, and behavioral changes by modulating sympathetic nerve activity. 19398663: Matrix metalloproteinase-7 and ADAM-12 (a disintegrin and metalloproteinase-12) define a signaling axis in agonist-induced hypertension and cardiac hypertrophy. In mice with angiotensin II-induced hypertension and cardiac hypertrophy, myocardial ADAM-12 and downstream hypertrophy marker genes were overexpressed. We observed that induction of acute hypertension by vasoconstrictors (ie, catecholamines, angiotensin II, and the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester) required the posttranscriptional activation of vascular MMP-7. 19581512: We targeted TACE in rodent models of spontaneous and agonist-induced hypertension using RNA interference combined with quantitative RT-PCR, activity determinations, and functional studies. 21464390: Inhibition of the AMP-activated protein kinase-alpha2 accentuates agonist-induced vascular smooth muscle contraction and high blood pressure in mice. 21943355: With high plasma concentration secondary to massive systemic overdose, the specificity for the alpha-2 receptor is lost and an alpha-1 agonist activity predominates and causes marked hypertension. 24077247: CONCLUSION: These results suggest that TIMP2 deficiency exacerbates renovascular remodelling in agonist-induced hypertension by a mechanism that may, in part, be attributed to increased activity of MMP-9. Angiotensin-II induced hypertension and renovascular remodelling in tissue inhibitor of metalloproteinase 2 knockout mice. 24900328: It has been postulated that fingolimod's efficacy is due to S1P1 agonism, while its cardiovascular side effects (transient bradycardia and hypertension) are due to S1P3 agonism. 27519818: Tissue selectivity could potentially differentiate S1PL inhibitors from S1P receptor agonists, the use of which also results in bradycardia, atrioventricular block, and hypertension. 2843054: Despite potentiating the systemic arterial pressor response to methoxamine, chloralose attenuated the reflex decrease in heart rate after alpha-agonist-induced hypertension. 3019261: Finally, alpha 1-agonists cause maximum arterial hypertension at all doses used, irrespective of induction of LE and of protective pretreatment against LE. 30941336: After extensive literature review, we found 3 other cases of HTN secondary to GnRHa, improving with endocrine treatment cessation. 34207980: The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of alpha 1 -adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing alpha 1A -adrenoceptor mRNA in the PVN. 7013572: With massive overdose, clonidine's partial alpha-agonist properties may predominate, resulting in marked hypertension requiring cautious therapy. 7987671: Central administration of the angiotensin II antagonist DuP 753 (5 nmol) 30 min before i.c.v. injection of [Asn1,Val5]AII totally prevented the tachycardia and reduced the hypertension induced by the angiotensin II agonist. 8067431: Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. 10604525: To demonstrate potential therapeutic effects of kallikrein gene delivery in salt-induced hypertension and renal diseases, we delivered adenovirus carrying the human tissue kallikrein gene (Ad.CMV-cHK) into deoxycorticosterone acetate (DOCA)-salt hypertensive rats. 10986555: These results indicate that human AM gene delivery protects against salt-induced hypertension and cardiac and renal lesions in DSS rats via activation of cAMP as a second messenger. 11161799: Concordance of murine quantitative trait loci for salt-induced hypertension with rat and human loci. To investigate the genetic control of salt-induced hypertension, we performed a quantitative trait locus analysis on male mice from a reciprocal backcross between the salt-sensitive C57BL/6J and the normotensive A/J inbred mouse strains after they were provided with water containing 1% salt for 2 weeks. 11179194: Compared with the wild-type controls, the B(2)R gene knockout mice had a higher baseline BP (109.7+/-1.1 versus 101.1+/-1.3 mm Hg, P:=0.002), developed salt-induced hypertension faster (in 19.3+/-2.3 versus 27.7+/-2.4 days, P:=0.024), and had a more severe end point BP (148+/-3.7 versus 133+/-3.1 mm Hg, P:<0.05). 1153885: Rapid onset of salt induced hypertension in rats with hereditary hydronephrosis. 11711500: The results of previous studies with genetically engineered mice have suggested that an intact central alpha(2B)-adrenergic receptor (alpha(2B)-AR) subtype mediates the development and maintenance of salt-induced hypertension. 11748085: Although gender had no effect on MR at any perfusion pressure or age, only male mice showed significant salt-induced hypertension and an associated increase in the set point and reduction in the extent of the MR. 11752095: This study investigated the importance of the male sex hormone testosterone on salt-induced hypertension, renal alpha(2)-adrenoceptor subtype distribution, and gene expression in salt-sensitive (SBH) male Sabra rats. In conclusion, testosterone is needed for the full expression of salt-induced hypertension in male salt-sensitive Sabra rats. In gonadectomized rats, testosterone replacement restores salt-induced hypertension, density of renal alpha(2B)-adrenoceptors, and gene expression to the intact levels observed both under normal and high salt diet. 11884268: This review discusses the view that the renal genotype is not the only determinant of salt-induced sympathetic hyperactivity and hypertension, and that changes in genetic control of neuronal responses to cerebrospinal fluid Na(+) may play a primary role. Neural mechanisms play an essential role in salt-induced hypertension, and recent studies indicate that centrally induced sympathetic hyperactivity actually causes the hypertension. 12675281: We concluded that, in rats with salt-induced hypertension, the myosin isoform shift from V1 to V3 starts at the base of the LV, and particularly at the base of the IVS, and then spreads across the entire LV. 14458005: Pathogenesis of experimental hypertension induced by salt. 14654758: Resistance to salt-induced hypertension in catechol-O-methyltransferase-gene-disrupted mice. OBJECTIVE: To test the hypothesis that COMT blockade protects from salt-induced hypertension. CONCLUSION: Our findings suggest that COMT deficiency in mice increases the availability of L-DOPA, leading to enhanced dopaminergic tone, which may be associated with resistance to salt-induced hypertension. 14746895: To characterize the involvement of specific alpha(1)-adrenergic receptor (alpha(1)-AR) subtypes in hypertension, parameters related to central salt- or angiotensin II (ANG II)-induced hypertension were investigated in alpha(1D)-AR-deficient mice (knockout). 1531344: We examined changes in the expression of fibronectin during the induction of cardiac hypertrophy by L-triiodothyronine administration and by mineralocorticoid- and salt-induced experimental hypertension. 16396943: These results indicate that transfer of the region of chromosome 5 between markers D5Rat108 to D5Rat31 from the Lewis rat into the Dahl S genetic background increases the renal production of 20-HETE, improves pressure-natriuresis and opposes the development of salt-induced hypertension. 1645980: Conversely, the absence of sodium regulation in SBN rats might represent a genetically mediated change responsible for the resistance to the development of salt-induced hypertension. 16466965: In TcDD, the expression of genes containing target sequences such as CAG repeating sequences or genes encoding for zinc-finger binding proteins were followed in an experimental rat model with salt-induced hypertension. 17070424: In alpha(2B)-AR gene knockout mice, blood pressure (BP) does not rise with salt loading, and in rats with salt-induced hypertension, BP decreases transiently with antisense (AS) treatment targeting the alpha(2B)-AR gene. BACKGROUND: Salt-induced hypertension is mediated via the alpha(2B)-adrenergic receptor (AR) subtype. CONCLUSIONS: These results indicate that our construct, when given by ICV means, could reach multiple sites of the central nervous system relevant to BP regulation and could safely inhibit the central alpha(2B)-adrenergic receptor, thereby achieving prolonged reversal of salt-induced hypertension. 17650543: Lewis Dahl and the genetics of salt-induced hypertension. 1797594: Genetic and maternal influences in rat models of spontaneous and salt-induced hypertension. 18084302: G12-G13-LARG-mediated signaling in vascular smooth muscle is required for salt-induced hypertension. In contrast, lack of G12-G13, as well as of their major effector, the leukemia-associated Rho guanine nucleotide exchange factor (LARG), did not alter normal blood pressure regulation but did block the development of salt-induced hypertension. Using genetically altered mouse models that allow for the acute abrogation of both signaling pathways by inducible Cre/loxP-mediated mutagenesis in smooth muscle cells, we show that G(q)-G11-mediated signaling in smooth muscle cells is required for maintenance of basal blood pressure and for the development of salt-induced hypertension. 18156195: Genes overexpressed in cerebral arteries following salt-induced hypertensive disease are regulated by angiotensin II, JunB, and CREB. Together, these results suggest that salt-induced hypertensive disease promotes changes in matricellular genes that are stimulated by ANG II, regulated by ERK, and selectively regulated by JunB and CREB. 18316652: The consomic SS-13(BN) rat, genetically similar to the Dahl salt-sensitive rat, while exhibiting a significant amelioration of salt-induced hypertension, was used as a control. 18420168: Estrogen effects on MMP-13 and MMP-14 regulation of left ventricular mass in Dahl salt-induced hypertension. 18430809: We studied the molecular networks that underlie the complex disease phenotypes in the SS model, using a design that involved two consomic rat strains that were protected from salt-induced hypertension and one that was not protected. Substitution of Brown Norway (BN) chromosome 13 or 18, but not 20, into the SS genome was found to significantly attenuate salt-induced hypertension and albuminuria. 18826995: Knockdown of renal medullary 11 beta-hydroxysteroid dehydrogenase type 1 with small-interfering RNA attenuated the early phase of salt-induced hypertension in Dahl salt-sensitive rats and reduced urinary excretion of corticosterone. In summary, we have demonstrated that suppression of 11 beta-hydroxysteroid dehydrogenase type 1 expression in the renal medulla attenuates salt-induced hypertension in Dahl salt-sensitive rats. Long-term attenuation of salt-induced hypertension was achieved with small hairpin RNA targeting renal medullary 11 beta-hydroxysteroid dehydrogenase type 1. 19079278: These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. The time course of salt-induced hypertension, and why it matters. 19330919: BACKGROUND: The kidney's role in the pathogenesis of salt-induced hypertension remains unclear. 1987017: Based on early experiments, it was thought that hypertension in Dahl salt-sensitive rats epitomized the overriding importance of renal and humoral mechanisms in salt-induced hypertension, but studies in the past 15 years have demonstrated that alterations in sympathetic neural mechanisms also participate critically in the genetic predisposition to salt-induced hypertension in Dahl salt-sensitive rats. This article briefly reviews sympathetic neural mechanisms in Dahl rats, including evidence for a role of afferent baroreceptor as well as central neural and peripheral adrenergic mechanisms in salt-induced hypertension in Dahl salt-sensitive rats. The Dahl strain provides a model for examining mechanisms involved in the genetic sensitivity or resistance to salt-induced hypertension. Sympathetic neural contribution to salt-induced hypertension in Dahl rats. 20538365: This work builds upon a recent study, which developed a grey-box multi-component model of salt-induced hypertension in the Dahl-S rat. Salt-induced hypertension has been demonstrated in a variety of species including rats, monkeys, chimpanzees and humans. A 5-component mathematical model for salt-induced hypertension in Dahl-S and Dahl-R rats. 21207253: In a subgroup of individuals with metabolic syndrome, adipocyte-derived aldosterone-releasing factors cause inappropriate secretion of aldosterone in the adrenal glands during salt loading, resulting in the development of salt-induced hypertension and cardiac and renal damage. Such a local control system for MR can also be relevant to the pathogenesis of salt-sensitive hypertension, and future studies will clarify the detailed mechanism for the intricate regulation of the aldosterone/MR cascade. 21208017: The aim of our study was to evaluate NO synthase (NOS) activity and protein expression of its three isoforms--neuronal (nNOS), endothelial NOS (eNOS) and inducible (iNOS)--in two brain regions involved in blood pressure control (diencephalon and brainstem) as well as in the kidney of young adult rats with either genetic (12-week-old SHR) or salt-induced hypertension (8-week-old Dahl rats). In conclusions, we disclosed similar changes of NO system in the brainstem (but not in the diencephalon) of rats with genetic and salt-induced hypertension. As far as peripheral NOS activity and expression is concerned, renal eNOS expression was considerably reduced in both genetic and salt-induced hypertension. 21572007: The elevated blood pressure in salt-induced hypertension is reduced below normotensive levels after MLCK attenuation. Role of myosin light chain kinase in regulation of basal blood pressure and maintenance of salt-induced hypertension. 21666123: Vascular reactivity to calcitonin gene-related peptide is enhanced in subtotal nephrectomy-salt induced hypertension. In subtotal nephrectomy (SN)- and salt-induced hypertension, calcitonin gene-related peptide (CGRP) plays a compensatory role to attenuate the blood pressure increase in the absence of an increase in the neuronal synthesis and release of this peptide. 21765214: Therefore, our data identify Rac1 as a determinant of salt sensitivity and provide insights into the mechanism of salt-induced hypertension and kidney injury. 22349312: As a result, hypertension induced by 2-week high salt was significantly attenuated in rats treated with HIF-1alpha plasmid or CoCl2. 22622494: Angiotensin II/salt caused hypertension in both the knockout and wild-type mice, an effect significantly blunted in the knockout mice. 22652430: The genetic deletion of Mas abolishes salt induced hypertension in mice. 22773773: In Dahl S rats and spontaneous hypertensive rats, high salt activates the CNS aldosterone-EO pathway, and the salt-induced hypertension can be prevented/reversed by specific CNS blockade of any of the steps in the cascade from aldosterone synthase to AT(1)R. 23702776: In this study, we tested the hypothesis that components of the SWI/SNF complex are activated and recruited to promoters that regulate the fetal cardiac gene program in hearts that become hypertrophic as a result of salt induced hypertension. Our data implicate SWI/SNF chromatin remodeling enzymes as regulators of gene expression in cardiac hypertrophy resulting from salt induced hypertension. Thus we provide novel insights into the epigenetic mechanisms by which salt induced hypertension leads to cardiac hypertrophy. 23911822: L-NAME salt-induced hypertension accelerated mesangial cell process invasion. 2393103: This study was designed to investigate the GABAergic neurons in specific regions of the brain possibly linked to salt-induced hypertension. This study provides new evidence to support further the idea that central GABAergic neurons are closely associated with pathogenesis of salt-induced hypertension. Different hypertensive mechanisms between salt-induced hypertension and genetic hypertension are also discussed. It is not clear, however, which GABAergic systems are involved in salt-induced hypertension. 24247285: Investigations have also demonstrated that immune reactivity to overexpressed heat shock protein 70 (HSP70) is involved in the pathogenesis of salt-induced hypertension. 24339896: BACKGROUND: Reactive oxygen species are implicated in the physiopathogenesis of salt-induced hypertension and the C242T polymorphism of the p22-phox gene has been associated with higher superoxide production. 25164814: We have recently shown that ENaC activity contributes to the development of salt-induced hypertension as a result of deficiency of EGF level. We conclude that changes in the RhoGDIalpha-dependent pathway have a permissive role in the Rac1-mediated enhancement of ENaC activity observed in salt-induced hypertension. 25304471: Deletion of interleukin-6 prevents cardiac inflammation, fibrosis and dysfunction without affecting blood pressure in angiotensin II-high salt-induced hypertension. 25420527: Thus, selected genes and genetic variants contributing to the development of salt-induced endothelial dysfunction and hypertension are discussed. 25520008: beta2-Adrenergic stimulation due to increased renal sympathetic activity in obesity- and salt-induced hypertension suppresses histone deacetylase 8 activity via cAMP/PKA signaling, increasing the accessibility of GRs to the negative GR response element in the WNK4 promoter. 2558064: This property may represent a genetically-mediated change responsible for the resistance to the development of salt-induced hypertension. These results also suggest an association between absence of sodium regulation of alpha 2-adrenoceptors and resistance to salt-induced hypertension. 25617698: BACKGROUND: The study was designed to explore the significance of endogenous H2S in the development of high-salt-induced hypertension in rats. Down-regulated CBS/H2S pathway is involved in high-salt-induced hypertension in Dahl rats. METHODS: High-salt-induced hypertension rat model was made by feeding Dahl rat high-salt diet containing 8% NaCl for 8 weeks with SD rats as control. 26103560: KEY RESULTS: 1K/DOCA/salt-induced hypertension in mice was associated with increased renal mRNA expression of inflammasome subunits NLRP3, ASC and pro-caspase-1, and the cytokine, pro-IL-1beta, as well as protein levels of active caspase-1 and mature IL-1beta. 26178554: Liddle's syndrome or pseudoaldosteronism is a rare autosomal dominant disease mimicking primary hyperaldosteronism, characterized by early-onset hypertension, hypokalemia and hypoaldosteronism, caused by excessive salt and water reabsorption in the distal nephron. 2632718: The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. 26438340: NF-kappaB Blockade in Hypothalamic Paraventricular Nucleus Inhibits High-Salt-Induced Hypertension Through NLRP3 and Caspase-1. 26534937: The goal of the present study was to further narrow that region to identify the gene(s) most likely to protect from salt-induced hypertension. A 1.37 Mbp region of chromosome 13 previously identified by exclusion mapping was consistently associated with a reduction of salt-induced hypertension in the Dahl salt-sensitive (SS) rat. We conclude that we have identified a variant form of Pappa2 that can protect against salt-induced hypertension in the Dahl S rat. The studies yielded a subcongenic SS rat strain containing a 0.71 Mbp insert from BN (26-P strain) in which salt-induced hypertension was reduced by 24 mmHg. 27431647: Genetic Abrogation of Adenosine A3 Receptor Prevents Uninephrectomy and High Salt-Induced Hypertension. 28185984: Hydrogen sulfide in paraventricular nucleus attenuates blood pressure by regulating oxidative stress and inflammatory cytokines in high salt-induced hypertension. These findings suggest that endogenous or exogenous H2S in the PVN attenuates sympathetic activity and hypertensive response, which are partly due to decrease of ROS and PICs within the PVN in high salt-induced hypertension. 2827643: These results indicates that vertebrate animals possess a regulator of Na, K-ATPase and suggests the possibility that it may be the mediator of salt-induced high blood pressure. The endogenous inhibitor of Na, K-ATPase has been implicated in the pathogenesis of salt-induced hypertension. 28298656: Immune system involvement may be a key component that initiates kidney damage in a genetic model of salt-induced hypertension. 28338001: This study was designed to explore the precise mechanisms of RAS acting on reactive oxygen species (ROS) in salt-induced hypertension. These results, for the first time, identified that the precise signaling pathway of RAS regulating ROS in PVN is via AT1R/PKCgamma/Rac1 in salt-induced hypertension. Male Wistar rats were administered with a high-salt diet (HS, 8.0% NaCl) for 8 weeks to induced hypertension. Renin-angiotensin system acting on reactive oxygen species in paraventricular nucleus induces sympathetic activation via AT1R/PKCgamma/Rac1 pathway in salt-induced hypertension. 2839785: [Hereditary resistance to salt-induced hypertension. What mechanisms?]. The demonstration of a similar pattern of response in the Dahl rats suggests that alpha 2 adrenoreceptor may be involved in the sensitivity or resistance to salt induced hypertension. 28409833: This pathway provides one of the mechanisms by which HS causes hypertension in Dahl SS rats. 28827472: We conclude that enhancement of intrarenal H2O2 with a 4.0% NaCl diet stimulates the mTORC1 pathway that is necessary for the full development of the salt-induced hypertension and kidney injury in the SS rat. Inhibition of Mammalian Target of Rapamycin Complex 1 Attenuates Salt-Induced Hypertension and Kidney Injury in Dahl Salt-Sensitive Rats. 28931751: To define the importance of Kir5.1 in blood pressure control under conditions of salt-induced hypertension, we generated a Kcnj16 knockout in Dahl salt-sensitive (SS) rats (SSKcnj16-/-). 29221166: High salt induced hypertension leads to cognitive defect. 29537860: With the SS- Rag1-/- rats utilized as a novel tool to explore the effects of lymphocyte deficiency, these results provide evidence that adaptive immune mechanisms contribute to the exacerbation of salt-induced hypertension and renal injury mediated by increased dietary protein intake. Rag1-null Dahl SS rats reveal that adaptive immune mechanisms exacerbate high protein-induced hypertension and renal injury. 29545262: This information paves the way for early prevention and treatments of salt-induced hypertension related to developmental problems in fetal origins. 29679484: Renal inflammation induced by immunity to HSP70 causes hypertension in laboratory animals, and administration of specific peptide sequences of HSP70 results in a protective anti-inflammatory response that prevents and corrects salt-induced hypertension. 29705701: Protective role of AgRP neuron's PDK1 against salt-induced hypertension. These results demonstrate a novel role of PDK1 in AgRP neurons to counteract the high salt diet-induced hypertension by preventing hyperactivation of PVN nesfatin-1 neurons. 29894319: Furthermore, knock out of Kir5.1 in Dahl salt-sensitive rat background revealed the crucial role of the Kir4.1/Kir5.1 channel in salt-induced hypertension. 30059752: However, the molecular mechanism of high-salt diet induced hypertension and the serious complications in cardiovascular system still remain unknown. CONCLUSION: Our study provided new insight about molecular mechanism of high-salt induced hypertension and heart and kidney damage. Differential expression gene (DEG) analysis and further functional annotation including Ingenuity Pathway Analysis (IPA) was performed to reveal the molecular mechanism of high-salt induced hypertension and organ injury. 30328008: These results suggest that the increased MAP and sympathetic activity in salt-induced hypertension can be suppressed by blockade of endogenous Ang-(1-7) in the PVN, through modulation of PICs and oxidative stress. This study was designed to determine whether inhibition of Ang-(1-7) in the hypothalamic paraventricular nucleus (PVN) attenuates sympathetic activity and elevates blood pressure by modulating pro-inflammatory cytokines (PICs) and oxidative stress in the PVN in salt-induced hypertension. 30354815: Role of DNA De Novo (De)Methylation in the Kidney in Salt-Induced Hypertension. Intrarenal administration of anti-DNA methyltransferase 3a/ten-eleven translocase 3 GapmeRs attenuated high salt-induced hypertension in SS rats. 30390036: Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity. Among the most promising approaches are dietary strategies for reducing the risk for salt-induced hypertension that do not depend on reducing salt consumption in the population. According to this theory, initiation of salt-induced hypertension usually involves abnormal vascular resistance responses to increased salt intake, not greater renal retention of a salt load in salt-sensitive subjects than in normal subjects. By shifting the focus from the historical theory to a contemporary final common pathway for the pathogenesis of salt sensitivity, research from Japan is building the scientific foundation for more effective approaches to the prevention and treatment of salt-induced hypertension. 3762307: Previously, altered aldosterone binding to corticoid receptor I was found in aortic smooth muscle cells cultured from Fischer 344 rats which are extremely resistant to steroid and salt induced hypertension. Rat models of genetic hypertension include spontaneous hypertension and resistance or sensitivity to mineralocorticoid and salt induced hypertension. 434173: Salt-induced hypertension in Dahl's genetically hypertensive rat has been attributed to humoral or renal factors. 4508561: Incidence of salt-induced hypertension in rats from different stocks. 6241934: The Fischer 344 rat strain represents a uniform population that is immune to salt induced hypertension and resistant to mineralocorticoid hypertension. 6280903: Feeding 8% NaCl diet for 5 weeks induced hypertension in young S rats but failed to alter renal or brain (Na+,K+)-ATPase activity. It appears unlikely that mutations in the structural locus for the renal (Na+,K+)-ATPase molecule are involved in the strain specific differences in susceptibility to salt-induced hypertension since the physical-chemical properties of the enzyme from the two strains were found to be similar. 7198908: Although originally developed for the study of salt-induced hypertension, special attention is given to the application of this animal model in behavior genetic research, stressing its inherent advantages and limitations. 8613201: However, phenotypic characteristics such as body weight, salt-induced hypertension, and mortality were significantly different in S(HSD) compared with S(Rapp). 862565: Pituitary R1 accumulation does, however, segregate with resistance to salt-induced hypertension in genetic experiments. 8747306: We examined the role of central GABAergic mechanisms in salt-induced hypertension and exaggerated responses to stress in borderline hypertensive rats (BHR), the first offspring of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Central GABAergic mechanisms are defective in salt-induced hypertension in borderline hypertensive rats. 8898010: We recently re-inbred the original colony of SBH-SBN rats, a model of salt-induced hypertension. 8977154: Cosegregation of the new region on chromosome 3 with salt-induced hypertension in female F2 progeny from stroke-prone spontaneously hypertensive and Wistar-Kyoto rats. 9353164: In this study, we examined the time course changes in the glomerulus associated with salt-induced hypertension using the inbred Dahl salt-sensitive rats. These findings indicate that salt-induced hypertension accelerates the age-dependent progression of glomerulosclerosis in Dahl salt-sensitive rats, and fibronectin may play a role in the pathogenesis, development, and progression of glomerulosclerosis associated with salt-induced hypertension. Progression of glomerulosclerosis, renal hypertrophy, and an increased expression of fibronectin in the renal cortex associated with aging and salt-induced hypertension in Dahl salt-sensitive rats. This age-dependent progression was further accelerated by the co-existence of salt-induced hypertension in the high salt diet group. 9389199: The results suggest that AT1a and AT1b receptors may be involved in the pathogenesis of salt-induced hypertension. 9488228: OBJECTIVE: To search for alterations of cytosolic pH and cell calcium handling in platelets and erythrocytes of Dahl rats susceptible and resistant to salt-induced hypertension. 9807020: , Liddle's syndrome, glucocorticoid-remediable hypertension, and apparent mineralocorticoid excess, has revived the interest in salt-induced hypertension, since the reported genetic defects decrease the ability of the kidneys to excrete sodium. 31894463: In conclusion, our results indicate that GBE prevents the symptoms of Al induced AD like pathophysiology by upregulating the HSPs levels and decreasing the aggregation load. Here, we have evaluated the possible effects of Ginkgo biloba (GBE) against aggregation of the Abeta through activation of heat shock proteins (HSPs) in the Aluminium (Al) induced AD based model. 31923036: Moreover, immunochemical and histopathological examination revealed marked protection with virgin coconut oil against aluminum-induced Alzheimer's disease-like pathology and cognitive deficit. 31958088: Human exposure to aluminum is linked to the etiology of Alzheimer's disease and recent research measured a high content of aluminum in brain tissue in familial Alzheimer's disease. 32201908: Among well-known environmental risk factors, prolonged exposure to several heavy metals, for example, aluminum, arsenic, cadmium, lead, and mercury; particulate air, and some pesticides as well as metal-containing nanoparticles have been participated to cause AD. 32473558: Synchrotron Fourier transform infrared microspectroscopy (sFTIRM) analysis of Al-induced Alzheimer's disease in rat brain cortical tissue. 32619464: ATR-IR and EPR spectroscopy for following the membrane restoration of isolated cortical synaptosomes in aluminium-induced Alzheimer's disease - Like rat model. Here we investigated the therapeutic potential of Lepedium sativum (LS) as a natural anti-inflammatory, antioxidant and as acetyl cholinesterase inhibitor in treating Al induced AD-like in rat model. 32900247: Aluminum (Al), a neurotoxic element, can induce Alzheimer's disease (AD) via triggering neuronal death. 32990282: RhoA/Rock2/Limk1/cofilin1 pathway is involved in attenuation of neuronal dendritic spine loss by paeonol in the frontal cortex of D-galactose and aluminum-induced Alzheimer's disease-like rat model.Alzheimer's disease (AD) has become the most prevalent neurodegenerative disorder. RhoA/Rock2/Limk1/cofilin1 pathway is involved in attenuation of neuronal dendritic spine loss by paeonol in the frontal cortex of D-galactose and aluminum-induced Alzheimer's disease-like rat model. 33022965: Aluminium (Al) is clearly neurotoxic and considerable evidence exists that Al may play a role in the aetiology or pathogenesis of Alzheimer's disease (AD). 33174148: Alteration in DNA methylation after aluminum exposure has been shown to contribute in pathogenesis of Alzheimer's disease (AD). 33464538: Aluminum demonstrates clear neurotoxicity and can cause Alzheimer's disease (AD)-like symptoms, including cognitive impairment. 34111442: Following CHIT1 treatment, we found that the protein and mRNA levels of HDAC3 and NF-kappaB were reduced, the expression level of IkappaBalpha increased, anti-inflammatory factors (Arg-1, IL-10, and CD206) were elevated while pro-inflammatory factors (TNF-a, iNOS, and IL-1beta) were decreased in D-gal/aluminum-induced AD rats. 34396567: It is not yet known whether aluminium can travel from the skin to brain to cause Alzheimer's disease. 34499332: Aluminum is a widespread environmental neurotoxicant that can induce Alzheimer's disease (AD)-like damage, such as neuronal injury and impairment of learning and memory. 34606775: Considering the suggested connection between aluminum exposure and Alzheimer's disease (AD) pathogenesis, there is a concern about the effect of nano-Al on cognitive function and brain health. 34706318: To explore the possible neuroprotective effect as well as mechanism of action of Vinpocetine either alone or in combination with EGCG, CoQ10, or VE & Se in ameliorating aluminum chloride-induced AD in rats. The influence of vinpocetine alone or in combination with Epigallocatechin-3-gallate, Coenzyme COQ10, Vitamin E and Selenium as a potential neuroprotective combination against aluminium-induced Alzheimer's disease in Wistar Albino Rats. 34771159: Attenuative Effects of Fluoxetine and Triticum aestivum against Aluminum-Induced Alzheimer's Disease in Rats: The Possible Consequences on Hepatotoxicity and Nephrotoxicity. 34982355: Necrostatin-1 Relieves Learning and Memory Deficits in a Zebrafish Model of Alzheimer's Disease Induced by Aluminum. 35313783: Aluminum (Al), a neurotoxic element, can induce Alzheimer's disease-like (AD-like) changes by triggering neuronal death. 35668264: The results conclude that BA administration modulated the expression of Wnt/beta-catenin pathway-related parameters, contributing to BA's role against Al-induced Alzheimer's disease. This study aimed to elucidate the role of the Wnt/beta-catenin pathway in BA protective activity against aluminum-induced Alzheimer's disease. 36306920: These results suggest that AS ameliorated Al-induced AD by affecting the expression of BACE1 and reducing the level of Abeta 1-42 , thereby exerting a neuroprotective effect. Combination of Alpinia Oxyphylla Fructus and Schisandra Chinensis Fructus ameliorates aluminum-induced Alzheimer's disease via reducing BACE1 expression. 36430429: In Vivo Preclinical Assessment of beta-Amyloid-Affine [ 11 C]C-PIB Accumulation in Aluminium-Induced Alzheimer's Disease-Resembling Hypercholesterinaemic Rat Model. The proposed in vivo Al-induced AD-resembling animal system seems to be adequate for the understanding of AD neuropathology and future drug testing and radiopharmaceutical development. 36462588: The potential ameliorative effect of bromelain compared to donepezil was evaluated in an aluminum chloride (AlCl3)-induced AD in rats. Ameliorative effects of bromelain on aluminum-induced Alzheimer's disease in rats through modulation of TXNIP pathway. 36516571: CONCLUSION: The combination of taurine and DFP is a potential candidate for the treatment of AD induced by Al exposure. 37077707: Garden Cress ( Lepidium sativum ) Seeds Ameliorated Aluminum-Induced Alzheimer Disease in Rats Through Antioxidant, Anti-Inflammatory, and Antiapoptotic Effects. 37631278: The aim of this study is to investigate the pathophysiological mechanisms underlying AD and explore the potential neuroprotective effects of cocoa, either alone or in combination with other nutraceuticals, in an animal model of aluminum-induced AD. These alterations contributed to the observed behavioral and histological changes in the AlCl 3 -induced AD model. 37801786: BACKGROUND: Studies have shown that aluminum (Al) is one of the environmental risk factors leading to Alzheimer's disease (AD), and Al exposure can cause elevated levels of BACE1mRNA, beta-secretase (BACE1), and amyloid beta (Abeta) in vivo and in vitro. 38057817: However, its effects on aluminum-induced AD model have not been studied much. A body of evidence suggest that oxidative stress and autophagy are involved in the pathogenesis of AD. 38070385: New bithiophene derivative attenuated Alzheimer's disease induced by aluminum in a rat model via antioxidant activity and restoration of neuronal and synaptic transmission. 22464639: DESIGN: Sixty female Sprague Dawley rats were divided into four groups n=15, (1) normal control group (con), (2) group underwent surgery to remove ovaries (ovx control group), (3) ovx group received aluminum chloride in a dose of 17 mg/kg daily for 2 months to induce AD (AD group), (4) AD group treated with alpha-chymotrypcin (alpha-ch) at dose (8.1 unit/rat/day) which is equivalent to the recommended human dose (alpha-ch-treated group) for three months. CONCLUSION: This study revealed that alpha-chymotrypcin significantly ameliorates the neuroinflammation characterizing Alzheimer's disease in ovariectomized rats due to it's proteolytic activity as well as it's anti-inflammatory effect. 23821590: Oral administration of aluminium chloride (AlCl3) in a dose of 17 mg/kg body weight (bw) daily for 45 days induced AD-like pathology in male rats with a significant increase in brain acetylcholinesterase (AchE) activity, transforming growth factor beta (TGF-beta), Fas and interleukin-6 (IL-6) levels. 25613582: Protective effect of selenium against aluminum chloride-induced Alzheimer's disease: behavioral and biochemical alterations in rats. 25630717: Neuroprotective effect of hesperidin on aluminium chloride induced Alzheimer's disease in Wistar rats. 25842984: The present study has been designed to explore the memory-enhancing effect of the tannoid principles of E. officinalis (EoT) at the biochemical, anatomical, behavioral, and molecular levels against aluminum chloride (AlCl3) induced Alzheimer's disease (AD) in rats. 26306462: Erratum to: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer's Disease in Wistar Rats. 26622218: 70 female albino rats were divided equally into 7 groups as follows: group 1: healthy control; group 2: Aluminium chloride induced Alzheimer disease; group 3: induced Alzheimer rats that received intravenous injection of MSCs; group 4: induced Alzheimer rats that received MSCs and HO inducer cobalt protoporphyrin; group 5: induced Alzheimer rats that received MSCs and HO inhibitor zinc protoporphyrin; group 6: induced Alzheimer rats that received HO inducer; group7: induced Alzheimer rats that received HO inhibitor. 26897372: AD was induced by aluminum chloride (17 mg/kg, p.o. for 6 weeks) and confirmed by Morris water maze and Y-maze behavioral tests. 28003750: Group I: normal control group treated with water; Group II: disease control treated with AlCl3 to induce the mimicking AD for 4 successive weeks (SW); Group III: normal control group treated with baicalein (5 mg/kg) for 2 SW followed by combination of baicalein and AlCl3 for 4 SW; Group IV: normal control group treated with baicalein (10 mg/kg) for 2 SW followed by combination of baicalein and AlCl3 for 4 SW; Group V: normal control group treated with rivastigmine (0.3 mg/kg) for 2 SW followed by combination of rivastigmine and AlCl3 for 4 SW. Baicalein improves behavioral dysfunction induced by Alzheimer's disease in rats. 28499970: Furthermore, anti-inflammation factors (Arginase 1, Arg-1, mannose receptor type C 1, MRC1/CD206) were increased and pro-inflammation factors (tumor necrosis factor alpha, TNFalpha, interleukin 1 beta, IL-1beta) were decreased in D-galactose/AlCl3-induced AD rats with chitinase1 treatment. We also detected that chitnase1 could weaken the deposition of Abeta oligomers in the brain of D-galactose/ AlCl3-induced AD rats. 28514831: The present study aimed to identify the potential neuroprotective of HPE on AlCl3-induced AD rats. Our results showed HPE improved cognitive function in AlCl3-induced AD rats, and attenuated AlCl3-induced increase in acetylcholinesterase activity and glutamic acid level as well as decreased in noradrenaline and dopamine level. Hypericum perforatum extract attenuates behavioral, biochemical, and neurochemical abnormalities in Aluminum chloride-induced Alzheimer's disease rats. Thus, HPE is conferred neuroprotection against AlCl3-induced AD like pathology. 28650335: These findings suggest that co-administration of AlCl3 and D-gal for one week could induce AD like symptoms and may be used to develop AD animal model. 28697918: In this study, the neuroprotective properties of a methanol extract of the leaves of Kigelia africana (KAE) and its flavonoid-rich fraction (FKAE) in aluminum chloride (AlCl3)-induced experimental AD was evaluated. Sausage tree (Kigelia africana) flavonoid extract is neuroprotective in AlCl3-induced experimental Alzheimer's disease. 28715867: Therapeutic impact of grape leaves polyphenols on certain biochemical and neurological markers in AlCl3-induced Alzheimer's disease. 29448848: Chronic treatment with morin-loaded micelles significantly increased the memory in AlCl3 induced Alzheimer's disease in Wistar rats. 29770796: In a D-galactose- and AlCl3-induced AD mouse model, administration of the FFDS composite solution significantly improved the learning and memory, as well as neuronal morphology, and decreased the serum levels of INF-gamma. 30010139: Our findings therefore show that VCO preserved the ultrastructural morphology of the hippocampus and cortex of the AlCl3-induced AD rat model, potentially providing protection against the neurodegeneration in AD of both cortical and hippocampal neurons. Moreover, VCO significantly increased the glutathione (GSH) level in both the hippocampus and cortex and significantly decreased the malondialdehyde (MDA) level in only the cortex of the AlCl3-induced AD rat model compared to an AlCl3-induced AD rat model with no VCO. 30537804: Furthermore, TM-10 exhibited a favorable dyskinesia recovery rate and response efficiency on an AlCl3-induced zebrafish AD model and a potent neuroprotective effect on Abeta1-40-induced zebrafish vascular injury. 30624431: Seeds of chia (Salvia hispanica L.) are highly rich in these nutrients, and thus, the present study investigated the effects of chia seeds on behavior and cognition in an aluminum-induced Alzheimer's disease model in rats. Detrimental effects of chia (Salvia hispanica L.) seeds on learning and memory in aluminum chloride-induced experimental Alzheimer's disease. 30802512: After molecular docking simulation, AlCl3-induced Alzheimer's disease zebrafish model was established. 31014012: The results clearly demonstrated for the first time that CA could alleviate d-gal/AlCl3 induced AD-like pathologies in rats via inhibition of hyperphosphorylated tau (P-tau) bio-synthetic proteins, anti-apoptosis and maintenance of cytoarchitecture. This study aimed to evaluate the effectiveness of CA in preventing d-galactose/aluminium chloride (d-gal/AlCl3) induced AD-like pathologies and the underlying mechanisms of action were further investigated for the first time. Results showed that co-administration of CA to d-gal/AlCl3 induced AD-like rat models significantly increased the levels of protein phosphatase 2 (PP2A) and decreased the levels of glycogen synthase kinase-3 beta (GSK-3beta). 31103976: Neuroprotective evaluation of Tribulus terrestris L. in aluminum chloride induced Alzheimer's disease. 31137621: Chenodeoxycholic Acid Ameliorates AlCl3-Induced Alzheimer's Disease Neurotoxicity and Cognitive Deterioration via Enhanced Insulin Signaling in Rats. 31148478: Both extracts significantly decreased the acetylcholinesterase activity and improved the histopathological changes in the cerebral cortex and cerebellum of rat model of aluminium chloride-induced Alzheimer disease. 31460853: This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl3)-induced Alzheimer's disease. Neuro-amelioration of cinnamaldehyde in aluminum-induced Alzheimer's disease rat model. 31553175: Lactoferrin Coupled Lower Generation PAMAM Dendrimers for Brain Targeted Delivery of Memantine in Aluminum-Chloride-Induced Alzheimer's Disease in Mice. The in vivo study in an AlCl3-induced Alzheimer's (AD) mice model showed a significant improvement in behavioral responses. The study reported improved brain bioavailability of MEM in AlCl3-induced Alzheimer's mice leading to improved memory, with the resultant mechanism behind in a descriptive manner. 31734542: Group II: received aluminum chloride to induce Alzheimer's disease. 31860774: Nootropic effect of neferine on aluminium chloride-induced Alzheimer's disease in experimental models.Alzheimer's disease (AD) is an age-associated neurodegenerative disease, which is developed by oxidative stress and acetylcholine contraction in the synaptic cleft of the neurons. Nootropic effect of neferine on aluminium chloride-induced Alzheimer's disease in experimental models. 32030557: The present study aimed to investigate the neuroprotective role of ethyl pyruvate against in vitro and in vivo model of aluminum chloride (AlCl 3 )-induced AD. Neuroprotective Effects of Ethyl Pyruvate against Aluminum Chloride-Induced Alzheimer's Disease in Rats via Inhibiting Toll-Like Receptor 4. Thus, ethyl pyruvate is effective against in vitro and in vivo models of AlCl 3 -induced AD. Neuroprotective Effects of Ethyl Pyruvate against Aluminum Chloride-Induced Alzheimer's Disease in Rats via Inhibiting Toll-Like Receptor 4.Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the formation of insoluble deposits of beta-amyloid (Abeta) plaques within the parenchyma of the brain. 32329360: Nutritional supplementation of GA preserve the morphological and physiological integrity of the hippocampus against environmental neurotoxins (AlCl 3 ) by mopping up free radicals associated with oxidative stress induced AD. This study aimed at investigating the neuroprotective effects of Gallic Acid (GA) against aluminum-chloride induced AD in adult Wistar rats. 32383521: Biotin, coenzyme Q10, and their combination ameliorate aluminium chloride-induced Alzheimer's disease via attenuating neuroinflammation and improving brain insulin signaling. 32932753: Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl 3 )-induced Alzheimer-like disease in rats using biochemical, histological, and ultrastructural approaches. 33327909: OBJECTIVE: Here the aim was to evaluate the antioxidant therapeutic effects of ellagic acid (EA) and EA-loaded nanoparticles (EA-NP) in an aluminum chloride-induced AD rat model. 33582452: Neuroprotective effect of Betalain against AlCl 3 -induced Alzheimer's disease in Sprague Dawley Rats via putative modulation of oxidative stress and nuclear factor kappa B (NF-kappaB) signaling pathway. The present investigation established that the betalain treatment ameliorated the AlCl 3 induced AD by modulating NF-kappaB pathway activation. AlCl 3 (100 mg/kg) was administrated orally to induce the AD in SD rats. Hence, this study was intended to investigate the possible protective effect of betalain against aluminum chloride (AlCl 3 ) induced AD on Sprague Dawley (SD) rats. 33587299: The objective of this study was to investigate the neuroprotective activity in an aluminum chloride (AlCl 3 )-induced AD in vivo model and phytochemical profile of the traditional Egyptian herb Mentha longifolia (Ml). 33971493: METHODS: Aluminum chloride (70 mg/kg, I.P for 5 weeks) was used to induce AD in rats that either normally fed or socially isolated and protein malnourished (SI&PM). Natural antioxidants enhance the power of physical and mental activities versus risk factors inducing progression of Alzheimer's disease in rats. 34070220: Additionally, histopathological analysis of hippocampus revealed the potential of CUR in decreasing the hallmarks in the AlCl 3 -induced AD. 34103557: An AD-like rat model was induced by aluminum chloride (AlCl 3 ; 50 mg/kg/day for six consecutive weeks; i.p), whereas a methanolic standardized P. harmala seed extract (187.5 mg/kg; p.o) was given to AD rats starting 2 weeks post AlCl 3 exposure. 34208063: A Leaf Extract of Harrisonia abyssinica Ameliorates Neurobehavioral, Histological and Biochemical Changes in the Hippocampus of Rats with Aluminum Chloride-Induced Alzheimer's Disease. 34354404: Neuroprotective effects of ononin against the aluminium chloride-induced Alzheimer's disease in rats. 34537230: Quercetin stimulates the non-amyloidogenic pathway via activation of ADAM10 and ADAM17 gene expression in aluminum chloride-induced Alzheimer's disease rat model. The present study aimed to evaluate the alpha-secretase stimulatory function of Q through activation of ADAM10 and ADAM17 gene expression in the aluminum chloride (AlCl3)-induced AD rat model. 34542066: Taurine and Camel Milk Modulate Neurobehavioral and Biochemical Changes in Aluminum Chloride-Induced Alzheimer's Disease in Rats. 34706318: To explore the possible neuroprotective effect as well as mechanism of action of Vinpocetine either alone or in combination with EGCG, CoQ10, or VE & Se in ameliorating aluminum chloride-induced AD in rats. The influence of vinpocetine alone or in combination with Epigallocatechin-3-gallate, Coenzyme COQ10, Vitamin E and Selenium as a potential neuroprotective combination against aluminium-induced Alzheimer's disease in Wistar Albino Rats. 34727278: The present research work is designed to investigate the neuroprotective effect of spermine in aluminium chloride (AlCl 3 ), and iron (Fe) induced AD-like symptoms in rats. 34954699: We also found that supplementation of B. coagulans JA845 alleviated amyloid-beta deposits and hyperphosphorylated tau in hippocampus of D-gal/AlCl3-induced AD model mice. 34971104: Effect of taurine and camel milk on amyloid beta peptide concentration and oxidative stress changes in aluminium chloride-induced Alzheimer's disease rats. 35236271: OBJECTIVES: The present study aimed to: (1) study the effect of MSCs with/without acitretin on the regulation of Adam10 gene expression in AlCl3-induced AD rat model, (2) validate the hypothesis that AD is a time-dependent progressive disease that spreads spontaneously even after the stopping of exposure to AlCl3. 35243060: Both Captopril and Perindopril protects against aluminium chloride induced amyloidogenesis and AD like pathology. Aluminium chloride induces AD like pathology in rats. Captopril is more effective than Perindopril against aluminium chloride induced amyloidogenesis and AD like pathology. 35453412: We evaluated the drug release profile and cytotoxicity of PGC and its effects on AD pathology through in vitro and in vivo studies and on cognitive function through an aluminum-chloride-induced AD rat model. 35507244: Correction to: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer's Disease in Wistar Rats. 35525893: Differential neuroprotective effect of curcuminoid formulations in aluminum chloride-induced Alzheimer's disease. 35596040: Hence, the present study aims to investigate the potential of chronic intranasal oxytocin in halting memory impairment & AD pathology in aluminum chloride-induced AD in female rats. 36015156: Neuroprotective Effects of Phytochemicals against Aluminum Chloride-Induced Alzheimer's Disease through ApoE4/LRP1, Wnt3/beta-Catenin/GSK3beta, and TLR4/NLRP3 Pathways with Physical and Mental Activities in a Rat Model. 36194986: Interestingly, treatment with p-CA alleviated all the above-mentioned neuropathological changes in the AlCl 3 -induced AD rat model. 36246933: Herein, we evaluated the protective effects of Lactobacillus casei ATCC 393 ( L. casei ATCC 393) and selenium nanoparticles-enriched L. casei ATCC 393 ( L. casei ATCC 393-SeNPs) against D-galactose/aluminum chloride-induced AD model mice. 36290710: The present study aims to evaluate the role of quercetin nanoemulsion (QCNE) in attenuating neuronal dysfunction in aluminum chloride (AlCl 3 )-induced experimental AD. 36312298: This work aimed to comprehend the role of naringin in the defense of the cerebellum against aluminum chloride (AlCl 3 )-induced AD in rats by investigating the behavioral, neurochemical, immunohistochemical, and molecular mechanisms that underpin its possible neuroprotective effects. Collectively, these findings suggested that naringin could contribute to the combat of oxidative and autophagic stress in the cerebellum of AlCl 3 -induced AD. 36385687: However, administration of leflunomide alone or with rivastigmine in AlCl 3 -induced AD rats restored most of the behavioral, biochemical, and histological parameters triggered by AlCl 3 in rats. In this study, for the first time, the potential prophylactic and therapeutic effects of leflunomide were investigated either alone or in combination with rivastigmine in aluminum chloride (AlCl 3 )-induced AD-like rats using behavioral, biochemical, and histological approaches. Our findings suggest that leflunomide can potentially restore most of the neuronal damage in the hippocampal tissues of AlCl 3 -induced AD rats. 36462588: The potential ameliorative effect of bromelain compared to donepezil was evaluated in an aluminum chloride (AlCl3)-induced AD in rats. Ameliorative effects of bromelain on aluminum-induced Alzheimer's disease in rats through modulation of TXNIP pathway. 36554305: Wistar rats were given an i.p. injection of 60 mg/kg D-gal and 10 mg/kg AlCl 3 to induce AD and three doses of 1 mg/kg, 5 mg/kg or 10 mg/kg 5-MTHF by oral gavage. 36678510: Characterization of Orange Peel Extract and Its Potential Protective Effect against Aluminum Chloride-Induced Alzheimer's Disease. 36761834: In the Alcl3-induced AD model in rats, disease progression was confirmed by Y-maze, the preliminary histopathology evaluation showed significantly higher efficacy of the prepared liposomes (CLCAE and CLAA) compared to the Centella asiatica extract (CAE) and they were found to have equivalent efficacy to the standard drug (rivastigmine tartrate). 37035098: Insights into the function of the retina by electroretinogram (ERG) and the changes thought to have occurred in the molecular structure of the retina and brain using Fourier transform infrared spectroscopy (FTIR) as a result of AD progression induced by AlCl 3 in rats were done. 37242536: Dapagliflozin Ameliorates Cognitive Impairment in Aluminum-Chloride-Induced Alzheimer's Disease via Modulation of AMPK/mTOR, Oxidative Stress and Glucose Metabolism. The current data demonstrate that dapagliflozin represents a possible approach to combat AlCl 3 -induced AD in rats through inhibiting oxidative stress, enhancing glucose metabolism and activating AMPK signaling. This study aims to examine the possible mechanisms of the neuroprotective effects of dapagliflozin against aluminum chloride (AlCl 3 )-induced AD. 37323056: Aluminum chloride was used to induce AD in rats, and afterward, a group of AD-induced rats received a single dose of Ad-MSCs (2 * 10 6 cell, I.V per rat). 37368609: Jambolan fruit extract and choline were investigated for Aluminum tri chloride (AlCl 3 )-induced Alzheimer's disease in rats. 37380861: The rats were administered 300 mg/kg of oral AlCl 3 to induce AD and were then treated with oral PB at a dosage of 50 mg/kg, BEE at a dosage of 50 mg/kg, and rivastigmine at a dosage of 1 mg/kg as a standard drug for 21 days. Therefore, its activity was evaluated against an aluminum chloride (AlCl 3 )-induced AD rat model, and a berberine-enriched extract (BEE) was used to determine if its activity is equivalent to pure berberine (PB). 37454825: AD was induced by AlCl 3 (50mg/kg) for 6 weeks. 37505462: The mice model of Alzheimer's disease (AD) induced by aluminum chloride (AlCl3) combined with D-galactose (D-gal) was established to comprehend the mechanism behind PAF's anti-AD activity from both behavioural and pathological perspectives. 37631278: The aim of this study is to investigate the pathophysiological mechanisms underlying AD and explore the potential neuroprotective effects of cocoa, either alone or in combination with other nutraceuticals, in an animal model of aluminum-induced AD. These alterations contributed to the observed behavioral and histological changes in the AlCl 3 -induced AD model. 37851769: In conclusion, the present study provided primary evidence for using a combination of B. papyrifera and S. aromaticum to treat cognitive dysfunction associated with AlCl3 Induced AD by improving the AChE levels and modulating oxidative stress in the brain. Neuroprotective effects of a combination of Boswellia papyrifera and Syzygium aromaticum on AlCl3 induced Alzheimer's disease in male albino rat. Therefore, the current study explored the possible mitigating effects of a combination of Boswellia papyrifera and Syzygium aromaticum against aluminum chloride (AlCl3) induced AD. 38052316: These findings suggest that coconut oil shows protective effects against cognitive and non-cognitive impairment, AD pathology markers, oxidative stress, synaptic transmission, and cholinergic function in a D-GAL/AlCl 3 -induced AD rat model. Thus, we investigated the effects of coconut oil on spatial cognitive ability and non-cognitive functions in a rat model of AD induced by G-galactose (D-GAL) and aluminum chloride (AlCl 3 ), and examined the changes in synaptic transmission, cholinergic activity, neurotrophic factors and oxidative stress in this process. 38074017: Enhanced Neuroprotective Synergy of Atorvastatin and Magnesium L-Threonate in a Rat Model of Alzheimer's Disease Induced by Aluminum Chloride. 38090736: The in-vivo studies were performed using aluminum chloride-induced experimental AD in rats. 38141332: This study was aimed at investigating the neuroprotective potential of a co-extract obtained by supercritical fluid extraction (SFE) of turmeric powder and dried coconut shreds against aluminium chloride (AlCl 3 )-induced Alzheimer's disease (AD) in male Wistar rats. Summarily, the results demonstrated intranasal delivery of CurCOO to show better efficacy than Cur and COO in preventing neurodegeneration associated with AlCl 3 induced Alzheimer's disease. A supercritical fluid co-extract of turmeric powder and dried coconut shreds shows neuroprotection against AlCl 3 -induced Alzheimer's disease in rats through nose to brain delivery. 38181932: Protective effect of a hydromethanolic extract from Fraxinus excelsior L. bark against a rat model of aluminum chloride-induced Alzheimer's disease: Relevance to its anti-inflammatory and antioxidant effects. 38448794: 3-Acetyl coumarin alleviate neuroinflammatory responses and oxidative stress in aluminum chloride-induced Alzheimer's disease rat model. 31852393: Methods and Results: To test the therapeutic potential of targeting Sirt3 expression we developed new transgenic mice with global Sirt3 overexpression (Sirt3OX) which protects from endothelial dysfunction, vascular oxidative stress and hypertrophy, attenuates angiotensin II- and DOCA-salt induced hypertension. 31865500: Previously we showed that elevated angiotensin II (Ang II) and angiotensin II type I receptor (AT1R) expression levels can increase neuroinflammation leading to hypertension. 31994810: Electrolyte and transporter responses to angiotensin II induced hypertension in female and male rats and mice.AIM: Sexual dimorphisms are evident along the nephron: Females (F) exhibit higher ratios of renal distal to proximal Na + transporters' abundance, greater lithium clearance (C Li ) more rapid natriuresis in response to saline infusion and lower plasma [K + ] vs. males (M). Electrolyte and transporter responses to angiotensin II induced hypertension in female and male rats and mice. 32027625: Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury.BACKGROUND Hypertension could induce many serious diseases, including damage to vascular endothelial cells. 32065054: Ang II induced hypertension caused significant change in the expression of 1380 T cell genes in WT, but only 51 in miR-214 -/- . 32447546: Angiotensin II exerts a cardinal role in the pathogenesis of hypertension and renal injury via action of angiotensin II type 1 (AT 1 ) receptors. 32500132: METHODS: In the present study, we examined the role of phosphoinositide-3 kinase gamma (PI3Kgamma) signaling in the recruitment of inflammatory cells and bone marrow-derived fibroblasts into the kidney and development of renal injury and fibrosis in an experimental model of hypertension induced by angiotensin II. 32502636: Hypertension induced by Ang II infusion rather than abdominal aorta constriction was mitigated by IMD. 32609312: MUMT-/- mice were also not protected from hypertension or end-organ damage induced by Ang II infusion or deoxycorticosterone acetate (DOCA)-salt treatment. METHODS AND RESULTS: We purified serum IgG from mice exposed to vehicle or angiotensin (Ang) II to induce hypertension and adoptively transferred these to wild type (WT) recipient mice receiving a subpressor dose of Ang II. 32683300: Angiotensin II (Ang II) as an important pathogenic factor, has been implicated in the pathogenesis of hypertension and associated renal injury, and inhibition of Ang II can reduce renal inflammation and exert renal protective effects. 32707188: Alamandine attenuated hypertension in mice induced by Ang II. 32709884: Therefore, we investigated the relationship between miR-124-3p and hypertension in Human Umbilical Vein Endothelial Cells (HUVECs) induced by angiotensin II (AngII). 32755037: Here, we aimed to demonstrate that HNK co-treatment attenuated the vasoconstriction, hypertension and H 2 S reduction caused by angiotensin II (AngII), a well-established inducer of hypertension. 32755412: This study was conducted to determine whether testosterone-CYP1B1 generated metabolite 6beta-hydroxytestosterone locally in the brain promotes the effect of systemic angiotensin II to produce hypertension in male mice. 32863942: As we have shown, hypertension induced by a prolonged Angiotensin II infusion is associated with increased permeability of the blood-brain barrier (BBB), chronic activation of microglia and myelin loss. 33017187: Evolving evidence shows that immune cell-derived EVs can modulate the IS in a paracrine fashion and therefore may mediate the effects of inflammation in the pathogenesis of HTN. Therefore, we aimed to understand if specific subtypes of leukocyte/immune-cell-derived EVs are altered in essential HTN using an in-vivo model of Angiotensin-II induced HTN. 33121424: Herein, its cardiovascular effects were evaluated on hypertension induced by angiotensin II (AngII) and NG-nitro-Larginine methyl ester (L-NAME), as well as baroreflex sensitivity (BRS). 33145641: Editing of the myosin phosphatase regulatory subunit suppresses angiotensin II induced hypertension via sensitization to nitric oxide mediated vasodilation. 33303682: Finally, TNFR1 silencing in the PVN inhibits elevated blood pressure induced by AngII. In the PVN, TNFR1 expression and plasma membrane localization are upregulated during hypertension induced by angiotensin II (AngII). 33657051: Angiotensin II caused hypertrophy and hypertension in the strain lacking AT1 receptor in the heart and conduit vessels, but not in the strain without AT1 receptors in resistance vessels. 33666098: Surviving obese-normotensive males displayed less left ventricular dilation and pulmonary congestion compared with chow-fed males after MI; hypertension reversed left ventricular dilation because of high-fat/fructose diet and promoted significant pulmonary congestion compared with chow-fed controls. Methods and Results Male and female C57BL/6J mice were provided standard chow or high-fat/fructose diet for 8 weeks and then infused with angiotensin II for 2 weeks to induce hypertension. 33707301: Therapeutic assessment of combination therapy with a neprilysin inhibitor and angiotensin type 1 receptor antagonist on angiotensin II-induced atherosclerosis, abdominal aortic aneurysms, and hypertension . 33708117: The actions of Ang II are mediated through binding to the Ang-II type 1 receptor (AT1R) which leads to increased blood pressure, fluid retention, and aldosterone secretion. 33745438: CONCLUSION: Hormonal imbalance between ANG II, VP, and SNS may induce hypertension and impaired water-electrolyte balance in cardiovascular diseases. 33815099: The elevated blood pressure caused by AngII was significantly attenuated by GTS-21. 33847027: The ARB (O) group received olmesartan (2 mg/kg/day) orally, and the ARB (T) group received two drops of olmesartan (5 mM) topically on the cornea; concurrently, both groups were treated with Ang-II (1 mg/kg/day, sc) to induce hypertension. 33890822: Loss of Soluble (Pro)renin Receptor Attenuates Angiotensin-II Induced Hypertension and Renal Injury. 33912493: This study examines the effect of aqueous extract of asafoetida on the cardiovascular parameters in acute hypertension induced by angiotensin II (AngII). Antihypertensive Effects of Standardized Asafoetida: Effect on Hypertension Induced by Angiotensin II. Los and extract were injected 30 min before hypertension induced by AngII. Conclusion: Our results indicated that aqueous extract of asafoetida ameliorated cardiovascular responses in acute hypertension induced by AngII. 34003901: Conclusions: Arterial hypertension, induced by continuous angiotensin-II infusion, results in reduced retinal blood flow, increased vascular resistance, and decrease in area of intravascular blood flow within retinal arterioles and venules. 34090935: Angiotensin II (Ang II) induces hypertension by activating angiotensin II receptor subtype 1 (AT1R). 34091009: The present study aims to understand the underlying vasoprotective effects of nutritional NO 2 - and NO 3 - co-therapy in mice with angiotensin-II (AT-II)-induced arterial hypertension. High-dose AT-II (1 mg/kg/d, 1w, s. c.) was used to induce arterial hypertension in male C57BL/6 mice. Arterial hypertension is one of the major health risk factors leading to coronary artery disease, stroke or peripheral artery disease. 34345384: This study evaluated the effect of the saffron petal on hypertension induced by angiotensin II (AII) and NG-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor). Effects of hydroalcoholic extract of saffron petal on blood pressure and heart rate in hypertension induced by angiotensin II and L-NAME in anesthetized rats. 34393778: This study aims to assess the effects of QDG treatment on Angiotensin II- (AngII-) induced hypertension and vascular function and explore its underlying mechanisms both in vitro and in vivo . 34400298: In this study, we aimed to examine whether RvD1 ameliorates cardiac remodeling and hypertension triggered by angiotensin II. 34428599: The aim was to elucidate the role of CX43 in hypertension induced by AngII. 34515350: In the present study, we examined the role of phosphatase and tensin homolog (PTEN), a major regulator of PI3K signaling, in the pathogenesis of renal inflammation and fibrosis in an experimental model of hypertension induced by AngII. Hypertension is a major cause of chronic kidney disease. 34669013: Moreover, grip strength and cardiac response to angiotensin II-induced high blood pressure were comparable with healthy control mice. 34970343: In summary, bazedoxifene could improve the protective role against hypertension induced by AngII. 34999197: Angiotensin II infusion results in both hypertension and increased AMPA GluA1 signaling in hypothalamic paraventricular nucleus of male but not female mice. 35058564: Herein, we reveal that PDE4D (one of PDE4 isoforms) expression is upregulated in the aortas of experimental hypertension induced by angiotensin II (Ang II). 35126818: Recently, we reported that Hdac8 inhibition alleviates isoproterenol-induced and angiotensin II-induced cardiac hypertrophy or hypertension in mice. 35177224: In vascular tissue, protease-activated receptor 1 activation leads to enhanced vascular reactivity to angiotensin II to cause hypertension. 35222039: In conclusion, these results indicate that blockade of VCAM-1 exerts a protective effect against Ang II-induced arterial hypertension and dysfunction by regulating monocytes adhesion and infiltration into the endothelium and represents a novel therapeutic approach for hypertension. 35276443: Inhibition of endothelial Nox2 activation by LMH001 protects mice from angiotensin II-induced vascular oxidative stress, hypertension and aortic aneurysm. The therapeutic potential of LMH001 was tested using a mouse model (C57BL/6J, 7-month-old) of AngII infusion (0.8 mg/kg/d, 14 days)-induced vascular oxidative stress, hypertension and aortic aneurysm. 35553515: In the present study, we investigated whether TLR4 activation contributes to renal ER stress and inflammation in Angiotensin-II (Ang-II) induced hypertension and whether TLR4 deficiency protects the kidney by suppressing ER stress. 35554138: Angiotensin II (Ang II) is a key regulator of blood pressure, and increased levels of Ang II are known to induce hypertension. 35555055: Moreover, reducing sPRR release into plasma decreased blood pressure and attenuated angiotensin II (AngII) induced hypertension. 35556318: Our study suggests that obesity significantly increases tissue inflammation following SARS-CoV-2 infection, with the heart at particular risk of higher SARS-CoV-2 infection; in contrast, acute hypertension induced by Ang-II infusion does not significantly alter SARS-CoV-2 infection or COVID-19 disease course. 35556428: The goal of this study is to identify the key mechanisms actuating the intrarenal accumulation of Ang II during hypertension induced by Ang II infusion. 35677431: The results showed that Nehesperidin acts as an antioxidant and could significantly inhibit angiotensin II induced hypertension and vascular remodeling in vitro and in vivo . In this study, angiotensin II was used to induce hypertension in mice (490 ng/kg/min, 14 days). 35730579: Cardiac hypertrophy resulting from hypertension induced by angiotensin II was reduced in these haploinsufficient PKN2 mice relative to wild-type littermates, with suppression of cardiomyocyte hypertrophy and cardiac fibrosis. 36070120: Angiotensin II (Ang II, 1.5 mg.kg -1 .12 h -1 , 2 weeks) was intraperitoneally injected to induce hypertension in mice. 36093879: Elevated angiotensin II (Ang II) produced by the renin-angiotensin-aldosterone system can lead to hypertension and its complications. 36206386: In males, AngII induced hypertension, and this resulted in an increase in the density of the astrocyte marker glial fibrillary acidic protein (GFAP) in the subgranular hilus and a decrease in the density of the microglial marker ionized calcium binding adapter molecule (Iba-1) in the CA1 region. 36290749: A Polyphenol-Rich Extract from Muscadine Grapes Prevents Hypertension-Induced Diastolic Dysfunction and Oxidative Stress. Thus, MGES may serve as a medical food to protect the heart from hypertension-induced diastolic dysfunction caused in part by excessive reactive oxygen species production. Male Sprague Dawley rats were treated for four weeks with drinking water, angiotensin II (Ang II) to induce hypertension, MGES, or both Ang II and MGES. 36406706: We aimed to evaluate the effects of angiotensin-II induced hypertension and deficiency of testosterone combined regarding the resistance coronaries found intramurally. 36422742: Herein, we aimed to elucidate the effects of Ang-(1-9) on endothelial apoptosis and the underlying molecular mechanism in angiotensin II (Ang II) induced hypertension. 36424917: Male and female Srf Itga8 mice exhibit vascular contractile incompetence, and angiotensin II causes elevated blood pressure in wild type, but not Srf Itga8 , male mice. 36629913: Whilst previous studies showed that inhibition of Gal-3 effectively ameliorates angiotensin II (Ang II)-induced atherosclerosis or hypertension, it remains unclear whether Ang II regulates Gal-3 expression and actions in vascular endothelium. 36931497: Effect of bempedoic acid on angiotensin-II induced hypertension and vascular tissue remodelling in renal hypertensive rats through AMPK multiple signalling pathways modulation. 37301198: Translationally, targeting endothelial FAM3D by adeno-associated virus or intraperitoneal injection of FAM3D-neutralizing antibodies markedly ameliorates AngII- or deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 37302617: In our previous studies, we observed that induction of hypertension with angiotensin II (Ang II) combined with simvastatin administration results in a high mortality rate or the appearance of signs of kidney failure in heme oxygenase-1 knockout (HO-1 KO) mice. 37308550: Infused juice concentrate of Japanese plum Prunus mume attenuates inflammatory vascular remodeling in a mouse model of hypertension induced by angiotensin II. Development of hypertension induced by Ang II was also prevented by bainiku-ekisu. 37449045: We found that chronic angiotensin II infusion induced hypertension and upregulated cardiac Erbb4-IR , which was associated with cardiac dysfunction, including a decrease in left ventricle ejection fraction (LVEF) and LV fractional shortening (LVFS) and an increase in LV mass. 37850974: In order to explore the function and mechanism of CTRP3 in hypertensive fibrosis, Angiotensin II (Ang II) was used to induce hypertension in primary neonatal rat cardiac fibroblasts in vitro. 38169582: In the present study, we investigated the protection and mechanisms of irisin against hypertension and vascular remodeling induced by angiotensin II (Ang II). 38383894: Mitochondrial fission inhibition protects against hypertension induced by angiotensin II. 38388918: Angiotensin II in combination with L-NAME-induced hypertension was used to elicit CMH. 38482554: Chronic angiotensin II (AngII) infusion is an experimental model that induces hypertension in rodents. 38597112: In line with this, tamoxifen-inducible, SMC-specific GPRC5C knockout mice showed reduced Ang II-induced arterial hypertension, and acute inactivation of GPRC5C was able to ameliorate established arterial hypertension. 11882589: In Wistar rats, hypercholesterolemia was established by high-cholesterol diet from Day -14 (HC rats), and hypertension was induced by a suprarenal aortic constriction at Day 0 (HT rats). 11884292: We have tested the effects of chronic hypertension induced by suprarenal aortic constriction on the development of atherosclerosis in apolipoprotein E-deficient (Apoe-/-) mice. 123285: Significantly augmented non-uniform flow changes, however, were produced by ganglion stimulation during hypertension caused by aortic constriction or by methoxamine. 1381284: OBJECTIVE: The aim was to investigate nucleic acid composition and rates of protein synthesis in cardiopulmonary tissues and skeletal muscle in response to hypertension induced by aortic constriction. Protein synthesis in pulmonary, cardiac, and skeletal muscle in acute hypertension induced by aortic constriction in the rat. 16777933: During hypertension induced by aortic constriction (mean arterial pressure, MAP = 140 +/- 6 mmHg) coronary vascular resistance (CVR), reactive hyperaemia (ratio of peak in hyperaemic flow to control flow and ratio of repayment to debt) and the decrease in CVR during the peak in hyperaemic flow were comparable to those during normotension. During hypertension induced by noradrenaline (MAP = 144 +/- 6 mmHg) CVR was 16% lower (P < 0.05), reactive hyperaemia was reduced by 14-25% (P < 0.05) and the decrease in CVR during the peak in hyperaemic flow was lower than the values of these parameters during normotension. 1735578: We studied the correlation of changes in gain sensitivity of the baroreceptors and the development of resetting of the baroreceptors 2 and 6 days after the onset of hypertension produced by subdiaphragmatic aortic constriction in rats. 18490734: Hypertension-induced cardiovascular hypertrophy and fibrosis are critical in the development of heart failure. We wondered whether vaccine bacillus Calmette-Guerin (BCG), which activated TLR4 to elicit immune responses, modulated the pressure overload-stimulated cardiovascular hypertrophy and cardiac fibrosis in the murine models of abdominal aortic constriction (AAC)-induced hypertension. 19424280: Seven-week-old male Wistar rats with hypertension induced by suprarenal aortic constriction (AC) were treated orally with 2 mg kg(-1) day(-1) of BAY 41-2272 for 14 days. 26735444: Male Wistar rats were subjected to 30 days aortic constriction to induce hypertension. 2782429: Rapid or acute resetting of the aortic baroreceptors was studied in anesthetized rats during the onset and maintenance of hypertension produced by subdiaphragmatic aortic constriction for up to 6 h. 28348018: AC produced hypertension in the right kidney (above AC) and near normal blood pressure in the left kidney (below AC), with both kidneys exposed to the same levels of glucose, circulating hormones, and neural influences. Hypertension was induced by aorta constriction (AC) between the renal arteries in 6-month-old male Goto-Kakizaki (GK) type 2 diabetic and control Wistar rats. 30431106: Aortic constriction induces hypertension and cardiac hypertrophy via (pro)renin receptor activation and the PLC-beta3 signaling pathway. Hypertension and cardiac hypertrophy were induced by partial abdominal aortic ligation in Sprague-Dawley rats. 34866402: HTN was induced by aorta constriction (AC) between the renal arteries. 3803614: The aortic caliber was studied in freely moving rats during the development of sustained hypertension produced by subdiaphragmatic aortic constriction. 6599686: By means of a chronically implanted electrolytic transducer, changes in the aortic calibre were studied in conscious rats during the onset of acute hypertension produced by subdiaphragmatic aortic constriction. 875466: Seven rats were subjected to acute hypertension produced by subdiaphragmatic aortic constriction after recording the control measurements. 8781754: UNLABELLED: In male Sprague Dawley rats with left ventricular hypertrophy (LVH) and hypertension induced by aortic constriction (AC) and subsequent myocardial infarction (MI) by occlusion of the left coronary artery the effects of ACE inhibition with ramipril (RA 1 mg/kg/day via the drinking water during 6 weeks) on survival as well as cardiac function and metabolism were investigated. 8967372: Thus we conclude that the remodeling processes of cells and matrices of the splenic and ileal arteries are dependent on the local blood pressure in aorta constriction-induced hypertension, and the indicial analysis is a useful approach in the description of the relationship between the blood pressure and the arterial remodeling processes. 9076550: The dihydropyridine calcium channel blocking agent amlodipine is an effective anti-hypertensive agent and its use (in doses of 5 or 10 mg/day/kg body weight) was investigated in male Wistar rats with hypertension induced by aortic constriction. 11464462: Many hypotheses have been proposed to explain the mechanism whereby one of the isoforms of apoE, apoE4, could cause AD. 16270302: We propose that the overproduction of apoE4 in neurons may suppress normal IK channel activities and thus be responsible for the late-developed neuronal damages related to the pathogenesis of AD. 20531185: ApoE4 carriers account for 65-80% of all Alzheimer's disease cases, highlighting the importance of apoE4 in Alzheimer's disease pathogenesis. 21266538: Our observations suggest that apoE4 strongly stabilizes Abeta oligomers, the pathological species responsible for Alzheimer's disease. 24386905: Emerging data indicate that levels of soluble oAbeta are increased with APOE4, providing a potential mechanism of APOE4-induced AD risk. Soluble apoE/Abeta complex: mechanism and therapeutic target for APOE4-induced AD risk. 25871773: ApoE4 confers a gain of toxic function, a loss of neuroprotective function or a combination of both in AD pathogenesis. 27788676: Developing therapeutic strategies based on AGFs may be particularly efficacious for APOE4-induced AD risk. 28550258: APOE?4 is central to the events that lead to AD in cognitively normal older adults, likely through a quantitative role in the disruption of A? clearance. 29133888: Given the observations of neuronal hyperactivity in prodromal AD, we propose that this APOE4-driven hyperactivity may be a causative factor driving increased risk of AD among APOE4 carriers. 29311783: These findings directly link the APOE4 genotype to endosomal-lysosomal dysregulation in an in vivo, AD pathology-free setting, which may play a causative role in the increased incidence of AD among APOE4 carriers. 31331998: In activating neuronal signaling, the three ApoE variants exhibit a differential potency of ApoE4>ApoE3>ApoE2, which mirrors their relative effects on AD risk, suggesting that differential signaling by ApoE variants may contribute to AD pathogenesis. 9894876: These findings suggest a relationship between APOE4 and a DLST locus in the pathogenesis of AD in very elderly subjects. 10218725: We and others demonstrated that long-term treatment with L-NAME causes hypertension and cardiovascular lesions (perivascular fibrosis and medial thickening), especially at microvascular levels. 10329876: RESULTS: Except for an increase on the day after insertion of the pump indomethacin had no significant effect on the hypertension induced by N G -nitro- L -arginine methyl ester. 10357253: Adrenomedullin attenuated the L-NAME induced hypertension and pup mortality. On the other hand, adrenomedullin administration in both pregnant rats in early gestation (5-11 days of pregnancy) and in non-pregnant rats did not show any significant effect on L-NAME-induced hypertension. 10523324: The observed effects of antioxidant drugs on ACE activation do not appear to involve the hypertension induced by L-NAME. 10523358: In conclusion, L-NAME-induced hypertension is accompanied by an increase in insulin resistance in rats. 10580377: We conclude that remodelling of the aorta in L-NAME-treated rats was rather associated with NO deficiency than L-NAME-induced hypertension. The aim of the present study was to determine whether decreased nitric oxide (NO) synthase production or rather N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension was responsible for metabolic and structural remodelling of the rat aorta during four-week L-NAME treatment. 10625224: Thus, NO deficiency rather than hemodynamic changes appears to be crucially involved in collagenous protein and fibrotic tissue changes of the left ventricle in hypertension induced by L-NAME. 10653835: BACKGROUND: Chronic N(G)-nitro-L-arginine methyl ester (L-NAME), which inhibits nitric oxide synthesis, causes hypertension and would therefore be expected to induce robust cardiac hypertrophy. Chronic N(G)-nitro-L-arginine methyl ester-induced hypertension : novel molecular adaptation to systolic load in absence of hypertrophy. Rats with L-NAME-induced hypertension had levels of systolic wall stress similar to those of rats with aortic stenosis (85+/-19 versus 92+/-16 kdyne/cm). CONCLUSIONS: When the expected compensatory hypertrophic response is suppressed during L-NAME-induced hypertension, severe chronic pressure overload is associated with a successful adaptation to maintain systolic performance; this adaptation depends on both LV remodeling and enhanced contractility in response to calcium. In the present study, we used L-NAME-induced hypertension to test the hypothesis that adaptation to pressure overload occurs even when hypertrophy is suppressed. 10707824: Our findings indicate that there is no change in energy utilization by the (Na,K)-ATPase during L-NAME induced hypertension in the heart. Functional alterations of cardiac (Na,K)-ATPase in L-NAME induced hypertension. 10707825: Cardiac membrane proteins and phospholipids in L-NAME induced hypertension. 10719388: To evaluate the role of renal nerve activity in L-NAME-induced hypertension, we compared the blood pressure response in four groups (N = 10 each) of male Wistar-Hannover rats weighing 200 to 250 g: 1) sham-operated vehicle-treated, 2) sham-operated L-NAME-treated, 3) denervated vehicle-treated, and 4) denervated L-NAME-treated rats. Much of the hypertension caused by chronic NO synthesis inhibition is thus dependent on renal nerve activity. 10720643: Chronic administration of the nitric oxide (NO) synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) to rats causes hypertension and morphological abnormalities in the heart, consisting mainly of ventricular hypertrophy and foci of necrosis and fibrosis. Our results show that chronic treatment of rats with a low dose of L-NAME for prolonged periods (up to 6 months) causes arterial hypertension accompanied by significant reductions in heart weight, left ventricular weight indexes, and cardiomyocyte size. 10722795: In this work, we examined the effect of spontaneous and captopril-induced recovery on LV hypertrophy and protein composition in rats with developed L -NAME-induced hypertension. We conclude that spontaneous regression of L -NAME-induced hypertension is not associated with regression of LV hypertrophy. 10805405: Captopril completely prevented L-NAME-induced hypertension and LV hypertrophy development. 10873511: Constriction of resistance arteries determines l-NAME-induced hypertension in a conscious hamster model. 10904020: Molecular plasticity of vascular wall during N(G)-nitro-L-arginine methyl ester-induced hypertension: modulation of proinflammatory signals. 10954000: METHODS: Hypertension, in Sprague-Dawley rats was induced by the oral administration of the arginine analog N(omega)-nitro-L-arginine methyl ester (L-NAME) in their drinking tap water for a period of 4 weeks. Enhanced expression of Gi proteins in non-hypertrophic hearts from rats with hypertension-induced by L-NAME treatment. 10978388: We examined the role of an increased haemodynamic burden on the development of renal damage combining unilateral nephrectomy (UNx)- and L-NAME-induced hypertension in F(1) and ACI rats. Blood pressure and the susceptibility to renal damage after unilateral nephrectomy and L-NAME-induced hypertension in rats. 10988276: L-NAME-induced HTN was reversible with L-arginine in the LFCC diet group; however, HTN was not corrected by L-arginine supplementation in the HFS diet group. We have recently demonstrated that long-term consumption of a high-fat, refined-carbohydrate (HFS) diet induces hypertension (HTN) in normal rats compared with a low-fat, complex-carbohydrate (LFCC) diet. 11078375: In this study, we determined plasma ET-1 levels and the expression of ET-1 mRNA in tissues of rats rendered hypertensive using distinct mechanisms: deoxycorticosterone acetate (DOCA)-salt hypertension: N(G)-nitro-L-arginine-methyl ester- (L-NAME) induced hypertension; and spontaneously hypertensive rats (SHR-SP). Whether ET-1 could be a primary cause of hypertension or a secondary factor associated with hypertension, however, remains unknown. Recent studies revealed important roles for endothelin-1 (ET-1) in the pathogenesis of hypertension. 11132603: The observed effects of the type 1 receptor antagonist was independent of the L-NAME-induced arterial hypertension. 11152369: L-NAME-induced hypertension was prevented by LY117018. 11213029: The existence of prior lesions in the AV3V area significantly attenuated the development of L-NAME-induced hypertension. 11566930: Cardiovascular neural reflexes in L-NAME-induced hypertension in mice. 11669463: Cortical infarct volume was not significantly modified by either 2-week or 6-week L-NAME treatment, despite induced hypertension, whereas it was significantly higher in SHRs than in normotensive rats. 11743626: These data show that L-NAME-induced hypertension causes alterations in body fluid distribution and in renal mass. 11875190: In this congenic strain, named ACI.FHH-D1Mit34/Rat156 or ACI.FHH-Rf1B, we challenged the renal hemodynamic function of these animals by studying the effects of unilateral nephrectomy (UNX) alone, or combined with N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 11893585: We previously reported that long-term inhibition of NO synthesis by administration of N(G)-nitro-L-arginine methyl ester (L-NAME) causes hypertension and activates vascular tissue angiotensin-converting enzyme (ACE) activity. 11904468: The following four models of HT were developed in rats: one kidney-one clip HT (1K-1C HT), two kidney-one clip HT (2K-1C HT), deoxycorticosterone acetate (DOCA) induced HT (15 mg/kg, 2 times/week, sc) and N-nitro L-arginine methyl ester (L-NAME) induced HT (50 mg/kg/day, 10 weeks, ip). 12149566: BACKGROUND: The rat model of chronic intoxication by N(G) -nitro-L-arginine methyl ester (L-NAME) induces severe systemic arterial hypertension and progressive ischemic lesions in the central nervous system and kidneys. 12175820: However, the responses were similar in L-NAME-induced hypertension (deltaMAP = 30 +/- 2 mm Hg). (iii) The vasodilator response to Ach was increased in rats with Ang II-induced hypertension (deltaMAP = 53 +/- 1 mm Hg) and in SHR (deltaMAP = 67 +/- 3 mm Hg). The principal findings of this study were: (i) The hypotensive response to RuNO was 150% higher in acutely (phenylephrine and Ang II) and chronically (SHR) hypertensive rats than in normotensive rats, except in the case of L-NAME-induced hypertension (deltaMAP = 10 +/- 1.4 mm Hg). 12176110: These findings indicate that L-NAME-induced hypertension in the rat relies on the marked impairment of the endothelial vasodilator function, with an ensuing contribution by a decreased production of prostacyclin by the endothelial cells. 12198334: N(G)-nitro-L-arginine methyl ester-induced hypertension and natriuretic peptide gene expression: inhibition by angiotensin II type 1 receptor antagonism. Results suggest that >l-NAME-induced hypertension and the associated activation of ventricular ANP and BNP gene expression are, at least in part, mediated by angiotensin II, whereas the resistance vessel hypertrophy following nitric oxide synthase inhibition is angiotensin II independent. 12218334: Chronic inhibition of nitric oxide (NO) synthesis by oral administration of N(G)-nitro-L-arginine methyl ester (L-NAME) causes hypertension and produces arteriosclerosis in rats. 12219175: The animal models of acquired hypertension studied were deoxycorticosterone-salt (DOC-salt), subtotal nephrectomy-salt (SN-salt), and Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertension during pregnancy in rats. 12377873: CONCLUSIONS: These results indicate that the association of hypertension and DM mimics the alterations induced by L-NAME in rats, which suggests a role for NO in the pathophysiology of hypertensive-diabetic cardiomyopathy. 12424422: The aim of this study was to investigate oxidant-antioxidant systems of renal tissue in rats with hypertension induced by L-NAME. Renal antioxidant status in rats with hypertension induced by N sup omega nitro-L-arginine methyl ester. 12495554: Oral administration of GSE significantly reduced systolic, mean and diastolic arterial pressure in Wistar rats with desoxycorticosterone acetate-salt and N(G)-nitro-L-arginine methyl ester (L-NAME) induced experimental hypertension. 12500028: Ouabain changes arterial blood pressure and vascular reactivity to phenylephrine in L-NAME-induced hypertension. The aim of this work was to determine whether ouabain can alter pressor responses to phenylephrine in rats with Nomega-nitro-l-arginine methyl ester (L-NAME)-induced hypertension. 12714875: Chronic inhibition of nitric oxide synthase induces hypertension and cardiomyocyte mitochondrial and myocardial collagen remodelling in the absence of hypertrophy. OBJECTIVES: To evaluate the morphometric and ultrastructural alterations of the heart produced by long-term inhibition of nitric oxide (NO) synthase with N(omega)-nitro-l-arginine methyl ester (l-NAME) and to examine whether the changes are caused by l-NAME-induced hypertension or a lack of NO. 14508194: Exogenous H2S effectively prevented the development of hypertension induced by l-NAME. METHODS: Hypertension in Wistar rats was induced by the oral administration of the l-arginine analog, NG-nitro-l-arginine methyl ester (l-NAME) in their drinking water for a period of 6 weeks. 15076158: CONCLUSION: Cerebral arterioles undergo hypertrophy and remodeling in WKY with L-NAME-induced hypertension. 15097241: OBJECTIVE: To test the hypothesis that the AT2 receptor affords protection from left ventricular hypertrophy and fibrosis in chronic hypertension induced by N-nitro-L-arginine methyl ester (L-NAME). 15106810: CONCLUSIONS: These results suggest the implication of AT1 receptors in enhanced expression of Gi alpha proteins and increased blood pressure in L-NAME-induced hypertension. 15257179: CONCLUSION: Our results provide evidence that Provinols partially prevents L-NAME-induced hypertension, cardiovascular remodeling and vascular dysfunction via the increase of NO-synthase activity and prevention of oxidative stress. Red wine polyphenols prevent cardiovascular alterations in L-NAME-induced hypertension. 15289382: BACKGROUND: Chronic inhibition of nitric oxide (NO) synthesis by N(omega)-nitro-L-arginine methyl ester (L-NAME) induces hypertension associated with remodeling of the arterial wall. 15605112: A greater RhoA expression and an enhanced RhoA activity have been observed in aortas of hypertensive rats, such as genetic spontaneously hypertensive rats and N(omega)-nitro-L-arginine methyl ester-induced hypertension. 15925750: CONCLUSIONS: We conclude that L-NAME-induced hypertension is associated with an upregulation of antioxidant SOD, GPX, and GR activities. RESULTS: Rats with L-NAME-induced hypertension showed increased copper-zinc (Cu-Zn) SOD activity in the renal cortex and medulla and the left and right ventricles, which was reduced by tempol administration. 15948896: L-arginine fails to protect against myocardial remodelling in L-NAME-induced hypertension. 15989079: We studied the involvement of both NO metabolism and oxidative stress in L-NAME-induced hypertension, and how AT1 receptor antagonism may interact. 16060136: Treadmill running exercise was prolonged for 4 weeks (60 min.day(-1), 5 days/week, 20 m.min(-1), no incline), and hypertension was induced by L-NAME given orally to rats for 4 weeks (25 mg.kg(-1).day(-1) in drinking water). 16060400: The aim of the study was to investigate the participation of autonomic nervous system on L-NAME-induced hypertension and also illuminate its effects on hepatic microcirculation in rats. 16111891: These observations highlight the importance of the local ACE particularly in organs regulating hypertension (aorta and heart) during development of L-NAME-induced hypertension. Investigation of local ACE activity and structural alterations during development of L-NAME-induced hypertension. 16156512: The aim of this study was to evaluate the production of superoxide anions as well as their role in the induction and/or maintenance of high blood pressure in rats with N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 16316323: METHODS: Differences in renal susceptibility between ACI, Rf-1A, and Rf-4 single congenics and Rf-1A+4 double congenics were assessed using four different treatments: control (two-kidney), two-kidney with l-arginine analogue N-nitro-l-arginine methyl ester (L-NAME)-induced hypertension, unilateral nephrectomy, and unilateral nephrectomy + L-NAME. 16392774: We concluded that the direct anti-inflammatory and antioxidative effects of calcium channel blockades in the aorta of rats with L-NAME-induced hypertension were not likely to have been mediated by the blood pressure-lowering action of these agents, but instead these beneficial effects appear to have been mediated by an augmentation of eNOS expression and by the inhibition of the expression of ACE. 16448880: CONCLUSIONS: The study showed that L-NAME-induced hypertension has differential effects on endothelial connexins, which respond variously to carvedilol and atenolol. 16541022: Differences in renal susceptibility between ACI (August x Copenhagen Irish) controls, Rf-1A and Rf-3 single congenics, and Rf-1A+3 double congenic rats were assessed using four different treatments: two-kidney control (2K), 2K plus N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (2K+L-NAME), unilateral nephrectomy (UNX), and UNX plus L-NAME-induced hypertension (UNX+L-NAME). 16633081: L-NAME + BAY cotreatment abolished the L-NAME-induced hypertension (112 +/- 5.1 mm Hg; P < 0.01). 16671958: These experiments indicate that L-NAME-induced hypertension is not relying only on ANS. 16691532: The rat model of hypertension induced by prolonged treatment with Nomega-nitro-L-arginine methyl ester (L-NAME) has been extensively used. Macrophage populations and cardiac sympathetic denervation during L-NAME-induced hypertension in rats. 16710099: CONCLUSIONS: L-NAME treatment leads to hypertension, proteinuria and renal fibrosis. METHODS: 36 Sprague-Dawley rats were divided into a control group and an experimental group, in which hypertension was induced by oral administration of L-NAME (100 mg/kg/day). 16710350: In conclusion, both captopril and spironolactone prevented L-NAME-induced hypertension and the decline of the antioxidant potential of the kidney tissue. Both NO itself and S-nitrosothiols may contribute to the preventive effect of spironolactone against development of L-NAME-induced hypertension. 16761190: Since chronic inhibition of nitric oxide (NO) synthase with N(omega)-nitro-L-arginine methyl ester (L-NAME) induces systemic hypertension associated with cardiovascular inflammation and remodeling, we examined the potential role of aldosterone in this process using eplerenone, a selective aldosterone receptor antagonist. 16832158: Oral administration of L-NAME for 2 weeks induced serious hypertension, and the HbNO concentration was reduced to 37.6% of the level in controls. 16915305: Run training prevented the arterial hypertension induced by L-NAME treatment (LN-SD: 135+/-2 and 141+/-2 mm Hg for both doses of L-NAME) compared to LN-SD groups (154+/-1 and 175+/-2 mm Hg, for 2 and 10 mg of L-NAME, respectively). 17218445: Chronic blockade of nitric oxide leads to hypertension that is sustained throughout the period of the blockade in baroreceptor-intact animals. The lack of change in renal sympathetic nerve activity during the L-NAME-induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits. 17353120: The herbal medicines Saireito and Boiogito improve the hypertension of pre-eclamptic rats induced by Nomega-Nitro-L-arginine methyl ester. 17460373: Developmental activity of the renin-angiotensin system during the \critical period\ modulates later L-NAME-induced hypertension and renal injury. Administration of L-NAME at age 18 weeks caused severe hypertension and renal injury. 17664861: In the present study, we examined the involvement of tissue inhibitor of metalloproteinase-3 (Timp-3) in N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension and accompanying vascular remodeling in mice. 17824806: Spontaneous, L-arginine-induced and spironolactone-induced regression of protein remodeling of the left ventricle in L-NAME-induced hypertension. N(G)-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension is associated with protein remodeling of the left ventricle. 17824810: The reactive growth of the heart and aorta seems to be controlled by different mechanisms in L-NAME-induced hypertension. Spironolactone differently influences remodeling of the left ventricle and aorta in L-NAME-induced hypertension. The aim of the present study was to determine whether the treatment with spironolactone can prevent hypertension, reduction of tissue nitric oxide synthase activity and left ventricular (LV) and aortic remodeling in N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 17898042: Substitution of chromosome 20 from the BN to the FHH attenuated the development of l-NAME-induced hypertension, normalized plasma renin activity, and decreased plasma creatinine in male rats. Male and female rats of each of the parental and consomic strains were maintained for 2 wk on high-salt (8.0% NaCl) chow with N(G)-nitro-l-arginine methyl ester (l-NAME) in the drinking water (12.5 mg/l) to induce hypertension and renal disease. 17924312: Carvacrol was observed to exhibit hypotension and to inhibit N((omega))-nitro- L-arginine methyl ester ( L-NAME)-induced hypertension. 18391099: These data demonstrate that collecting duct-derived endothelin-1 is important in the following: (1) chronic N(G)-nitro-l-arginine methyl ester-induced hypertension; (2) full expression of pressure-dependent changes in sodium excretion; and (3) control of inner medullary NOS1 and NOS3 activity. 18419778: AIM: We investigated, whether the substrate for nitric oxide (NO) formation -L-arginine - and the aldosterone receptor antagonist - spironolactone - are able to reverse alterations of the left ventricle (LV) and aorta in N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 18496584: We have confirmed a strain-dependent difference in susceptibility to L-NAME-induced hypertension between BN and Fischer rats. 18633192: Regression of L-NAME-induced hypertension: the role of nitric oxide and endothelium-derived constricting factor. N(G)-Nitro-L-arginine-methyl ester (L-NAME)-induced hypertension is a well established model of experimental hypertension. 18753302: Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 +/- 8.9 vs. L-NAME 6.0 +/- 3.1 arbitrary units). 18923385: Chronic inhibition of nitric oxide synthase by N(omega)-nitro- L-arginine methyl ester (L-NAME) causes progressive renal injury with systemic hypertension and interstitial macrophage infiltration. 18935914: L-NAME caused systemic hypertension, decrease in plasma nitrate/nitrite, increases in blood urea nitrogen and creatinine, impairment of glomerular dynamics. 1908734: Comparison of NA responsiveness during vasopressin and L-NMMA/L-NAME-induced hypertension shows that increasing the blood pressure may modify LPS-induced hyporeactivity, but cannot account for the complete restoration of responses to NA by L-NMMA and L-NAME. 19100733: However, in L-NAME-induced hypertension the enhanced vasorelaxation to anandamide in the mesenteric vasculature was due to increased sensory nerve-mediated activity. Pre-treatment with capsaicin prevented the enhancement of vasorelaxation by anandamide in mesenteric arterial beds from rats with L-NAME-induced hypertension. 19116642: Inhibition of the nitric oxide pathway by N(omega)-nitro-l-arginine methyl ester (l-NAME) is well known to produce hypertension and proteinuria, but the mechanisms are less straightforward. 19151535: Chronic administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) caused systemic arterial hypertension, endothelial injury, and renal dysfunction. 19633445: DESIGN: We investigated whether melatonin was able to prevent left ventricular hypertrophy (LVH) and fibrosis associated with N(G)-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension. CONCLUSION: Melatonin prevented the development of left ventricular fibrosis and the increase in oxidative load in rats with L-NAME-induced hypertension. 19889865: Therefore, the present study was undertaken in conscious rats in which hypertension was induced by treatment with l-NAME over the course of either 2 or 14 days. The role played by the sympathetic drive in the development of N(G)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension is not firmly established. In conclusion, the evaluation of the sympathetic drive in conscious rats demonstrated that the arterial hypertension induced by l-NAME treatment over the course of 2 and 14 days does not show sympathetic overactivity. 20002674: Chronic inhibition of nitric-oxide synthase induces hypertension and erectile dysfunction in the rat that is not reversed by sildenafil. STUDY TYPE: Aetiology (case control) Level of Evidence 3b OBJECTIVE To evaluate the effect of N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (HT) on erectile function in the rat and determine if the phosphodiesterase (PDE)-5 inhibitor, sildenafil, can reverse the effects of nitric oxide (NO) deficiency, as HT is a risk factor for erectile dysfunction (ED) and the NO synthase (NOS) inhibitor L-NAME induces NO-deficient HT. 20041987: Chronic L-NAME treatment induced hypertension, elevated the oxidative load and inhibited NOS activity. To elucidate the possible role of the nitric oxide (NO) pathway in the hemodynamic actions of melatonin, the effects of this indolamine on vascular function during hypertension induced by the NO-synthase (NOS) inhibitor, N(omega)-nitro-L-arginine-methyl ester (L-NAME) were investigated. Melatonin interactions with blood pressure and vascular function during L-NAME-induced hypertension. 20154263: In conclusion, we have identified the NK gene complex as an important determinant in the genetically determined sensitivity to develop l-NAME-induced hypertension in mice. 20305675: Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension: effect of sildenafil. 20823711: RESULTS: The continuous light and L-NAME treatment led to hypertension, left ventricular hypertrophy (LVH) and fibrosis. 20823712: RESULTS: L-NAME caused hypertension, reduced NO-signalling and arterial diameter and increased oxidative load and EDCF-signalling. We investigated whether melatonin can accelerate the recovery from N(G)-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension after the cessation of L-NAME administration. 20845411: ADMA and L-NAME induced hypertension (PAS 167 +/- 16 and 168 +/- 10 versus 100 +/- 4 mmHg, p < 0.01, respectively). 21350197: CONCLUSIONS: These results suggest that endothelial cPLA2alpha may play a principal role in L-NAME-induced hypertension and may be a target molecule for maintaining endothelial function under NO inhibition. 21448566: Antioxidant and vascular protective effects of curcumin and tetrahydrocurcumin in rats with L-NAME-induced hypertension. Inhibition of nitric oxide synthesis with N ( omega )-nitro-L-arginine methyl ester (L-NAME) induces marked hypertension and oxidative stress. 21971659: Effects of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor, in L-NAME-induced hypertension in rats. 22072109: The aim of this study was to investigate the effect of THC on hemodynamic status, aortic elasticity and oxidative stress in rats with N-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 22115075: We therefore conclude that even though pressor response was unaffected, reversal of cardiac autonomic responses and decline in oxidative stress following sympathectomy in L-NAME-treated rats reflects a significant role for sympathetic innervation in acute L-NAME-induced hypertension. 22210049: Moreover, CYP1B1 contributes to the development and/or maintenance of hypertension produced by Ang II-, deoxycorticosterone (DOCA)-salt-, and N(omega)-nitro-L-arginine methyl ester-induced hypertension and in spontaneously hypertensive rats. The pathophysiological changes, including cardiovascular hypertrophy, increased vascular reactivity, endothelial and renal dysfunction, injury and inflammation associated with Ang II- and/or DOCA-salt induced hypertension in rats, and Ang II-induced hypertension in mice are minimized by inhibition of CYP1B1 activity with 2,4,3',5'-tetramethoxystilbene or by Cyp1b1 gene disruption in mice. 22215717: We investigated whether compound 21 alone or in combination with angiotensin II type 1 receptor blockade by olmesartan medoxomil could prevent PWV increase and aortic remodeling in N(omega)-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension. Direct angiotensin II type 2 receptor stimulation in Nomega-nitro-L-arginine-methyl ester-induced hypertension: the effect on pulse wave velocity and aortic remodeling. 22467300: Systolic blood pressures did not differ between wild-type (WT) and Alox15(-/-) mice between 8-12 wk of age, but Alox15(-/-) mice exhibited resistance toward both N(G)-nitro-L-arginine-methyl ester (L-NAME)- and deoxycorticosterone acetate (DOCA)/high-salt-induced hypertension. Injection of WT PM, a primary source of Alox15 protein, into Alox15(-/-) mice abolished their resistance toward L-NAME-induced hypertension. On the other hand, WT mice acquired resistance to L-NAME-induced hypertension after depletion of macrophages by clodronate injection. 22626924: (Loranthaceae) in Nomega-nitro-L-arginine methyl ester induced hypertension and renal dysfunction. AIM OF THE STUDY: The present study was designed to evaluate the antihypertensive activity of the methanolic extract of Viscum articulatum (MVA) against N(omega)-nitro-L-arginine methyl ester (L-NAME) induced hypertension in rats. 22923949: N(G)- nitro- l- arginine methyl- ester (L- NAME) is L- arginine analogue, which by binding to Nitric Oxide Synthase (NOS) may induce hypertension partly due to increase in tissues oxidative stress. 22994444: DISCUSSION AND CONCLUSION: L-NAME induced hypertension in rats was reduced by treatment with LS. OBJECTIVE: To evaluate antihypertensive and cardioprotective effects of the Lagenaria siceraria fruit powder in N(G)-nitro-L-arginine methyl ester (L-NAME) induced hypertension in rats. 23053479: Chronic delivery of angiotensin II (Ang II, 400 ng/kg/min) or N(omega)-nitro-L-arginine-methyl-ester (L-NAME, 0.1 g/L) was used for a 2-week period to induce hypertension. Arterial hypertension is a major risk factor that can lead to complication of peripheral vascular disease due, in part, to endothelial dysfunction. 23788129: Propolis reduces oxidative stress in l-NAME-induced hypertension rats. 24092817: Plasminogen activator inhibitor-1 antagonist TM5441 attenuates Nomega-nitro-L-arginine methyl ester-induced hypertension and vascular senescence. 24163073: The PPARgamma antagonist treatment also prevented L-NAME-induced hypertension in thioglycollate-injected Alox15(-/-) mice, indicating a PPARgamma-mediated effect in macrophage elicitation and the resultant hypertension. WT mice treated with 50 MUg/kg daily dose of GW9662 for 12 days became resistant to L-NAME-induced hypertension. These results indicate a regulatory role for macrophage-localized PPARgamma in L-NAME-induced experimental hypertension. Targeted disruption of the Alox15 gene makes mice resistant to angiotensin II-, DOCA/salt-, and N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced experimental hypertension. 24164360: Because of a recent report of aldehyde dehydrogenase 2 (ALDH2)-catalyzed glyceryl trinitrate (GTN) vasorelaxation by denitration of GTN to 1,2-glyceryl dinitrate (1,2-GDN) and nitrite, we therefore investigated a catalytic activity of ALDH2 for nitrite reduction and subsequent effect on N(omega)-nitro-l-arginine methyl ester (l-NAME)-induced hypertension in normoxic rat. 24726875: We investigated the effects of upregulating heme-oxygenase (HO) on myocardial histo-pathological lesions, proinflammatory cytokines/chemokines, oxidative mediators and important markers of heart failure such as osteopontin and osteoprotergerin in N(omega)-nitro-l-arginine methyl ester (L-NAME)-induced hypertension. Heme oxygenase suppresses markers of heart failure and ameliorates cardiomyopathy in L-NAME-induced hypertension. These data suggest a cardio-protective role of the HO system against L-NAME-induced hypertension that could be explored in the design of novel strategies against cardiomyopathy. 24772821: The effect of an aqueous Mentha cordifolia (MC) extract on the haemodynamic status, vascular remodeling, function, and oxidative status in NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension was investigated. Vascular and antioxidant effects of an aqueous Mentha cordifolia extract in experimental N(G)-nitro-L-arginine methyl ester-induced hypertension. 25194632: In rats with L-NAME induced hypertension there was a significant reduction of the blood pressure after two weeks treatment. 25294342: Involvement of inducible nitric oxide synthase and dimethyl arginine dimethylaminohydrolase in Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 25395680: Maternal CIT therapy prevented L-NAME-induced programmed hypertension, which was associated with a decreased asymmetric dimethylarginine (ADMA) concentration and an increased L-arginine-to-ADMA ratio in the kidney, increased urinary cGMP levels, and decreased renal protein levels of type 3 sodium hydrogen exchanger (NHE3). L-NAME exposure during pregnancy induces hypertension in the 12-wk-old offspring. We examined whether maternal CIT supplementation can prevent L-NAME-induced programmed hypertension. Nitric oxide (NO) deficiency induced by the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAME) resulted in hypertension. Maternal citrulline supplementation prevents prenatal N(G)-nitro-L-arginine-methyl ester (L-NAME)-induced programmed hypertension in rats. 25498996: Heme Oxygenase Improves Renal Function by Potentiating Podocyte-Associated Proteins in Nomega-Nitro-l-Arginine-Methyl Ester (l-NAME)-Induced Hypertension. 25517031: L-NAME exposure induced hypertension in the 12-week-old offspring, which CIT therapy prevented. We examined whether maternal CIT supplementation can prevent N(G)-nitro-L-arginine-methyl ester (L-NAME, NO synthase inhibitor)-induced programmed hypertension and examined their effects on the renal transcriptome in male offspring using next generation RNA sequencing (RNA-Seq) technology. 25623850: SIGNIFICANCE: These findings indicate that NO induced-hypertension is associated with up-regulation of NADPH oxidase, oxidative stress production and overexpression of key inflammatory mediators. Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension. Nitric oxide (NO) inhibition with N(w)-nitro-L-arginine methyl ester (L-NAME) has previously been reported to produce hypertension, increased expression of Angiotensin II (Ang II) and renal dysfunction. The current study was designed to test the hypothesis that AT1R activation promotes renal NAD(P)H oxidase up-regulation, oxidative stress and cytokine production during L-NAME induced-hypertension. KEY FINDINGS: After two weeks, L-NAME induced high blood pressure, renal overexpression of AT1R, NAD(P)H oxidase sub-units gp91, p22 and p47, increased levels of oxidative stress, interleukin-6 (IL-6) and interleukin-17 (IL-17). 25761067: We investigated the involvement of cyclooxygenase-2 (COX-2) and the renin-angiotensin system in N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. Early co-expression of cyclooxygenase-2 and renin in the rat kidney cortex contributes to the development of N(G)-nitro-L-arginine methyl ester induced hypertension. These findings indicate that renal COX-2 expression increased in parallel with renin expression, renal PGI2 synthesis, and plasma Ang II in L-NAME-induced hypertension. 25872005: Chronic inhibition of nitric oxide synthase by N(omega)-nitro-L-arginine methyl ester (L-NAME) causes progressive renal injury and systemic hypertension. 26068063: Cardiac-specific overexpression of metallothionein attenuates myocardial remodeling and contractile dysfunction in l-NAME-induced experimental hypertension: Role of autophagy regulation. Our results revealed that l-NAME treatment (14 days) led to hypertension and myocardial anomalies evidenced by interstitial fibrosis, cardiomyocyte hypertrophy, increased LV end systolic and diastolic diameters (LVESD and LVEDD) along with suppressed fractional shortening. l-NAME compromised cardiomyocyte contractile and intracellular Ca(2+) properties manifested as depressed peak shortening, maximal velocity of shortening/relengthening, electrically-stimulated rise in intracellular Ca(2+), elevated baseline and peak intracellular Ca(2+). This study was designed to examine the effect of cardiac-specific overexpression of metallothionein, a cysteine-rich antioxidant, on myocardial contractile and intracellular Ca(2+) anomalies in N(G)-nitro-l-arginine methyl ester (l-NAME)-induced experimental hypertension and the mechanism involved with a focus on autophagy. 26187312: In conclusion, besides to its efficacy in reducing the elevated SBP, amelioration of vascular function, modulation of arterial and renal eNOS expressions as well as reduction of the plasma levels of oxidative and inflammatory biomarkers are possible supportive mechanisms mediating the favorable implications of Barnidipine in L-NAME-induced hypertension model. 26644935: Comparative study of cardio protective effect of aliskiren, telmisartan, and torsemide was carried out on l-nitro arginine methyl ester (l-NAME) induced hypertension in rats. Effect of aliskiren, telmisartan and torsemide on cardiac dysfunction in l-nitro arginine methyl ester (l-NAME) induced hypertension in rats. 26701333: Hypertension was induced by L-NAME which was given to rats orally over 6 weeks (25 mg/kg/day in drinking water). The present study suggests that Mg supplementation has the potential to prevent VEP changes in the L-NAME-induced hypertension model. 26938552: This study examined the effect of Carthamus tinctorius (CT) extract plus captopril treatment on blood pressure, vascular function, nitric oxide (NO) bioavailability, oxidative stress and renin-angiotensin system (RAS) in N(omega)-Nitro-l-arginine methyl ester (l-NAME)-induced hypertension. 28195070: The aim of this study was to show, whether ivabradine, the blocker of If-channel in sinoatrial node, is able to modify the behaviour of rats in L-nitro-arginine methyl ester (L-NAME)-induced hypertension and to compare the effect of ivabradine with captopril and melatonin. In conclusion, ivabradine, besides its potentially protective hemodynamic actions, does not seem to exert any disturbing effects on behaviour in L-NAME-induced hypertension in rats, while some of its effects were similar to captopril or melatonin. Effect of ivabradine, captopril and melatonin on the behaviour of rats in L-nitro-arginine methyl ester-induced hypertension. Chronic administration of L-NAME induced hypertension without a change in HR. 28257997: Hypertension was induced by N-nitro-l-arginine methyl ester (25 mg/kg/day in drinking water), and exercise training comprised swimming 1 h/day, 5 days/week, for 6 weeks. This study aimed to assess the effect of the HO/CO system on the vascular tone in exercise-trained rats with hypertension induced by chronic NO synthase (NOS) inhibition. 28455132: These data suggest that GME had a protective effect against l-NAME-induced hypertension and cardiovascular remodeling via suppressing p47phox NADPH oxidase subunit and iNOS protein expression resulting in enhancing NO bioavailability. Male Sprague-Dawley rats were given 40mg/kg/day of l-NAME in drinking water to induce hypertension, and were simultaneously treated with GME at a dose of 200mg/kg/day. Nomega-Nitro-l-arginine methyl ester (l-NAME)-induced hypertension and cardiovascular remodeling are associated with oxidative stress and inflammation. GME prevented the development of hypertension and cardiovascular remodeling induced by l-NAME with reduced oxidative stress and inflammation. 28567090: SUBJECTS AND METHODS: We used three different hypertensive animal models: (i) Wistar-Kyoto rats (n=8) and spontaneously hypertensive rats (SHR; n=8), (ii) mice infused with saline or angiotensin II to induce hypertension, via osmotic mini-pump for 2 weeks, and (iii) mice that were allowed to drink L-NG-nitro-L-arginine methyl ester (L-NAME) to induce hypertension. 28640644: CONCLUSION: Our data indicate a protective role of nebivolol on the high blood pressure and vascular remodeling induced by l-NAME. PURPOSE: To investigate the effect and mechanism of nebivolol on aortic remodeling in N-nitro-l-arginine methyl ester (l-NAME)-induced hypertension. 28757582: In addition, the lactacystin-model was compared with NG-nitro-l-arginine-methyl ester (L-NAME)- and continuous light-induced hypertension. LV weight and the cross-sectional area of the aorta were increased only in L-NAME-induced hypertension. 28760945: Compared with normotensive APPPS1 mice, those with l-NAME-induced hypertension had greater amyloid burden (P<0.05), increased cortical amyloid angiopathy (P<0.01), decreased regional microvascular density (P<0.05), and deficient long-term spatial reference memory (P<0.001). We previously reported that hypertension aggravates the Alzheimer-like pathology in APPPS1 mice (amyloid precursor protein/presenilin-1, mouse model of Alzheimer disease) with angiotensin II-induced hypertension, in relation with hypertension and nitric oxide deficiency. These results suggest that impaired nitric oxide bioavailability exacerbates the pathophysiology of Alzheimer disease, essentially impacting amyloid load and cognitive impairment, independently of l-NAME-induced hypertension. 29851183: Therefore, it is for the first time found that GSP exerts protective effect against Nomega-Nitro-L-arginine methyl ester-induced hypertension in pregnant mice, which provided a theoretical basis for potential application in the clinic. 29920624: The present study investigated the protective effect of the polyphenol-rich fraction (PRF) of the methanol-extract of Azadirachta indica against Nomega-Nitro-L-Arginine Methyl Ester (L-NAME) induced hypertension and cardiorenal dysfunction in rats. Antihypertensive Effect of Polyphenol-Rich Fraction of Azadirachta indica on Nomega-Nitro-L-Arginine Methyl Ester-Induced Hypertension and Cardiorenal Dysfunction. 30021237: Correction: Antihypertensive Effect of Polyphenol-Rich Fraction of Azadirachta indica on Nomega-Nitro-L-Arginine Methyl Ester-Induced Hypertension and Cardiorenal Dysfunction. 30217638: METHODS: Starting from the 10th day of gestation, pregnant rats were given L-NAME for 10 days to produce hypertension and proteinuria. 30336562: Renoprotective Effects of Antroquinonol in Rats with Nomega-Nitro-l-Arginine Methyl Ester-Induced Hypertension. 30668387: PURPOSE: This study investigated whether aqueous extract of Moringa oleifera leaves (MOE) could alleviate Nomega-nitro-L-arginine-methyl ester (L-NAME)-induced high blood pressure via modulation of vascular function and antioxidant properties. 30696976: We investigated the influence of in vivo 5-HT by characterizing the implicated serotonergic receptors on the mesenteric sympathetic outflow in rats with N-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. Our findings suggest that L-NAME-induced hypertension modifies the 5-HT modulation of the rat mesenteric sympathetic drive: prejunctional 5-HT4 receptors are involved in the serotonergic sympathoinhibitory effect. 30819180: This study aimed at investigating the antihypertensive effects of the hydroethanol extract of S. serratuloides (HESS) in N-Nitro-L-arginine methyl ester (L-NAME) induced hypertension in rats. 31196042: CONCLUSION: Polysaccharide from XJEK exerts protective effects against Ang II-induced injury in HUVECs and L-NAME-induced hypertension in mice and the underlying mechanism may be attributed to improving endothelial dysfunction, OS and the inflammation status in mice. The protective effects of polysaccharide extract from Xin-Ji-Er-Kang formula on Ang II-induced HUVECs injury, L-NAME-induced hypertension and cardiovascular remodeling in mice. 31325242: Hypertension was induced by L-NAME (20 mg/kg per day, by gavage, for seven consecutive days) in male Wistar rats. 31326379: Furthermore, in rats with hypertension induced by N?-nitro-L-arginine methyl ester (L-NAME), oral administration of morin (50 mg/kg/day) decreased systolic blood pressure. Thus, we demonstrated that morin induces endothelium-dependent relaxation in the rat mesenteric artery by acting on TRPV4 channels to mediate Ca2+ influx and attenuate blood pressure in L-NAME-induced hypertension, thereby highlighting the potential of morin in the treatment of hypertension. 31673446: Effect of Hydroalcoholic Extract of Ribes khorasanicum on Acute Hypertension Induced by L-NAME in Rat. Objectives: The aim of this study was to evaluate the effect of Ribes khorasanicum (R. khorasanicum); a plant growing in north Khorasan of Iran; on cardiovascular and stress oxidative in acute hypertension induced by N-nitro-l-arginine methyl ester (L-NAME), anitric oxide synthase inhibitor. 31721202: Nomega -nitro-L-arginine methyl ester (L-NAME) can induce hypertension with no deficiency on mice. Here, we investigated the effects of ethanol extract from C. brevistyla seed pomace (CBPE) in L-NAME-induced hypertension mice. 31730865: PPAR-gamma agonist, pioglitazone, reduced oxidative and endoplasmic reticulum stress associated with L-NAME-induced hypertension in rats. The aim of the present study was to investigate the effect of pioglitazone on cardiovascular complications of N-nitro-L-arginine methyl ester (L-NAME)-induced hypertension and to determine the role of oxidative and endoplasmic reticulum (ER) stress in its activity. 31769908: Here we show parallel time-dependent changes of 35 HPs and some of their cross-relationships in condition of high BP induced by L-NAME. 31817916: Materials and Methods: L-NAME was given orally to male Wistar rats for 6 weeks to induce hypertension concurrently with treatment of ethyl rosmarinate at 5, 15, or 30 mg/kgor enalapril at 10 mg/kg Systolic blood pressure (SBP), heart rate, and body weight of all experimental groups were recorded weekly, while the vascular sensitivity and histological changes of the aorta were evaluated at the end of the experiment. 31868952: Effects of Hydrogen Sulfide on Oxidative Stress, Inflammatory Cytokines, and Vascular Remodeling in L-NAME-induced Hypertension. This study was designed to evaluate the protective effects of hydrogen sulfide (H 2 S) against NG-Nitro L-Arginine Methyl Ester (L-NAME)-induced hypertension and its possible effects on the inflammatory process, oxidative stress, and vascular remodeling in rats. 32031202: In this study, the aim was to test the effect of tangeretin on Nomega-Nitro-l-arginine methyl ester (l-NAME)-induced high blood pressure, and left ventricular dysfunction and remodeling in rats. 32076406: The results showed that L-NAME induced hypertension and disordered the endothelial nitric oxide synthase (eNOS)-NO pathway in the treated rats. 32088240: VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. 32422184: The present study investigated the novel antihypertensive and neuroprotective effect of Naringenin on L-N G -Nitro arginine methyl ester (L-NAME) induced hypertension together with possible molecular mechanism of action. 32684805: Conclusion: The results of the current study showed that both the aqueous and ethyl acetate fractions of ZJ through the effect on nitric oxide system can prevent the development of HTN induced by L-NAME. In this regard, the present study investigated the effect of aqueous and ethyl acetate fractions of ZJ extract on acute hypertension (HTN) induced by nitro-L-arginine methyl ester (L-NAME). 32750643: RESULTS: Prophylactic administration of low and high doses of tadalafil improved l-NAME induced hypertension, proteinuria, maternal weight loss during pregnancy, fetal growth restriction and flow-mediated dilatation, balanced endothelial-relative factors, and alleviated inflammation activation in placenta and kidney tissue. 32754607: Ivabradine Ameliorates Kidney Fibrosis in L-NAME-Induced Hypertension. Thirty-six adult male Wistar rats were divided into non-diseased controls and rats with N G -nitro-L-arginine methyl ester (L-NAME)-induced hypertension to assess ivabradine's site-specific effect on kidney fibrosis. 32763289: MATERIALS AND METHODS: The animals were treated for 56 days, 28 days with N (omega) -nitro-L-arginine methyl ester to induce hypertension, and then treated for another 28 days with the new di- hydropyridine and the standard drug nifedipine. 32767352: TPPU and lisinopril resulted in normalization of L-NAME-induced hypertension. CONCLUSIONS: This study demonstrates that TPPU effectively lowers L-NAME-induced hypertension in rats. 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), a soluble epoxide hydrolase inhibitor, lowers L-NAME-induced hypertension through suppression of angiotensin-converting enzyme in rats. 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), a soluble epoxide hydrolase inhibitor, lowers L-NAME-induced hypertension through suppression of angiotensin-converting enzyme in rats.OBJECTIVE: This study evaluated the efficacy of the soluble epoxide hydrolase (sEH) inhibitor, TPPU on chronic NG-Nitro L-arginine methyl ester (L-NAME)-induced hypertension in rats and its effects on plasma Angiotensin II (Ang II), cardiac Angiotensin-converting enzyme (ACE) and Angiotensin II receptor type 1 (AT1R) expressions. 32863247: Skeels of Wampee (WP) fruits extract attenuate the progression of high blood pressure, endothelial dysfunction and preservation of antioxidant status with using a nitric oxide synthase (NOS) inhibitor, N (G) (-nitro-L-arginine methyl ester (L-NAME) induced hypertension and oxidative stress in rats. 33243020: The antihypertensive activity of the complex (assessed in an N(G)-Nitro-L-arginine methyl ester-induced hypertension model) was significantly higher. 33442028: Crocin further alleviated the inflammatory signals and oxidative stress in the serum, as well as in placental tissues, in rats with L-NAME-induced hypertension. 33641368: Male wild-type and alphaCGRP knockout mice received L-nitro-arginine methyl ester (150 mg/kg in drinking water) to induce a sustained hypertension with evidence of cardiovascular remodeling. 33826116: CONCLUSION: This study therefore demonstrates that MEADF possesses an in vivo ACE inhibitory activity, hypotensive potential and the ability to avert further degeneration of biochemical and physiological upsets associated with L-NAME induced hypertension. Fruit Pulp on N G -Nitro-L-Arginine Methyl Ester (L-NAME) Induced Hypertension in Rats. AIM: This study investigated the effect of methanol extract of Adansonia digitata fruit (MEADF) pulp on N G -nitro-L-arginine methyl ester (L-NAME) induced hypertension in rats. 34543638: MATERIALS AND METHODS: Male Wistar rats (220-250 g) were given l-NAME (0.5 mg/mL in drinking water) to induce hypertension for 5 weeks. 34581043: The Sennae Folium-induced diarrhea model, streptozotocin(STZ)-induced diabetes model and L-nitro-arginine methyl ester(L-NAME)-induced hypertension model were used to compare the pharmacodynamic differences in anti-diarrhea, blood glucose reduction and blood pressure lowering among raw, roasted and vinegar-processed PLR and PTR. 34925007: Conclusion: C. asiatica extract can prevent the development of hypertension and cardiac damage induced by l-NAME, and these effects were comparable to captopril. 35366256: Since the BP increase persisted after 7 weeks of L-NAME treatment, we hypothesize that central regulation of BP may contribute significantly to L-NAME-induced hypertension. 35517807: Conclusion: In conclusion, SMI improved the antihypertensive efficacy of LOS in the L-NAME-induced hypertension rat model by increasing the concentration of LOS, while leaving the concentration of EXP3174 intact. 36570254: The results revealed that the ethanolic extract of the leaves in two doses (250 and 500 mg/kg b.wt.) significantly normalized the elevated systolic blood pressure in N(G)-nitro-l-arginine-methyl ester-induced hypertension in rats. 38034670: AEGL was subjected to LC-MS analysis, and its effect (75, 150, and 300 mg/kg/day; by gavage) was evaluated against Nomega-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg)-induced hypertension in adult male Wistar rats for four consecutive weeks. 38672089: The aim of this study was to show whether an ARNI exerts a protective effect in a model of Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertension with a hypertensive heart and to compare this potential benefit with an angiotensin-converting enzyme inhibitor, captopril. In conclusion, in L-NAME-induced hypertension, the dual inhibition of neprilysin and AT1 receptors by ARNI reduced SBP and prevented the development of LV hypertrophy, fibrosis, and systolic and diastolic dysfunction. Sacubitril/Valsartan Alleviates Cardiac Remodeling and Dysfunction in L-NAME-Induced Hypertension and Hypertensive Heart Disease. 7562480: We found that two separate pharmacologic maneuvers which normalized BP after a transient period of hypertension, namely the NO donor sodium nitroprusside (SNP) or the calcium entry blocker verapamil (VER), did not reverse the increased renal vascular resistance (RVR) produced by acute NAME. 7619348: Previous studies have demonstrated that an acute intravenous administration of nitro-L-arginine methyl ester (L-NAME) causes a sustained hypertension and widespread vasoconstriction. 7684026: Although less potent than A-81988, the angiotensin II antagonist losartan and the angiotensin converting enzyme inhibitor enalapril also blocked L-NAME-induced hypertension. 7906520: Evidence that the autonomic nervous system plays a major role in the L-NAME-induced hypertension in conscious rats. 8012697: L-Arginine pretreatment attenuated L-NAME-induced hypertension for 5 min.8. 8081303: Spontaneous daily oral intake of L-NAME (1 mg/ml for 6 days) caused marked hypertension and tachycardia (176 +/- 5 mmHg and 418 +/- 16 bpm), when compared to untreated rats (111 +/- 2 mmHg and 354 +/- 8 bpm). 8181036: Long term oral administration of L-arginine in MWF rats increases NO production (as assessed by the urinary excretion rates of NO3- and cyclic GMP), but does not significantly influence systolic blood pressure, whereas L-NAME induces sustained hypertension and cardiac hypertrophy due to inhibition of NO formation. 8203552: Thirty days of treatment with L-NAME resulted in marked hypertension, hyperreninemia, interstitial expansion, and glomerular ischemia. 8205318: Hence, as with shorter periods of exposure to the less potent NO synthase inhibitor, NG-monomethyl-L-arginine, the hypertension caused by L-NAME is dependent on its continued administration, and is associated with a particularly marked hindquarters vasoconstriction. 8206637: To evaluate the potential role of the renal sympathetic nerves in L-NAME-induced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n = 8 each): (1) sham-operated vehicle-treated, (2) sham-operated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves. Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent. 8349331: This initial study of the relation between left ventricular weight and L-NAME-induced hypertension has now been extended by giving 50 mg/kg per day L-NAME to Wistar rats (n = 30) for 8 weeks and comparing results with those from control rats (n = 10) and two-kidney, one clip rats (n = 14). 8566127: Captopril (140 mumol/rat/day) significantly lowered the high blood pressure levels induced by L-NAME but did not significantly affect the inhibition of paw oedema caused by L-NAME. 8621212: Low-dose L-NAME treatment induced hypertension only when associated with sodium overload. 8666033: In rats, chronic administration of the nitric oxide (NO) inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) causes arterial hypertension, cardiac hypertrophy and myocardial ischemic alterations such as necrosis and fibrosis. 8723992: Vascular reactivity and flow-pressure curve in isolated kidneys from rats with N-nitro-L-arginine methyl ester-induced hypertension. 8797148: Quinapril significantly reversed the high BP induced by L-NAME without changing the decrease in the aortic wall cyclic GMP. 8845069: Oral administration of the nitric oxide biosynthesis inhibitor, N-nitro-L-arginine methyl ester (L-NAME), causes hypertension, but not glucose intolerance or insulin resistance, in rats. 8934362: L-NAME treatment resulted in higher blood pressure and increased severity of conduit artery hypertrophy, but reduced cardiac and small artery hypertrophy, and enhanced aortic endothelin-1 mRNA. 8994442: In the chronic model of L-NAME-induced hypertension, blockade of the renin-angiotensin system does not unmask an endothelin-dependent vasopressor tone. 9007669: SNP (1 microgram/kg/min; n = 6) virtually abolished L-NAME-induced hypertension and significantly attenuated both the increase in the ISVR (< 3.0 mg/kg) and the decrease in CO. Iloprost (50 ng/kg/min; n = 6) also abolished L-NAME-induced hypertension and markedly attenuated the increase in SVR. 9039102: Thus, increased renal sympathetic nerve activity does not contribute significantly to L-NAME-induced hypertension. 9052893: We studied the effect of chronic therapy with bosentan, a combined endothelin-A/endothelin-B receptor antagonist, on blood pressure and vascular function and structure of small arteries as well as on the reactivity of the aorta in N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. 9125618: CONCLUSIONS: Calcitonin gene-related peptide reverses the N(G)-nitro-L-arginine methyl ester-induced hypertension during pregnancy, when progesterone levels are elevated, but not post partum or in ovariectomized nonpregnant rats. Progesterone up-regulates vasodilator effects of calcitonin gene-related peptide in N(G)-nitro-L-arginine methyl ester-induced hypertension. 9189854: Acute systemic inhibition of NO synthesis with n-nitro L-arginine methyl ester (L-NAME) leads to hypertension, renal vasoconstriction, and natriuresis in rats with intact renal nerves. 9194516: In conclusion, acute L-NAME induced hypertension does not result in glucose intolerance, hyperinsulinemia, or decreased [3H]-deoxyglucose muscle uptake. 9231822: From these experiments, we conclude that the importance of the sympathetic system in the pathogenesis of L-NAME-induced hypertension accrues slowly over hours and days, and thus its importance can be overlooked by focusing on the initial phase of the hypertension. Using 8-hour infusions of L-NAME, we found that 60 minutes was the minimum time required for detecting a sympathectomy-sensitive component of L-NAME-induced hypertension. 9251774: Special emphasis is placed on the experimental model of arterial hypertension induced by N-nitro-L-arginine methyl ester (L-NAME) in which the interplay of these three reflexes is demonstrable. 9370381: Our findings clearly show that FHL rats are more susceptible to developing renal damage after induction of hypertension by chronic L-NAME treatment. Difference in susceptibility of developing renal damage in normotensive fawn-hooded (FHL) and August x Copenhagen Irish (ACI) rats after N(omega)-nitro-L-arginine methyl ester induced hypertension. This was further investigated by comparing the effects of N(omega)-nitro-L-arginine methyl ester (L-NAME) induced hypertension on functional and structural renal damage in two normotensive strains, the resistant August x Copenhagen Irish rat (ACI) and the normotensive fawn-hooded (FHL) rat, which also appears to carry a susceptibility locus for renal failure. 9446711: NomegaNitro-L-arginine methyl ester (L-NAME)-induced hypertension was significantly reduced after chronic nicotine treatment. 9464471: It was found that L-NAME induced arterial hypertension on weeks 1-4 in control rats but not in garlic-fed rats, whose blood pressure remained essentially as the basal values. It has been reported that garlic activates nitric oxide synthase in vitro and that chronic inhibition of nitric oxide (NO) synthesis by N omega-nitro-L-arginine-methyl-ester (L-NAME) induces arterial hypertension in rats. 9488223: RESULTS: L-NAME treatment induced hypertension (systolic blood pressure control 129.2+/-2.7 mmHg and SBP L-NAME treatment 176.3+/-5.2 mmHg, P< 0.001). 9513898: Genetic differences define severity of renal damage after L-NAME-induced hypertension in rats. 9614642: Bosentan-blunted, L-NAME-induced hypertension at the beginning (P < .05), but not at the end of the treatment period in all rats examined. 9752900: The combination of L-NAME and the NO-independent vasodilator, verapamil, attenuated the hypertension induced by L-NAME and prevented the following rise in insulin level. 9794721: CONCLUSIONS: Results indicate that L-NAME-induced hypertension is associated with a deficiency of nitric oxide, both peripherally and centrally. RESULTS: The chronic treatment with L-NAME induced a sustained dose-dependent hypertension with a decrease in heart rate. 9870689: We investigated the mechanisms of renal vascular wall thickening in a rat model of N-nitro L-arginine methyl ester (L-NAME)-induced hypertension. To separate the effects of L-NAME-induced hypertension from other effects of nitric oxide (NO) inhibition, we created two models of L-NAME-induced hypertension: both had the same blood pressure level but NO inhibition was moderate in one group (group M) and severe in the other (group S). Lipid deposition and increased production of extracellular matrix may contribute to renal vascular wall thickening in L-NAME-induced hypertension. 9892169: Chronic administration of N(G)-nitro-L-arginine methyl ester (L-NAME) to rats induces systemic hypertension and progressive development of preglomerular sudanophilic (SB+) lesions. 15614428: Thus, upregulation of BACE1 transcription by oxidative stress may contribute to the pathogenesis of Alzheimer's disease. Oxidative stress has been shown to affect A(beta) generation in the AD pathogenesis and the mechanism of such effect is unknown. 18695942: The identification of the aspartic protease BACE1 (beta-secretase) was a defining event in research aimed at understanding the molecular mechanisms that underlie Alzheimer's disease (AD) pathogenesis. 19486882: BACE1 is a novel type I transmembrane aspartyl protease that has been implicated in the pathogenesis of Alzheimer's disease. 20731874: BACKGROUND: BACE1 is a key enzyme in the generation of the Abeta peptide that plays a central role in the pathogenesis of Alzheimer's disease. 23770985: It was particularly interesting to discover a dual inhibitor that targets both Abeta42 aggregation and BACE1, the two crucial players in the pathogenesis of Alzheimer's disease. 23816176: BACE1, a beta secretase candidate enzyme, initiates the Alzheimer's disease (AD) pathogenesis via amyloid beta (Abeta) peptide production serving as a potential therapeutic target. 25609634: BACE1 is a key protease controlling the formation of amyloid beta, a peptide hypothesized to play a significant role in the pathogenesis of Alzheimer's disease (AD). 25716831: The beta-secretase BACE1 is widely known for its pivotal role in the amyloidogenic pathway leading to Alzheimer's disease, but how its action on transmembrane proteins other than the amyloid precursor protein affects the nervous system is only beginning to be understood. 28946017: Together, our studies provide mechanistic insight into a novel role for Par3 and aPKC in regulating the retrograde endosome-to-TGN trafficking of BACE1 and shed light on the mechanisms of AD pathogenesis. The cleavage of amyloid precursor protein (APP) by beta-site APP cleaving enzyme 1 (BACE1) is the rate-limiting step in beta amyloid generation during Alzheimer's disease (AD) pathogenesis. In human AD brains, there is a significant decrease in Ser498 phosphorylation of BACE1 suggesting that defective phosphorylation-dependent retrograde transport of BACE1 is important in AD pathogenesis. 29371969: Our results demonstrated that miR-124 is a potent negative regulator of BACE1 in the cellular AD phenotype and might be involved in the pathogenesis of AD. 30496823: Beta secretase 1 (BACE1) is an enzyme involved in the pathogenesis of Alzheimer's disease (AD). 30530107: Several lines of evidence suggest that BACE1 is a key enzyme in the pathogenesis of AD and its inhibition is of particular importance in AD treatment. 30930125: Analysis of microRNAs (miRNAs) revealed that miR-9 and miR-181a negatively coregulated BACE1 and TGFBIp, which was directly associated with the pathogenesis of AD and GCD2, respectively. 31223308: Increased amyloid-beta (Abeta) plaque deposition is thought to be the main cause of Alzheimer's disease (AD). Therefore, revealing the underlying mechanism of BACE1 in the pathogenesis of AD might have a significant impact on the future development of therapeutic agents targeting dementia. 31608840: BACE1 is a beta-secretase involved in the cleavage of amyloid precursor protein and the pathogenesis of Alzheimer's disease. 17105834: Angiotensin-converting enzyme inhibitors for bevacizumab-induced hypertension. 18842611: CONCLUSIONS: Our data indicate that bevacizumab-induced hypertension may represent an interesting prognostic factor for clinical outcome in advanced colorectal cancer patients receiving first-line bevacizumab. 19151582: [A case of therapy for bevacizumab-induced hypertension]. 19643598: Bevacizumab is recognised to cause hypertension, arterial and venous thrombosis, intestinal perforation and impairment of wound healing but can be safely used in patients undergoing surgery, particularly when the timing of surgery is controlled. 19921473: CONCLUSIONS: Our data indicate that bevacizumab-induced hypertension may represent an interesting prognostic factor for clinical outcome in advanced colorectal cancer patients receiving bevacizumab. 20817652: The efficacy of antihypertensive medications for this cause of hypertension has not been demonstrated. CONCLUSIONS: This is the first data that demonstrates individual classes of antihypertensives are effective in bevacizumab-induced hypertension. The management of bevacizumab-induced hypertension is important in order to avoid dose interruption/discontinuation and/or end organ damage. 20878444: Patients received amlodipine 5 mg daily for grade >= 2 bevacizumab-induced hypertension. 21368463: CONCLUSION: Bevacizumab-induced hypertension may represent a prognostic factor for clinical outcome in advanced, recurrent colorectal cancer patients treated with first-line bevacizumab. 21627340: Bevacizumab-induced hypertension: pathogenesis and management. 21804330: Recently, much evidence has suggested that bevacizumab-induced hypertension might be predictive of the effect of bevacizumab. Our data suggested that bevacizumab-induced hypertension may be predictive of the effect of bevacizumab in Japanese metastatic colorectal cancer patients. 21807768: An observational study of bevacizumab-induced hypertension as a clinical biomarker of antitumor activity. This study aimed to describe the incidence of bevacizumab-induced hypertension and factors associated with its development, then to retrospectively assess its relation with activity. CONCLUSIONS: Our preliminary results indicate that home-based measurement and grading according to the ESH criteria represents a reliable method to detect bevacizumab-induced hypertension. 22531628: The development of bevacizumab-induced arterial hypertension has recently been suggested as a potential predictive biomarker. CONCLUSION: Bevacizumab-induced hypertension did not predict radiological response or survival in our study. In this analysis, the development of bevacizumab-induced hypertension was correlated with clinical outcomes. 23509076: The role of the endothelium in the mechanism of bevacizumab-induced hypertension deserves further exploration. 24153157: Antiangiogenic agents such as bevacizumab commonly cause hypertension (HTN) and proteinuria (PTN), which may be biomarkers of response and clinical outcome. 24283603: Several clinical studies have evaluated bevacizumab-induced hypertension in patients with metastatic colorectal cancer. CONCLUSIONS: Bevacizumab-induced hypertension may represent a prognostic factor in patients with metastatic colorectal cancer. This meta-analysis was performed to better determine the association of bevacizumab-induced hypertension with outcome in patients with metastatic colorectal cancer, and to assess whether bevacizumab-induced hypertension can be used as a prognostic factor in these patients. Correlation of bevacizumab-induced hypertension and outcomes of metastatic colorectal cancer patients treated with bevacizumab: a systematic review and meta-analysis. 24558090: Genetic markers of bevacizumab-induced hypertension. Overall, 194 white patients had grade 1-4 bevacizumab-induced hypertension. 24867380: For example, both bevacizumab and vascular endothelial growth factor receptor (VEGFR) kinase inhibitors cause hypertension; both epidermal growth factor receptor (EGFR) antibodies and kinase inhibitors cause rash; and these toxicities correlate with response. 25117820: No reliable markers are available for predicting bevacizumab-induced hypertension. Genetic variant predicts bevacizumab-induced hypertension in ECOG-5103 and ECOG-2100. 25557543: Patients were classified as normotensive or hypertensive depending on whether hypertension developed that was attributable to therapy. Bevacizumab-induced hypertension is a predictive marker for improved outcomes in patients with recurrent glioblastoma treated with bevacizumab. Bevacizumab-induced hypertension is a well-documented side effect, and some reports have suggested this occurrence to be related to treatment outcome in other cancers. Bevacizumab-induced hypertension may be a physiologic marker of outcome in patients with recurrent GBM. 26721240: The results presented here indicate that CTCAE version 3.0 may underreport the incidence and grade of BEV-induced hypertension within clinical trials. 27109438: Retrospective analysis of bevacizumab-induced hypertension and clinical outcome in patients with colorectal cancer and lung cancer. Bevacizumab-induced hypertension may represent a biomarker for clinical benefit in cancer patients treated with bevacizumab. However, the relationship between bevacizumab-induced hypertension and clinical outcome remains unclear. 27617286: Hypertension (HTN) induced by bevacizumab is a side effect that is often thought to resolve after treatment. Hypertension induced by bevacizumab resolved in 82% of patients in a median of 87 days. 27956931: Angiogenesis inhibitors, such as sunitinib and bevacizumab, can cause hypertension, one of the many medical conditions associated with the posterior reversible encephalopathy syndrome. 28792121: Female sex, good performance status, and bevacizumab-induced hypertension associated with survival benefit in Asian patients with recurrent glioblastoma treated with bevacizumab. 28882537: In this review, we outline research efforts to understand the mechanisms and pathophysiology of hypertension resulting from bevacizumab treatment. Bevacizumab-induced hypertension: Clinical presentation and molecular understanding. Moreover, we highlight current knowledge of the pharmacogenetics of bevacizumab-induced hypertension, which may be used to develop strategies to prevent or minimize this toxicity. 28969913: Genetic predisposition to bevacizumab-induced hypertension. 29284349: Background Studies suggest that bevacizumab-induced hypertension is prognostic of better outcomes in bevacizumab-treated patients with metastatic colorectal, HER2-negative breast, kidney, and pancreatic cancer. 29333527: AAs also had significantly more grade 3-4 TIPN (OR=2.9; p=2.4 *10-11) and grade 3-4 bevacizumab-induced hypertension (OR=1.6; p=0.02), with a trend for more CHF (OR=1.8; p=0.08). 29632638: Anti-vascular endothelial growth factor (VEGF) therapeutics such as bevacizumab, which are widely used in cancer treatment, commonly leads to hypertension. Moreover, bevacizumab-induced hypertension is associated with improved clinical outcomes in several cancers. 29765225: This study was conducted with the aim, primarily, to assess the overall incidence and risk of common toxicities associated with bevacizumab in patients with advanced or metastatic breast cancer and, secondarily, to descriptively review study results concerning a potential correlation between bevacizumab-induced hypertension and its efficacy for breast cancer treatment. The prognostic value of bevacizumab-induced hypertension for its antitumor efficacy among patients with breast cancer remains controversial, with mixed results presented in the five retrospective studies that were identified from our additional literature search. 29871907: Experimental Design: To identify genomic regions associated with bevacizumab-induced hypertension risk, sequencing of candidate genes and flanking regulatory regions was performed on 61 patients treated with bevacizumab (19 cases developed early-onset grade 3 hypertension and 42 controls had no reported hypertension in the first six cycles of treatment). Conclusions: The genomic region between SLC29A1 and HSP90AB1 and its role in regulating adenosine signaling are key targets for further investigation into the pathogenesis of bevacizumab-induced hypertension. 29969436: Taken together, our findings indicate that bevacizumab-induced hypertension can predict progress-free survival and overall survival in patients with metastatic colorectal cancer, whereas its prediction for objective response rate was nonsignificant. We tested the hypothesis that bevacizumab-induced hypertension may be a useful predictor for objective response rate, progression-free and overall survival in patients with metastatic colorectal cancer via a comprehensive meta-analysis. Usefulness of bevacizumab-induced hypertension in patients with metastatic colorectal cancer: an updated meta-analysis. Overall relative risk of objective response rate for bevacizumab-induced hypertension was 2.03 (95% confidence interval [CI]: 1.18-3.48, p=0.01), with significant heterogeneity and publication bias, whereas unbiased estimate was nonsignificant after considering potentially missing studies. 31262878: BACKGROUND/AIM: Both bevacizumab (BEV) and soluble fms-like tyrosine kinase-1 (sFlt-1) have demonstrated anti-angiogenic effects, thereby causing hypertension and proteinuria. 31384312: As bevacizumab may cause hypertension (HTN) and increase the risk of cardiac failure, we performed a pilot study to evaluate the feasibility and toxicity of a non-anthracycline-containing combination of docetaxel with cyclophosphamide and bevacizumab in early stage breast cancer patients. 32067605: However, compared with FOLFOX4+bevacizumab, FOLFOX4+selective VEGFR inhibitors, led to increased hypertension, neutropaenia, fatigue, thrombocytopaenia and asthaenia. 32136179: Bevacizumab-induced hypertension correlation with survival in recurrent glioblastoma multiforme. 34028627: This is the first study providing evidence of plasma proteins with potential value to predict patients at risk of developing bevacizumab-induced hypertension. There are no biomarkers to predict the risk of bevacizumab-induced hypertension. Plasma levels of angiopoietin-2, VEGF-A, and VCAM-1 as markers of bevacizumab-induced hypertension: CALGB 80303 and 90401 (Alliance). 34616010: Bevacizumab-induced hypertension and proteinuria: a genome-wide study of more than 1000 patients. SNP in KCNAB1 validated in an independent dataset provides evidence toward its clinical applicability to predict bevacizumab-induced hypertension. 34775477: In the discovery set, rs444904 (G > A) in PIK3R5 was associated with an increased risk of sorafenib-induced hypertension (p = 0.006, OR = 3.88 95% CI 1.54-9.81). In the replication set, rs427554 (G > A) in PIK3R5 (in complete linkage disequilibrium with rs444904) was associated with an increased risk of bevacizumab-induced hypertension (p = 0.008, OR = 1.39, 95% CI 1.09-1.78). This study aimed to identify predictive biomarkers of hypertension induced by these drugs using a discovery-replication approach. 34853435: Correction: Bevacizumab-induced hypertension and proteinuria: a genome-wide study of more than 1000 patients. 35016085: A positive prognostic impact of bevacizumab-induced HTN was reported in the 58% of the analyses reporting Progression Free Survival (PFS) and in the 54% of the analyses reporting Overall Survival (OS) data. CONCLUSIONS: Bevacizumab-induced HTN during the first-line treatment of mCRC is an independent prognostic factor, also adopting a time-dependency correction. BACKGROUND: Retrospective series suggest that bevacizumab-induced hypertension (HTN) is a prognostic and potentially predictive biomarker of efficacy of the antiangiogenic drug in the upfront treatment of metastatic colorectal cancer (mCRC) patients. Bevacizumab-induced hypertension as a predictor of clinical outcome in metastatic colorectal cancer: An individual patient data-based pooled analysis of two randomized studies and a systematic review of the literature. 35527502: Patients in the top quintile had a higher risk of developing bevacizumab-induced hypertension compared to patients in the bottom quintile using SNPs associated with SBP (p=4.75x10 -4 , OR=3.72, 95% CI: 1.84-8.16) and DBP (p=0.076, OR=1.83, 95% CI: 0.95-3.64). 35735428: However, while bevacizumab-induced hypertension has been linked to increased overall survival (OS), data on proteinuria are controversial. 35847929: In conclusion, RASIs and Bev have synergistic effect in the treatment of colorectal cancer and RASIs might be an optimal choice for the treatment of Bev-induced HT. However, at present, appropriate antihypertensive agents for Bev-induced HT are unavailable. Bev-induced hypertension (HT) is the most common adverse reaction during clinical practice. 36277543: Bevacizumab-Induced Hypertension as a Potential Physiological Clinical Biomarker for Improved Outcomes in Patients With Recurrent Glioblastoma Multiforme: A Systematic Review. In conclusion, bevacizumab-induced hypertension may represent a prognostic factor in patients with rGBM. Several clinical studies have evaluated bevacizumab-induced hypertension as a potential marker in patients with different malignancies, including recurrent glioblastoma multiforme (rGBM). 37322624: Our study suggests that the SBP and DBP variability of amlodipine in the treatment of hypertension induced by apatinib and bevacizumab is slightly better than that of perindopril, but the effect of perindopril in improving endothelial function indices NO and echocardiographic data is better than that of amlodipine. Comparison of antihypertensive drugs amlodipine and perindopril on blood pressure variability after long-term treatment of hypertension induced by apatinib and bevacizumab. The purpose of this study was to elucidate the therapeutic effect of different antihypertensive drugs (amlodipine and perindopril) on hypertension induced by apatinib and bevacizumab. 37340980: Bevacizumab-Induced Hypertension in Glioblastoma Patients and Its Potential as a Modulator of Treatment Response. 10564528: S100beta is an astrocyte-derived uritotrophic' cytokine which has been implicated in the pathogenesis of Alzheimer's disease. 10782042: Prostaglandins and proinflammatory cytokines are implicated in the etiology of neurodegenerative diseases, such as Alzheimer's disease. 11578774: This multifunctional cytokine might be centrally involved in several aspects of AD pathogenesis by regulating beta-amyloid precursor protein synthesis and processing, plaque formation, astroglial and microglial response and neuronal cell death. Recent studies have implicated pro- and anti-inflammatory cytokines as integral to Alzheimer's disease (AD) pathogenesis. 1491745: These findings span many of the major immune system phenomena, from major histocompatibility complex (MHC) antigens through cytokines and the complement cascade and suggest that some facets of AD pathogenesis may be immune related. 17420099: To further investigate the proposed association and to clarify the role of cytokines as a potential cause for AD susceptibility, we analyzed genotypes, allele distributions and haplotypes of IL10 promoter polymorphisms -1082 (rs1800896) and -819 (rs1800871) in an Italian sample of 222 sporadic AD patients and 179 normal controls. 21143158: Under stress and injury, astrocytes become astrogliotic leading to an upregulation of the expression of proinflammatory cytokines and chemokines, which are associated with the pathogenesis of AD. 21482536: OBJECTIVE: Serum amyloid A (A-SAA) is an acute-phase protein with cytokine-like properties implicated in the pathogenesis of rheumatoid arthritis (RA), atherosclerosis, diabetes and Alzheimer's disease. 22408651: Neuroinflammatory Cytokines-The Common Thread in Alzheimer's Pathogenesis. 22437436: Amyloid beta42 (Abeta42) and proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) have been suggested to contribute to the pathogenesis of Alzheimer's disease (AD) and vascular dementia (VaD). 22970774: The potential role of proinflammatory and antiinflammatory cytokines in Alzheimer disease pathogenesis. 24054992: Previously we identified that palmitate can induce primary astrocytes to produce cytokines, causing AD-like changes in primary neurons. 24141019: Together our data suggest a cell-autonomous role of microglia, and identify TNFalpha as the responsible cytokine, in promoting neuronal CCEs in the pathogenesis of AD. 24478534: Furthermore, findings in brains of patients dying with conditions known to predispose to Alzheimer's disease suggest that activation of glia and overexpression of glial cytokines are early events in Alzheimer pathogenesis. 25078115: However, accumulating evidence indicates that Abeta may activate astrocytes, which leads to an increase in cytokines that has been suggested to be a causative factor in the cognitive dysfunction of AD; thus, a vicious circle may be created. 25620241: The biology of NF-kappaB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. 27054030: Here, we review the progress in understanding the important role that these cytokines or neuroinflammation has played in AD etiology and pathogenesis. 27474414: To further investigate the proposed association and to clarify the role of cytokines as a potential cause for AD susceptibility, we analyzed genotypes, allele distributions and haplotypes of IL-10 promoter polymorphisms -1082 (rs1800896) and -819 (rs1800871) in a Mexican population: 986 normal controls and 221 cases divided as follows: 122 with Alzheimer disease (AD), 67 with (VaD) and 32 with mixed dementia (AD/VaD). 31044031: Conclusion: Altogether, our results show that treatment with serotype b-LPS triggers the secretion of proinflammatory cytokines by microglia, induces neurite shrinking, and increases the extracellular Abeta1-42 levels, all features strongly associated with the etiology of AD. 31217937: S100B is an astrocytic cytokine with a possible role in the pathogenesis of AD. 34685770: The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer's Disease. 8164471: Since IL-1 and tumor necrosis factor (TNF) tend to act synergistically in physiological conditions and in some pathological processes, we have studied the concentration of TNF-alpha in patients with Alzheimer's disease (AD) or multi-infarct dementia (MID) and in age-matched control subjects (CS) in order to evaluate possible changes in the levels of this cytokine with potential influence on the pathogenesis of AD. 8793035: The participation of interleukin-6, a stress-inducible cytokine, in the pathogenesis of Alzheimer's disease. 8892353: These findings are supported by numerous circumstantial findings suggesting a role for cytokines and acute phase reactants in the pathogenesis of AD. 31852393: Methods and Results: To test the therapeutic potential of targeting Sirt3 expression we developed new transgenic mice with global Sirt3 overexpression (Sirt3OX) which protects from endothelial dysfunction, vascular oxidative stress and hypertrophy, attenuates angiotensin II- and DOCA-salt induced hypertension. 31871958: Adipose Mesenchymal Cells-Derived EVs Alleviate DOCA-Salt-Induced Hypertension by Promoting Cardio-Renal Protection. 31902933: Grape Extract from Chardonnay Seeds Restores Deoxycorticosterone Acetate-Salt-Induced Endothelial Dysfunction and Hypertension in Rats.Grape extract (GE), which contains various polyphenolic compounds, exerts protective effects against lifestyle-related diseases, such as diabetes and hypertension. Grape Extract from Chardonnay Seeds Restores Deoxycorticosterone Acetate-Salt-Induced Endothelial Dysfunction and Hypertension in Rats. 32072406: In this study, the hepatoprotective effect and mechanism of TUDCA were investigated in the deoxycorticosterone acetate (DOCA)-salt-induced hypertension. Our findings indicate that the detrimental effect of DOCA-salt-induced hypertension on the liver was defended by the inhibition of ERS. 32187164: (Euphorbiaceae) on DOCA-salt-induced hypertension, cardiac hypertrophy and dysfunction, and endothelial dysfunction in rats. 32335091: Previous studies demonstrated that morin is capable of resolving deoxycorticosterone acetate-salt-induced hypertension and possess strong vasorelaxant properties. 32393187: There was no difference in DOCA-salt-induced hypertension between WT and KO mice. 32609312: MUMT-/- mice were also not protected from hypertension or end-organ damage induced by Ang II infusion or deoxycorticosterone acetate (DOCA)-salt treatment. METHODS AND RESULTS: We purified serum IgG from mice exposed to vehicle or angiotensin (Ang) II to induce hypertension and adoptively transferred these to wild type (WT) recipient mice receiving a subpressor dose of Ang II. 32799674: In contrast, intravenous infusion of PRO20 was less effective in attenuating DOCA-salt-induced hypertension and cardiorenal injury. 32824935: In conclusion, the minipig model of DOCA-induced HTN is feasible, showing durable effects. RDN may partially offset the DOCA-induced HTN. 32829380: Moreover, in heterozygous ELA knockout mice (ELA +/- ), the ELA deficiency remarkably accelerated the onset of DOCA/salt-induced hypertension. Our data demonstrate that ELA prevents DOCA/salt-induced hypertension by inhibiting NADPH oxidase/ROS/NLRP3 pathway in the kidney, which is APJ independent. ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway. Next, overexpression of ELA in the kidney was found to attenuate DOCA/salt-induced hypertension and renal injury, including lower blood pressure, reversed glomerular morphological damage, decreased blood urea nitrogen (BUN), and blocked the accumulation of fibrotic markers. ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.ELABELA (ELA), a 32-residue hormone peptide abundantly expressed in adult kidneys, has been identified as a novel endogenous ligand for APJ/Apelin receptor. The aim of this study was to investigate the role of ELA in deoxycorticosterone acetate (DOCA)/salt-induced hypertension and further explore the underlying mechanism. 32908237: Sodium butyrate ameliorates deoxycorticosterone acetate/salt-induced hypertension and renal damage by inhibiting the MR/SGK1 pathway. These results provide evidence that NaBu may attenuate DOCA/salt-induced hypertension and renal damage by inhibiting the MR/SGK1 pathway. 33080347: Dietary supplementation of Huangshan Maofeng green tea preventing hypertension of older C57BL/6 mice induced by desoxycorticosterone acetate and salt. The current study investigated the effect and mechanism of dietary supplement of Huangshan Maofeng green tea (HSMF) on prevention of hypertension induced by deoxycorticosterone acetate (DOCA) and salt in old C57BL/6 mice. 33097689: Correction: ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway. Correction: ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.An amendment to this paper has been published and can be accessed via a link at the top of the paper. 33363344: TVHE and captopril therapy also improved glomerular damage in DOCA-salt-induced hypertension rats. This study aimed to investigate TVHE therapy effect on MDA levels and renal histological conditions in deoxycorticosterone acetate (DOCA)-salt-induced hypertension rats. Tilapia viscera hydrolysate extract alleviates oxidative stress and renal damage in deoxycorticosterone acetate-salt-induced hypertension rats. Conclusion: TVHE has antioxidant ability, decreased MDA level, and decreased glomerular damage in DOCA-salt-induced hypertension rats. 33450051: Combining mesenchymal stem cells with serelaxin provides enhanced renoprotection against 1K/DOCA/salt-induced hypertension. 34226678: The purpose of the present study was to immunohistochemically evaluate and compare the expression of WNT4, WNT10A, Fzd8, beta-catenin, and GSK-3ss (glycogen synthase kinase 3beta) in the kidneys of rats with essential arterial hypertension (SHR), renal-renal hypertension (2K1C), and DOCA-salt-induced hypertension. 34607108: Only RLX and BM-MSCs, but not RLX and/or BM-MSC-EXO, also attenuated the 1K/DOCA/salt-induced hypertension. 34679745: Effects of Black Garlic Extract and Nanoemulsion on the Deoxy Corticosterone Acetate-Salt Induced Hypertension and Its Associated Mild Cognitive Impairment in Rats. Organosulfur compounds, phenolic acids and flavonoids in raw and black garlic were determined, and followed by preparation of black garlic nanoemulsion for studying their effects on deoxycorticosterone acetate-salt-induced hypertension and associated mild cognitive impairment in rats. 34756849: Dietary Supplementation of Huangshan Maofeng Green Tea Preventing Hypertension of Older C57BL/6 Mice Induced by Desoxycorticosterone Acetate and Salt: Green Tea Preventing Senior Hypertension. The current study investigated the effect and mechanism of dietary supplement of Huangshan Maofeng green tea (HSMF) on prevention of hypertension induced by deoxycorticosterone acetate (DOCA) and salt in old C57BL/6 mice. 34840266: ABSTRACT: The present study aimed to explore the contribution of mTOR in deoxycorticosterone acetate (DOCA)-salt-induced hypertension and related pathophysiological changes in cardiovascular and renal tissues. Pharmacological inhibition of mTOR attenuates DOCA-salt-induced hypertension and related pathophysiology: regulation of oxidative stress, inflammation and cardiovascular hypertrophy in male rats. 34857899: This study aims to test the hypothesis that gut microbiota dysbiosis is associated with DOCA-salt-induced hypertension, while captopril, an antihypertensive drug, is able to rebalance the gut microbiota alterations caused by hypertension. 35322744: This study aimed to investigate the cardiovascular protective effect of astaxanthin (ASX) in DOCA-salt-induced hypertension and its possible underlying mechanisms. CONCLUSION: ASX has beneficial protective effects on DOCA-salt-induced hypertension via DNA fragmentation protection, apoptosis inhibition, antioxidant, anti-inflammatory, and its effects on lipid levels. Astaxanthin attenuates cardiovascular dysfunction associated with deoxycorticosterone acetate-salt-induced hypertension in rats. 35556816: These results suggested that the overexpression of S1PR1 in the renal medulla attenuates sodium retention by the inhibition of ENaC function in the DOCA-induced SS-HTN. The mice were then implanted with the silastic DOCA sheet subcuntaneously and 1% NaCl drinking water to induce salt-sensitive hypertension (SS-HTN). 35862128: To determine mechanisms, we analyzed inflammasome activation in mouse models of deoxycorticosterone acetate salt-induced hypertension as well as salt-sensitive mice with ENaC inhibition or expression, IsoLG scavenging, and adoptive transfer of wild-type dendritic cells into NLRP3 deficient mice. 35949696: Objectives: Because the damage of kidney tissue is associated with hypertension and impaired nitric oxide (NO) synthesis, and as aspirin is reported to stimulate the synthesis of renal r-cortexin, an anti-hypertensive protein, we investigated the role of aspirin as bolus dose on elevated blood pressure induced by deoxycorticosterone acetate (DOCA)-salt in animal model. 36139008: Notably, we found that renin mRNA was significantly elevated in the SFO and PVN in a mouse model of DOCA-salt-induced hypertension. Importantly, renin-a ablation in the SFO attenuated the maintenance of DOCA-salt-induced hypertension and improved autonomic function without affecting fluid or sodium intake. 36231135: DOCA-induced hypertension induced p16INK4a+ senescent cells (SnCs) accumulation not only in the aorta and kidney ( p < 0.05) but also knee joint, which contributed to articular cartilage degradation and subchondral bone disturbance. 37107314: The deoxycorticosterone acetate (DOCA) and sodium chloride (DOCA-salt) model was used to induce hypertension in pregnancy. 37171128: CONCLUSION: These results suggested that activation of S1PR1 in the renal medulla attenuates DOCA-induced sodium retention and salt-sensitive hypertension associated with inhibition of ENaC. 37248323: JMJD3 ablation in myeloid cells confers renoprotection in mice with DOCA/salt-induced hypertension. In summary, JMJD3 ablation in myeloid cells reduces kidney inflammation and fibrosis in DOCA salt-induced hypertension. 37290410: METHODS: Intracranial aneurysms were induced using deoxycorticosterone acetate-salt-induced hypertension and a single injection of elastase into the cerebrospinal fluid of the basal cistern. 37301198: Translationally, targeting endothelial FAM3D by adeno-associated virus or intraperitoneal injection of FAM3D-neutralizing antibodies markedly ameliorates AngII- or deoxycorticosterone acetate (DOCA)-salt-induced hypertension. 37893466: To gauge the cardio-protective impact of SNEC in DOCA salt-induced hypertension, molecular docking was undertaken, uncovering curcumin's high affinity and adept binding capabilities to the active site of angiotensin-converting enzyme (ACE). 38047378: TLGMNKO mice exhibited reduced Ang II-induced or deoxycorticosterone acetate/salt-induced hypertension and target organ damage relative to wild-type (WT) mice. 38164960: Adipose c-Jun NH2-terminal kinase promotes angiotensin II-induced and deoxycorticosterone acetate salt-induced hypertension and vascular dysfunction by inhibition of adiponectin production and activation of SGK1 in mice. In addition, chronic treatment of recombinant mouse APN significantly augments the beneficial effects of adipose JNK1/2 inactivation in DOCA salt-induced hypertension. Specific inactivation of JNK1/2 in adipocytes significantly alleviates Ang II-induced and DOCA salt-induced hypertension and target organ damage in mice. 38690943: RESULTS: Blocking the afferent sensory nerves of PRAT with RTX can alleviate DOCA-Salt-induced hypertension and renal injury in rats. However, DOCA-Salt-induced hypertension and renal injury can be treated in Trpv1+/- mice but not alleviated or even worsened in Trpv1-/- mice, possibly because of compensatory increase of Trpv5 in DRG of Trpv1-/- mice. We also constructed Trpv1-/- mice and Trpv1+/- mice or used the injection of AAV2-retro-shTrpv1 to detect the effects of Trpv1 knockout or knockdown of PRAT-projected DRGs on deoxycorticosterone acetate (DOCA)-Salt-induced hypertension and kidney injury. TRPV1 signaling of perirenal adipose tissue promotes DOCA-Salt-induced hypertension and kidney injury. 32305658: Gut dysbiosis contributes to high fructose-induced salt-sensitive hypertension in Sprague-Dawley rats.OBJECTIVES: Although it is known that high fructose intake causes salt-sensitive hypertension, the underlying mechanism remains unclear. Gut dysbiosis contributes to high fructose-induced salt-sensitive hypertension in Sprague-Dawley rats. METHODS: For 8 wk, Sprague-Dawley rats were given 20% fructose in drinking water and 4% sodium chloride in their diet to induce hypertension. 32475636: Corrigendum to <'Gut dysbiosis contributes to high fructose-induced salt-sensitive hypertension in Sprague-Dawley rats'> <[Nutrition Volumes 75-76, July-August 2020, 110766]>. 32532282: CONCLUSION: We conclude that CX3CR1-microglia represses the nNOS signaling pathway and promotes chronic inflammation in fructose-induced hypertension. METHODS: The hypertensive rat model was used to study the role of CX3CR1-microglia in NTS inflammation following hypertension induction by oral administration of 10% fructose water. 33061560: Discussion: Thus, short-term consumption of high fructose plus high salt diet by rats results in modest hypertension, insulin resistance, diminished aortic and renal artery compliance, and left ventricular diastolic dysfunction. Existing studies show that a rat model reflecting a diet of fructose and salt consumed by the upper 20th percentile of the human population results in salt-sensitive hypertension mitigated by treatment with an antioxidant. 33189838: MATERIALS AND METHODS: Aqueous-ethanolic extract and activity based fractions of I. hederacea were evaluated using invasive blood pressure measuring technique, isolated tissue experiments, fructose induced hypertension/metabolic syndrome and biochemical analysis. 33800916: Moreover, minocycline- and HF-induced hypertension, individually or together, is associated with the aberrant activation of the renin-angiotensin system (RAS). 34259014: Conclusion HFr-induced hypertension and renal damage are exaggerated in DS rats via renal renin-angiotensin system activation, which can be controlled by renin-angiotensin system inhibitors. High Fructose-Induced Hypertension and Renal Damage Are Exaggerated in Dahl Salt-Sensitive Rats via Renal Renin-Angiotensin System Activation. Enalapril and candesartan attenuated the HFr-induced hypertension, albuminuria, glomerular hyperfiltration, and renal damage in DS rats. However, it has been unknown whether the HFr-induced hypertension and renal damage are exaggerated in subjects with salt sensitivity. Background High-fructose diet (HFr) induces hypertension and renal damage. 34281445: CONCLUSION: In summary, the obtained results suggest that AELC can prevent and reverse the high blood pressure induced by fructose, probably by restoring nitric oxide level and by improving altered metabolic parameters. PURPOSE: Since metabolic abnormalities such as elevated glucose level and imbalanced lipid profiles increase the risk for hypertension and cause endothelial dysfunction, we evaluated the effect of aqueous extract of large cardamom (AELC) on fructose-induced metabolic hypertension and oxidative stress. 34617181: The decrease in the CGRP content was found during the development of fructose-induced hypertension, but not L-NAME-caused hypertension. We studied the effect of CCK-8 on BP and blood content of CGRP in rats with hypertension caused by fructose or inhibition of NO synthase with L-NAME. These findings suggest that CGRP mediates the hypotensive effect of CCK-8 in fructose-induced hypertension, but not in NO-deficient hypertension. Effect of Cholecystokinin-8 (CCK-8) on Blood Pressure and Blood Content of Calcitonin-Gene-Related Peptide (CGRP) in Rats with Hypertension Caused by Fructose or Inhibition of Nitric Oxide Synthesis. 34687200: Glut5 Knockdown in the Nucleus Tractus Solitarii Alleviates Fructose-Induced Hypertension in Rats. Fructose-induced hypertension was assessed via the tail-cuff technique, a non-invasive blood pressure measurement approach. OBJECTIVE: Herein, we investigated whether NTS Glut5 knockdown can alleviate fructose-induced hypertension in rat models. 35113090: A combined intake of high fructose and high salt induced salt-sensitive hypertension and maternal high-fructose consumption induced programmed hypertension in adult offspring. 35153813: Salt-induced hypertension and fructose-induced hypertension are manifested in different mechanisms, including Inflammation, aldosterone-mineralocorticoid receptor pathway, aldosterone independent mineralocorticoid receptor pathway, renin-angiotensin system (RAS), sympathetic nervous system (SNS) activity, and genetic mechanisms. This review describes the evolution of hypertension and cardiovascular diseases (CVDs) in Lebanon and aims to elucidate potential mechanisms where salt and fructose work together to induce hypertension. These mechanisms increase salt absorption, decrease salt excretion, induce endogenous fructose production, activate fructose-insulin-salt interaction, and trigger oxidative stress, thus leading to hypertension. High intakes of salt and sugar (mainly fructose from added sugars) have been linked to the etiology of hypertension, and this may be particularly true for countries undergoing the nutrition transition, such as Lebanon. 35534765: These results suggest that JQ-R can reduce blood pressure and improve glucose and lipid metabolism in fructose-induced hypertension rats. 35555082: Gut microbiota depletion with antibiotics enhances fructose induced salt-sensitive hypertension in normal rats. INTRODUCTION-: We reported that 20% fructose in drinking water induced salt-sensitive hypertension in normal rats. CONCLUSION: - Chronic antibiotic treatment induced gut microbiota depletion and enhanced fructose induced salt-sensitive hypertension in normal rats, an effect that was associated with decreased plasma beta-hydroxy-butyrate, lactate and insulin. The contribution of the gut microbiota to fructose induced salt-sensitive hypertension or renal function has not been studied. Aim- We hypothesized that gut microbiota depletion with antibiotics (ABX) would change fructose induced salt-sensitive hypertension, renal excretory function and plasma levels of bacterial metabolites (lactate, beta-hydroxy-butyrate). 35708145: This study aimed to investigate the anti-hypertensive effect of CGA on high-fructose-induced salt-sensitive hypertension and the underlying mechanism. Moderation of gut microbiota and bile acid metabolism by chlorogenic acid improves high-fructose-induced salt-sensitive hypertension in mice. 35792095: Renal Farnesoid X Receptor improves high fructose-induced salt-sensitive hypertension in mice by inhibiting DNM3 to promote nitro oxide production. This study aimed to investigate the anti-hypertensive effect of renal FXR on high-fructose-induced salt-sensitive hypertension and underlying mechanism. 35846749: Modulation of the Gut Microbiota by Fufang-Zhenzhu-Tiaozhi Capsule Attenuates Hypertension Induced by a High-Fructose and High-Salt Diet. 36200315: Proximal tubule fructose metabolism is key to fructose-induced hypertension, but the roles of sex and stress are unclear. Independent effects of sex and stress on fructose-induced salt-sensitive hypertension. We conclude that fructose-induced salt-sensitive hypertension is similar in males and females unlike other forms of hypertension, and the increase in blood pressure depends in part on an augmented response of the sympathetic nervous system to stress. 36604264: We previously showed that dietary inulin can prevent fructose-induced hypertension in rats. 36729699: INTRODUCTION: High-fructose diet (HFr) causes metabolic syndrome, and HFr-induced hypertension and renal damage are exaggerated in Dahl salt-sensitive (DS) rats. Exercise Training Prevents High Fructose-Induced Hypertension and Renal Damages in Male Dahl Salt-Sensitive Rats. CONCLUSIONS: Ex prevents HFr-induced hypertension and renal damages in DS rats. 38045685: Objective: We aimed to investigate the hypothesis that B cells play a crucial role in the development of fructose-induced hypertension. Single cell transcriptome analyses reveal the roles of B cells in fructose-induced hypertension. This finding suggests that targeting B cells could be a potential strategy to mitigate high blood pressure in fructose-induced hypertension. Moreover, the simultaneous increase in follicular B cells and Tfh cells in LPs, along with the upregulation of interferon pathway genes in B cells, underscores a potential autoimmune factor contributing to the pathogenesis of fructose-induced hypertension in the intestine. 38059297: Conclusion: A FHS diet enhances the sensitivity of proximal tubule O 2 - production to Ang II, and this contributes to fructose-induced salt-sensitive hypertension. We hypothesized that FHS augments the ability of Ang II to stimulate superoxide production by proximal tubules, and this contributes to fructose-induced salt-sensitive hypertension. 38187558: Elevated dietary fructose leads to salt-sensitive hypertension, in part by fructose reabsorption in the proximal tubule (PT). 38442503: Baroreflex sensitivity (BRS) tested with PE/SNP, distribution/expression of Leptin/receptors in the NG/nucleus tractus solitary (NTS) examined using immumostaining and qRT-PCR, and serum concentrations of Leptin/NE measured by ELISA were observed in control and high fructose-drinking induced hypertension (HTN-HFD) rats. 38474316: Elevated dietary fructose leads to salt-sensitive hypertension, in part, through fructose reabsorption in the proximal tubule (PT). 38505704: In this study, we determine if NO in the NTS is involved in the synaptic plasticity underlying the elevated sympathetic outflow in fructose-induced hypertension. Synaptic mechanisms underlying the elevated sympathetic outflow in fructose-induced hypertension. 38545789: We hypothesized that PT fructose reabsorption by SGLT5 initiates a genetic program enhancing Ang II-stimulated oxidative stress in males and females, thereby causing fructose-induced salt-sensitive hypertension. CONCLUSIONS: SGLT5-mediated PT fructose reabsorption is required for FHS to augment Ang II-stimulated proximal nephron O 2 - production, and increases in PT oxidative stress likely contribute to FHS-induced hypertension. SGLT4 (sodium glucose-linked cotransporters 4) and SGLT5 are implicated in PT fructose reabsorption, but their roles in fructose-induced hypertension are unclear. Knocking Out Sodium Glucose-Linked Transporter 5 Prevents Fructose-Induced Renal Oxidative Stress and Salt-Sensitive Hypertension. 32382276: Preventive Electroacupuncture Ameliorates D-Galactose-Induced Alzheimer's Disease-Like Pathology and Memory Deficits Probably via Inhibition of GSK3beta/mTOR Signaling Pathway. 32959549: [Effects of electroacupuncture on cognitive function and neuronal autophagy in rats with D-galactose induced Alzheimer's disease]. 32990282: RhoA/Rock2/Limk1/cofilin1 pathway is involved in attenuation of neuronal dendritic spine loss by paeonol in the frontal cortex of D-galactose and aluminum-induced Alzheimer's disease-like rat model.Alzheimer's disease (AD) has become the most prevalent neurodegenerative disorder. RhoA/Rock2/Limk1/cofilin1 pathway is involved in attenuation of neuronal dendritic spine loss by paeonol in the frontal cortex of D-galactose and aluminum-induced Alzheimer's disease-like rat model. 33727095: Taken together, these findings suggest the role of LAP in ameliorating D-gal-induced AD in OVX rats via activating the pro-survival pathway; PI3K-Akt-GSK-3beta, while inhibiting p-mTOR, NOX-1, and p38 MAPK pathways. 33995945: Preventive electroacupuncture ameliorates D-galactose-induced Alzheimer's disease-like inflammation and memory deficits, probably via modulating the microbiota-gut-brain axis. 34481907: As an epilogue, targeting MPC-1 in the D-gal-induced AD in OVX rats resulted in the enhancement of autophagy, and suppression of neuroinflammation and excitotoxicity. 35721206: In the present study, we focused on the microbiome-gut-brain axis to investigate the mechanism of action of Gas using a D-galactose (Dgal)-induced AD model. 36554305: Wistar rats were given an i.p. injection of 60 mg/kg D-gal and 10 mg/kg AlCl 3 to induce AD and three doses of 1 mg/kg, 5 mg/kg or 10 mg/kg 5-MTHF by oral gavage. 37329974: The multifactorial role of vanillin in amelioration of aluminium chloride and D-galactose induced Alzheimer's disease in mice. 37414289: Here, we investigated the effect and mechanism of DAU on D-galactose and AlCl 3 combined-induced AD mice based on the Ca 2+ /CaM pathway. 37460908: Neuromodulatory effect of vardenafil on aluminium chloride/D-galactose induced Alzheimer's disease in rats: emphasis on amyloid-beta, p-tau, PI3K/Akt/p53 pathway, endoplasmic reticulum stress, and cellular senescence. The current study explored the potential therapeutic effect of vardenafil (VAR), a phosphodiesterase-5 inhibitor, in AlCl 3 /D-galactose (D-gal)-induced AD in rats and its possible underlying mechanisms. 38052316: These findings suggest that coconut oil shows protective effects against cognitive and non-cognitive impairment, AD pathology markers, oxidative stress, synaptic transmission, and cholinergic function in a D-GAL/AlCl 3 -induced AD rat model. Thus, we investigated the effects of coconut oil on spatial cognitive ability and non-cognitive functions in a rat model of AD induced by G-galactose (D-GAL) and aluminum chloride (AlCl 3 ), and examined the changes in synaptic transmission, cholinergic activity, neurotrophic factors and oxidative stress in this process. 38617712: The objective of the current investigation was to examine the neuroprotective and anti-ferroptotic role of nanocurcumin and Donepezil against model of aluminum chloride AlCl 3 and D-galactose induced ad. 11152688: Processing of the beta-amyloid precursor protein (betaAPP) by beta- and gamma-secretases generates the amyloidogenic peptide Abeta, a major factor in the etiology of Alzheimer's disease. 11316808: Generation of the amyloid peptide through proteolytic processing of the amyloid precursor protein by beta- and gamma-secretases is central to the etiology of Alzheimer's disease. 11744687: The presenilin (PS) proteins are components of the gamma-secretase activity, which is central in the pathogenesis of Alzheimer's disease. 12697771: The ability to isolate gamma-secretase from post-mortem human brain may facilitate the identification of brain-specific modulators of beta-APP processing and provide new insights into the biology of this important factor in the pathogenesis of Alzheimer's disease. 12944419: Thus, identifying components and pathways by which the gamma-secretase activity is regulated is crucial to understanding the mechanisms underlying AD pathogenesis, and may provide new diagnostic tools and therapeutic targets. 14505382: gamma-Secretase cleaves the transmembrane domain of the amyloid precursor protein, a process implicated in the pathogenesis of Alzheimer's disease, and this enzyme is a founding member of an emerging class of intramembrane proteases. 16046406: Gamma-secretase activity leads to generation of the amyloid beta-peptide, a key event implicated in the pathogenesis of Alzheimer disease. 16181553: OBJECTIVE: To study the role of presenilin1 (PS1) in the processing of beta-amyloid precursor protein (APP) to amyloid beta-peptide (Abeta) and its relation to gamma-secretase in the pathogenesis of Alzheimer's disease (AD). 16562666: OBJECTIVE: To identify the promoter of human nicastrin (NCT) gene, a major component of gamma-secretase which is closely related with pathogenesis of Alzheimer's disease. 16597739: Our finding supports a protective role of Abeta40 against amyloid pathology and raises the possibility that impaired gamma-secretase activity could be the basis for AD pathogenesis in general. 16978875: Proteolysis of beta-amyloid precursor protein (APP) into amyloid beta peptide (Abeta) by beta- and gamma-secretases is a critical step in the pathogenesis of Alzheimer's Disease (AD), but the pathways regulating secretases are not fully characterized. 17115048: Thus, beta(2)-AR activation can stimulate gamma-secretase activity and amyloid plaque formation, which suggests that abnormal activation of beta(2)-AR might contribute to Abeta accumulation in Alzheimer disease pathogenesis. 17156133: Generation and deposition of the amyloid beta (Abeta) peptide following proteolytic processing of the amyloid precursor protein (APP) by BACE-1 and gamma-secretase is central to the aetiology of Alzheimer's disease. 18061918: Improper functioning of gamma-secretase was found to be critical in the pathogenesis of Alzheimer's disease. 18276590: Accumulation of extracellular amyloid beta peptide (Abeta), generated from amyloid precursor protein (APP) processing by beta- and gamma-secretases, is toxic to neurons and is central to the pathogenesis of Alzheimer disease. 18575606: Thus, identification of factors that regulate APP steady state levels and/or APP cleavage by gamma-secretase is likely to provide insight into AD pathogenesis. 19114088: Presenilin-1 is required for gamma-secretase activity, which participates in Notch receptor processing, the pathogenesis of Alzheimer's disease and the modulation of Ca(2+) signaling. 19299585: The Aph1B complex contributes to total gamma-secretase activity in the human brain, and thus specific targeting of Aph1B-containing gamma-secretase complexes may help generate less toxic therapies for Alzheimer's disease. 20062056: Therefore, this mode of regulation represents an unprecedented mechanism for modulating gamma-secretase, providing insight into the molecular basis of Alzheimer's disease pathogenesis and a potential strategy for the development of therapeutics. 20237298: Inhibition of gamma-secretase activity is thus an attractive therapeutic strategy to slow down the pathogenesis of AD. 20297736: Amyloid beta protein (Abeta), the major component of senile plaques, is a 40 to 43 amino acid peptide cleaved from amyloid precursor protein (APP) by beta-secretase and gamma-secretase and has been implicated as the primary cause of AD. 21106832: gamma-Secretase is an intramembrane-cleaving protease that is responsible for the generation of amyloid-beta peptides linked to the pathogenesis of Alzheimer's disease. 21119643: gamma-Secretase generates the peptides of Alzheimer's disease, Abeta(40) and Abeta(42), by cleaving the amyloid precursor protein within its transmembrane domain. gamma-Secretase also cleaves numerous other substrates, raising concerns about gamma-secretase inhibitor off-target effects. 21248114: Presenilin 1 (PS1) is an integral component of gamma-secretase and is also a protein closely linked to the etiology of Alzheimer's disease (AD). 22170863: APP processing is linked to Alzheimer disease (AD) pathogenesis, which is consistent with a common mechanism involving toxic APP metabolites in both dementias. Processing of beta-CTF by gamma-secretase releases amyloid-beta (Abeta), which is assumed to cause AD. 22479317: CONCLUSIONS: Gradual saturation of gamma-secretase with its substrate can be the pathogenic process in different alleged causes of AD. Modulation of gamma-secretase activity by multiple enzyme-substrate interactions: implications in pathogenesis of Alzheimer's disease. Membrane-imbedded Abeta-bundles generated by gamma-secretase could be neurotoxic and thus crucial for our understanding of the amyloid hypothesis and AD pathogenesis. 22792182: Our findings allude to an integration of signaling pathways that utilize gamma-secretase activity, which may have significant implications for our understanding of Alzheimer's pathogenesis vis-a-vis vascular changes that set the stage for ensuing neurodegeneration. 23359429: Not exempt from this rule is gamma-secretase, an intramembrane-cleaving protease complex regulating a multitude of signaling pathways and biological processes by influencing gene transcription. gamma-Secretase is also implicated in the pathogenesis of Alzheimer's disease and several types of cancer. 23396974: gamma-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic beta-amyloid peptides (i.e. Abeta42) that have been implicated in the pathogenesis of Alzheimer disease. 23517619: Processing of beta-amyloid precursor protein (APP) by beta- and gamma-secretases in neurons produces amyloid-beta (Abeta), whose excess accumulation leads to Alzheimer's disease (AD). Knowledge on subcellular trafficking pathways of APP and its fragments is important for the understanding of AD pathogenesis. 25037285: Toxic amyloid-beta40-42 (Abeta40-42) peptide cleaved from Abeta protein precursor by beta- and gamma secretases plays a crucial role in the etiology of Alzheimer's disease (AD). 25108625: It is the catalytic subunit of gamma-secretase, which plays critical roles in developmental biology and the molecular etiology of Alzheimer disease, together with three membrane protein cofactors, nicastrin, Aph-1 and Pen-2. 25545059: gamma-Secretase cleaves amyloid beta-precursor protein (APP) to generate amyloid-beta peptide (Abeta), which is a causative molecule of Alzheimer disease (AD). 25893612: The transmembrane protease complex gamma-secretase is a key enzyme in Alzheimer disease pathogenesis as it liberates the neurotoxic amyloid beta-peptide (Abeta); however, the mechanism of regulation of its activity in various cell types and subcellular compartments is largely unknown. 26280335: Dysfunction of the intramembrane protease gamma-secretase is thought to cause Alzheimer's disease, with most mutations derived from Alzheimer's disease mapping to the catalytic subunit presenilin 1 (PS1). 27038342: Among them are the archaeal enzyme FlaK, processing its substrate FlaB2 during the formation of flagella and gamma-secretase, which is centrally involved in the etiology of the neurodegenerative Alzheimer's disease. 28065262: gamma-Secretase is a key player in the pathogenesis of Alzheimer's disease (AD). 28332150: Dynamic Nature of presenilin1/gamma-Secretase: Implication for Alzheimer's Disease Pathogenesis. 29103038: The processing of the amyloid-beta protein precursor (AbetaPP) by beta- and gamma-secretases is a pivotal event in the genesis of Alzheimer's disease (AD). Besides familial mutations on the AbetaPP gene, or upon its overexpression, familial forms of AD are often caused by mutations or deletions in presenilin 1 (PSEN1) and 2 (PSEN2) genes: the catalytic components of the proteolytic enzyme gamma-secretase (GS). 30926830: Cleavage of the amyloid precursor protein's (APP) transmembrane domain (TMD) by gamma-secretase is a crucial step in the aetiology of Alzheimer's Disease (AD). 32091332: Moreover, in AD, oxidative stress is generated by both genetic and biochemical factors as well as the functioning of the systems responsible for their formation and removal. 32111138: Here, I champion a hypothesis whereby AD is initiated on a disruption of the blood-brain barrier (BBB) caused by either genetic or non-genetic risk factors. 32192521: Dynamics of plasma biomarkers in Down syndrome: the relative levels of Abeta42 decrease with age, whereas NT1 tau and NfL increase.BACKGROUND: Down syndrome (DS) is the most common genetic cause of Alzheimer's disease (AD), but diagnosis of AD in DS is challenging due to the intellectual disability which accompanies DS. 32429084: Our analyses provided stronger evidence for possible roles of four genes (i.e., AIM2 , C16orf80 , DGUOK , and ST14 ) in AD pathogenesis as they were also transcriptionally associated with AD. Exploring the genetic and non-genetic contributors to AD pathogenesis is essential to better understand its underlying biological mechanisms, and to develop novel preventive and therapeutic strategies. 32568209: Identification of environmental risk factor(s) and elucidation of the complex interactions between genetic and environmental risk factors plus aging and female sex in the onset of AD will be a key to our understanding of the etiology and pathogenesis of AD and the development of the strategies for its prevention and treatment. 33027797: OBJECTIVE: Bioinformatic analysis at the genetic level has become the best way for the pathogenesis research of AD, which can analyze the abovementioned relationship. 33231156: Next, we represent the probable molecular mechanism which might elucidate the genetic etiology of AD and highlight the role of massively parallel sequencing technologies for novel gene discoveries. 33269107: Studies have found many significant genetic and environmental factors, but the pathogenesis of AD is still unclear. 33596794: BACKGROUND: Alzheimer's disease is a nervous system destructive disease which causes structural, biochemical and electrical abnormalities inside the human brain and results due to genetic and various environmental factors. 33665345: Insight into the genetic etiology of Alzheimer's disease: A comprehensive review of the role of rare variants. 33892965: Investigation of the role of matrix metalloproteinases in the genetic etiology of Alzheimer's disease. Consequently, we investigated the role of MMP1, 3, 13, MT1-MMP, and MT5-MMP in the genetic etiology of AD. 34034776: Mutations in the Presenilin genes are the major genetic cause of Alzheimer's disease (AD). 34276349: Down syndrome (DS) is the most common genetic cause of Alzheimer's disease (AD) due to trisomy for all or part of human chromosome 21 (Hsa21). 34961556: Down syndrome (DS), as the most common genetic cause of AD, presents promising opportunities to compare such features between early and advanced AD. 34971181: BACKGROUND: Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is a leading genetic cause of Alzheimer's disease. 34978149: INTRODUCTION: The National Institute on Aging Late-Onset Alzheimer's Disease Family Based Study (NIA-LOAD FBS) was established to study the genetic etiology of Alzheimer's disease (AD). DISCUSSION: The NIA-LOAD FBS is the largest collection of familial AD worldwide, and data or samples have been included in 123 publications addressing the genetic etiology of AD. 35379992: New insights into the genetic etiology of Alzheimer's disease and related dementias. 35383839: Altered RNA editing may be one possible mechanism for the functional effect of ad associated variants and may contribute to observed differences in the genetic etiology of ad between ancestries. 35946953: BACKGROUND: The interaction of aging-related, genetic, and environmental factors is thought to contribute to the etiology of late-onset, sporadic Alzheimer's disease (AD). 35966919: In the United States, the Alzheimer Disease Sequencing Project (ADSP) has taken a leading role in sequencing AD-related samples at scale, with the resultant data being made publicly available to researchers to generate new insights into the genetic etiology of AD. 36056839: Genetic Causes of Alzheimer's Disease and the Neuroprotective Role of Melatonin in its Management. 36809524: Therefore, understanding the genetic etiology of AD is essential to identifying targeted therapeutics. 37024647: Rare, autosomal dominant forms of AD occur in middle age as a result of highly penetrant genetic mutations, but the most common form of AD occurs later in life. As in other complex diseases, uncovering genetic causes of AD could identify underlying pathological mechanisms and lead to potential treatments. 37170141: BACKGROUND: APP duplication is a rare genetic cause of Alzheimer disease and cerebral amyloid angiopathy (CAA). 37577182: This article aims to briefly summarize the utilization of next-generation sequencing in deciphering the genetic causes of Alzheimer's disease and address the limitations of whole genome and exome sequencing. 37867597: A list of 15 candidate genes for AD risk was also generated to provide data support for further studies on the genetic etiology of AD. 38270275: Of the genetic causes of AD, people with DS represent the largest cohort. 38559257: Down syndrome (DS), or trisomy 21, is the most common genetic cause of AD. 38565895: Evidence from genetic and epidemiological studies point to lipid metabolism defects in both the brain and periphery being at the core of Alzheimer's disease (AD) pathogenesis. 38646507: Shared genetic aetiology of Alzheimer's disease and age-related macular degeneration by APOC1 and APOE genes. 17522446: Homocysteine (HC) and its derivatives may be involved in the etiology of Alzheimer's Disease (AD), although the precise mechanisms by which these compounds could cause cellular pathology are still unclear. 17537547: These results suggest that homocysteine may be an upstream effector to induce AD-like tau hyperphosphorylation through inactivating PP2A. 19087670: OBJECTIVE: To investigate the plasma levels of endogenous hydrogen sulfide (H2S), a gasotransmitter, and homocysteine (Hcy) in patients with Alzheimer's disease (AD), vascular dementia (VD), and cerebrovascular disease (CVD) and their role in the pathogenesis of AD and VD. 21978079: Our data suggest that ALC could be a promising candidate for arresting Hcy-induced AD-like pathological and behavioral impairments. 23837610: Our data suggest that HSYA might be a promising therapeutic candidate for attenuating Hcy-induced AD-like pathological and behavioral deficits. Hydroxysafflor yellow A ameliorates homocysteine-induced Alzheimer-like pathologic dysfunction and memory/synaptic disorder. 24549986: Recent findings shown that Betaine rescued neuronal damage due to homocysteine induced Alzheimer's disease (AD) like pathological cascade, including tau hyperphosphorylation and amyloid-beta (Abeta) deposition. 26019015: Hydrogen Sulfide Ameliorates Homocysteine-Induced Alzheimer's Disease-Like Pathology, Blood-Brain Barrier Disruption, and Synaptic Disorder. 29254095: Dissecting the Role of 5-Lipoxygenase in the Homocysteine-Induced Alzheimer's Disease Pathology. 29710724: Moringa Oleifera Alleviates Homocysteine-Induced Alzheimer's Disease-Like Pathology and Cognitive Impairments. Homocysteine (Hcy) injection for 14 days was used to induce AD-like pathology. 30065790: On the other hand, betaine has been demonstrated to attenuate Alzheimer-like pathological changes induced by homocysteine. 30425189: Our data for the first time provide evidence that TG attenuates Hcy-induced AD-like pathological changes and cognitive impairments, making TG a promising candidate for the treatment of AD-associated pathological changes. In the present study, Tamarix gallica (TG), a naturally occurring plant known for its strong antioxidative, anti-inflammatory and anti-amyloidogenic properties, was evaluated on homocysteine (Hcy) induced AD-like pathology and cognitive impairments in rats. 34122042: Background: Recent studies have reported that homocysteine (Hcy) may play a vital role in the pathogenesis of vascular dementia (VaD) and Alzheimer's disease (AD). 34169425: Here, we investigated whether homocysteine (Hcy) can induce AD-like pathologies and the effects of ligustrazine on these pathologies. Our data demonstrate that ligustrazine may be used as a promising neuroprotective agent to treat the Hcy-induced AD-like pathologies. 9359935: Homocysteine (Hcy) may represent a metabolic link in the pathogenesis of atherosclerotic vascular diseases and old-age dementias. 18479899: Soy protein hydrolysate ameliorates cardiovascular remodeling in rats with L-NAME-induced hypertension. In the present study, we investigated the effects of soy protein hydrolysate with angiotensin-converting enzyme (ACE) inhibitory potential on the blood pressure and cardiovascular remodeling in rats with N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension. 18559295: It is well known that hypertension is closely associated to the development of vascular diseases and that the inhibition of nitric oxide biosynthesis by administration of Nomega-Nitro-L-arginine methyl ester hydrochloride(L-NAME) leads to arterial hypertension. 18957819: In the present study, we investigated the effects of SPH with angiotensin-converting enzyme (ACE) inhibitory potential on blood pressure and renal injuries in rats with N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension. 22961602: The present study investigated the effects of a 6-week swimming training on blood pressure, nitric oxide (NO) levels and oxidative stress parameters such as protein and lipid oxidation, antioxidant enzyme activity and endogenous non-enzymatic antioxidant content in kidney and circulating fluids, as well as on serum biochemical parameters (cholesterol, triglycerides, urea and creatinine) from Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension treated rats. Physical training prevents oxidative stress in L-NAME-induced hypertension rats. 24705342: The present study was aimed to investigate the antihyperlipidemic and renoprotective potential of valproic acid against N(omega)-nitro-L arginine methyl ester hydrochloride (L-NAME) induced hypertension in male albino Wistar rats. These results suggest that VPA has enough potential to attenuate hypertension, dyslipidemia and renal damage in nitric oxide deficiency induced hypertension. 25218092: Vanillic acid: a potential inhibitor of cardiac and aortic wall remodeling in l-NAME induced hypertension through upregulation of endothelial nitric oxide synthase. The objective of the present study is to investigate the effects of vanillic acid on blood pressure, cardiac marker enzymes, left ventricular function and endothelial nitric oxide synthase (eNOS) expression in N(omega)-nitro-l-arginine methyl ester hydrochloride (l-NAME) induced hypertension in male albino Wistar rats. 26133972: Ellagic Acid Prevents L-NAME-Induced Hypertension via Restoration of eNOS and p47phox Expression in Rats. L-NAME induced high systolic blood pressure (SBP) and increased heart rate (HR), hindlimb vascular resistance (HVR) and oxidative stress. The effect of ellagic acid on oxidative stress and hypertension induced by Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME) was investigated. 29087727: In this study, we investigated the effects of 20-HETE on the vascular responsiveness and BP in an L-NAME-induced hypertension. This study demonstrates an important role of 20-HETE in increasing BP and altering vascular responsiveness in L-NAME-induced hypertension model, which suggests a possible involvement of 20-HETE in essential hypertension development in humans. Although various experimental animal hypertension models demonstrated that 20-HETE contributes to increased vascular resistance and BP, these effects have not been studied in Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertension model. 20-HETE inhibition by HET-0016 significantly decreased BP in L-NAME-induced hypertension model. Effect of 20-HETE inhibition on L-NAME-induced hypertension in rats. 31486326: The Effects of Irisin on Nomega-Nitro-L-arginine Methyl Ester Hydrochloride-Induced Hypertension in Rats 33244785: N omega -nitro-L-arginine methyl ester hydrochloride (L-NAME; 40 mg kg -1 day -1 ) was administered for 5 weeks to induce hypertension in male Sprague-Dawley rats, and treated with CF extract (100, 300 or 500 mg kg -1 day -1 ) or sildenafil (5 mg kg -1 day -1 ) during the final 2 weeks (n = 8/group). 35822591: METHODS AND RESULTS: We determined whether TRF can decrease blood pressure in two separate mouse models of hypertension, N(G)-nitro-L-arginine methyl ester hydrochloride-induced hypertension (LHTN) and salt-sensitive hypertension (SSHTN). 10405195: Moreover, the GBS-induced cascade deregulates the gene expression of interacting inflammatory mediators and may cause a net vasoconstrictor/vasodilator imbalance, leading to cerebral hypertension and edema in the early stages of infection. 10921530: The common finding of an autonomic imbalance in these patients contributes not only to the etiology of hypertension itself, but also to the cardiac risk and resulting adverse sequelae. 11323020: Alterations in the synthesis or enhanced inactivation of nitric oxide (NO) and an increase in endothelin-1 production lead to an imbalance that can induce arterial hypertension. 14040260: An analysis of the hypertension due to sympathetic imbalance. 14329335: HORMONAL HYPERTENSION RESULTING FROM PITUITARY IMBALANCE. 14713339: As oxidative stress plays a crucial role in the development and pathogenesis of hypertension, we analyzed the redox (reduction/oxidation) status in tissues from Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). Redox imbalance in essential organs may play a crucial role in the development and pathogenesis of hypertension. 15134517: Indeed, an imbalance in the production or effect of these products is deleterious for the circulatory system and can lead to characterized vascular diseases such as hypertension, stroke, atherosclerosis or myocardial infarction. 15586412: CONCLUSION: These data suggested that the imbalanced synthesis of hCG alpha and beta subunits may cause hypertension. 17287431: The human ET+/+ eNOS-/- mice therefore represent a novel model of hypertension as a result of an imbalance between the vascular ET-1 and NO systems. 17569300: INTRODUCTION: It is generally thought that development of hypertension in preeclampsia (PE) is due to generalized endothelial dysfunction and/or results from an imbalance in the production and/or action of vasoactive factors, resulting in higher cytosolic Ca2+ concentration which in turn leads to vasoconstriction and decreased blood pressure perfusion in organs, including the fetoplacental unit. 18077564: The metabolic syndrome is a cluster of metabolic abnormalities, including hyperinsulinemia, hypertension, dyslipidemia, and abdominal obesity, and is probably triggered by initial imbalances at the cellular level in various critical metabolic pathways. 19169850: Hypertension results from osmotic imbalance during renin-angiotensin cycle inefficiency. 1926814: [Characteristics of sodium metabolism in rats with experimental hypertension caused by chronic alimentary imbalance]. At the age of 14-16 months when a stable hypertension developed due to the above alimentary imbalance, their sodium metabolism was studied using whole-body radiometry with 22Na. 20490579: Hypertension can result from neuronal network imbalance in areas of central nervous system that control blood pressure, such as the nucleus tractus solitarius (NTS). 21631986: The pathogenesis of PPHT may result from an imbalance between vasoconstrictor and vasodilating factors. 2189444: This imbalance of endothelium-derived relaxing and contracting factors may be important in the pathogenesis of hypertension and its cardiovascular complications. 25104455: Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension. 25104456: The blood vessel functional imbalance trends to induce atherosclerosis, hypertension, and pulmonary arterial hypertension. 26974824: PE-associated pathologies, including thrombosis, hypertension, and impaired placental development, may result from imbalances between thromboxane A2 (TXA2) and prostacyclin. Preeclampsia (PE) is a potentially fatal pregnancy-related hypertensive disorder characterized by poor placenta development that can cause fetal growth restriction. 28225041: The imbalance of neurotransmitters and excessive oxidative stress responses contribute to the pathogenesis of hypertension. 28320892: Our results suggest that the hypertension with fluctuation and bradycardia of Spr-/- mice would be caused by an imbalance of sympathetic and parasympathetic input and impaired nitric oxide production in endothelial cells. 29495951: Herein, we hypothesize that a late autonomic imbalance-induced hypertension might be related to long-lasting effects of protein restriction during the critical period of the CNS development on the mitochondrial function and oxidative stress in the brainstem of adult (i.e. 150 days of age) male Wistar rats. 343905: On the assumption that the increased peripheral resistance responsible for hypertension results from an imbalance or a disturbance of the equilibrium between the sympathetic nervous system and norepinephrine on one hand, and the vascular tone, sensitivity and responsiveness of the arterial smooth muscle to norepinephrine and to angiotensin II on the other hand, three models that fit the experimental and clinical facts as known at present are described. Role of the adrenal cortex and sodium in the pathogenesis of human hypertension. 3605364: This work is based on the premise that hypertension in the spontaneously hypertensive rat (SHR) is a consequence of an imbalance in autonomic cardiovascular control. 3977442: If pulsatile compression of the left lateral medulla occurs, hypertension may develop as a consequence of an imbalance in the neural control systems that normally regulate blood pressure. 7010944: A neural or neurochemical imbalance in brain can produce hypertension. 8305164: An imbalance in the activity of the vasopressor renin-angiotensin and vasodepressor kallikrein-kinin systems may play an important role in the pathogenesis of hypertension after unilateral renal artery constriction. 9648078: CONCLUSIONS: We conclude that hypoxia-induced HTN is associated with depressed NO production and can be mitigated by L-arginine supplementation. This study was designed to test the hypothesis that hypoxia-induced HTN may be mediated by increased endothelin and/or decreased NO production. BACKGROUND: We have recently demonstrated that prolonged hypobaric hypoxia can lead to a hematocrit-independent sustained arterial hypertension (HTN) in genetically normotensive Sprague-Dawley rats. Role of endothelin and nitric oxide imbalance in the pathogenesis of hypoxia-induced arterial hypertension. 10404393: Imbalances of cytoskeletal organization can lead to disease such as Alzheimer's, muscular disorders, and cancer. 12862394: Amyloid precursor protein gene mutations responsible for early-onset autosomal dominant Alzheimer's disease. The imbalance between A beta production and A beta clearance releases a cascade of subsequent cellular processes leading to AD. 16360221: An accumulation of amyloid beta peptide (Abeta) due to an imbalance between anabolism and catabolism triggers Alzheimer's disease (AD). 16781020: Much experimental evidence suggests that an imbalance in cellular redox status is a major factor in the pathogenesis of Alzheimer's disease (AD). 1717039: Alzheimer's disease (AD) and its hallmark, plaques, may be due to an imbalance of trophic support. 18085519: Chronic imbalance between production and degradation of the human amyloid-beta peptide (Abeta) is assumed to play an important role in pathogenesis of Alzheimer's disease (AD). 18393845: An imbalance between the production and clearance of Abeta is thought by many to represent the earliest event in the pathogenesis of AD. 19413589: Imbalanced generation of the Abeta42 peptide from the amyloid beta protein precursor (APP) is implicated in the pathogenesis of Alzheimer's disease. 20463236: The accumulation of amyloid beta (Abeta) in Alzheimer's disease is caused by an imbalance of production and clearance, which leads to increased soluble Abeta species and extracellular plaque formation in the brain. 21148344: Alzheimer's disease is hypothesized to be caused by an imbalance between beta-amyloid (Abeta) production and clearance that leads to Abeta accumulation in the central nervous system (CNS). 21551909: Moreover, since alpha1-antitrypsin, the principal inhibitor of elastase, is highly susceptible to oxidative stress, our findings suggest a link between proteolytic imbalance and oxidative stress in the pathogenesis of Alzheimer disease. 22055653: DISCUSSION: The positive correlation between sAPPalpha and sAPPbeta challenges the hypothesis that AD is caused by an imbalance of the alpha- and beta-secretase APP proteolysis through competing mechanisms. 22241730: These observations are consistent with the hypothesis that AD proceeds as a result of an imbalance between Abeta production and Abeta clearance, suggesting a role for myosin Vb in this process. 22415062: The possible imbalance between the Abeta production/degradation process was suggested to contribute to the pathogenesis of AD. 22491325: Therefore, restoration of sAPP-alpha or enhancement of its association with BACE may be viable strategies to ameliorate imbalances in APP processing that can lead to AD pathogenesis. 23378928: Alzheimer's disease (AD) is characterized by the accumulation of beta-amyloid peptide (Abeta) in the brain because of an imbalance between Abeta production and clearance. 24115839: Metal imbalance is the leading cause for many neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. 24310478: Imbalance of zinc ion (Zn(2+)) in human body causes diseases like Alzheimer's and Parkinson's and therefore Zn(2+) estimation in biological fluids has diagnostic values. 24983737: Alzheimer's disease is a consequence of an imbalance between the generation and clearance of amyloid-beta peptide in the brain. 25649650: In particular, our previous studies on GSH redox imbalance have implicated oxidative stress induced by excessive reactive oxygen species as a major mediator of AD-like events, with the presence of S- glutathionylated proteins (Pr-SSG) appearing prior to overt AD neuropathology. 25866779: The identified common subnetworks showed that inflammation of the brain nerves is one of the critical factors of AD and calcium imbalance may be a link among several causative factors in AD pathogenesis. 26254061: The imbalance between beta-amyloid (Abeta) generation and clearance plays a fundamental role in the pathogenesis of Alzheimer's disease (AD). 26390937: An imbalance of intracellular calcium homeostasis induced by amyloid beta-protein (Abeta) contributes to the pathogenesis of Alzheimer's disease (AD), such as deficits in learning and memory. 26639718: AD is caused by an imbalance between Abeta production and clearance, resulting in increased amount of Abeta in various forms [2]. 27031475: Although the pathogenesis of AD remains unclear, AD is thought to result from an imbalance in the production and clearance of amyloid-beta protein (Abeta). 27234294: AD is associated with increased oxidative stress, resulting from imbalance in production and clearance of reactive oxygen species (ROS). 27412291: Strong evidence indicates that an imbalance between production and degradation of key proteins contributes to the pathogenesis of AD. 28281098: The metal imbalance is also among leading causes of AD, owing to the fact that Abeta aggregation takes place in the synaptic cleft where Abeta, Cu(II) and Fe(III) are found in abnormally high concentrations. 28666362: Although it has been reported that AD is strongly affected by CNVs, most of AD-causing genes with pathogenic CNVs have not been identified yet. Inference of Causative Genes for Alzheimer's Disease Due to Dosage Imbalance. 29609077: In the present study, we investigated whether this neurotrophic imbalance can produce an AD-like retrograde degeneration of BFCNs. 30098078: Oxidative stress and oxidative DNA damage are early features of mild cognitive impairment and Alzheimer's disease (AD), occurring before the formation of classical AD neuropathology, and resulting from an imbalance between pro- and anti-oxidants. 30595042: Alzheimer's disease (AD) is considered as a potential risk factor for the development of seizure due to neurodegeneration and imbalance between stimulatory and inhibitory circuits in the brain. 30822648: An imbalance in Ca2+ homeostasis represents an early event in the pathogenesis of Alzheimer's disease (AD). 30866445: Imbalances of excitatory/inhibitory synaptic transmission occur early in the pathogenesis of Alzheimer's disease (AD), leading to hippocampal hyperexcitability and causing synaptic, network, and cognitive dysfunctions. 31379578: Alzheimer's disease (AD) is characterized by two landmark pathologies, the overproduction of amyloid-beta peptides (Abeta), predominated by the beta-amyloid protein precursor cleaving enzyme 1 (BACE1), and hyperphosphorylation of the microtubule protein, tau, because of an imbalance in a kinase/phosphatase system that involves the activation of the protein kinase A (PKA). 31795606: We surmise that any imbalance in MeCP2 function would accelerate or cause Alzheimer disease pathogenesis, implying that MeCP2 may be a potential drug target for the treatment and prevention of Alzheimer disease. 835158: Apparently, this vasocontrictive reflex becomes excessive in Alzheimer's disease, possibly due to cerebral neurogenic imbalance. 9603784: These findings demonstrate that oxidative imbalance and stress are key elements in the pathogenesis of Alzheimer disease. 10567200: Both hypertension and cataract formation have been associated with reductions in sodium pump activity, possibly as a result of an endogenous inhibitor. 11425780: Renal activity of 11beta-HSD is decreased in patients with apparent mineralocorticoid excess (SAME), licorice-induced hypertension, and essential hypertension. CONCLUSIONS: Chronic ET(A) receptor blockade normalizes blood pressure, prevents upregulation of vascular ET-1, and improves endothelial dysfunction in 11beta-HSD inhibitor-induced hypertension and may emerge as a novel therapeutic approach in cardiovascular disease associated with reduced 11beta-HSD activity. 12974300: Many studies employed L-NAME (N(G)-nitro-L-arginine methyl ester), an L-arginine antagonist and nitric oxide (NO) synthase (NOS) inhibitor, to produce hypertension experimentally in male animals. 14558211: However, both COX inhibitors caused hypertension and adverse renal effects. 14639023: NO inhibitor-induced hypertension caused no changes in ANP concentrations. 1481381: Cumulation of endogenous inhibitors of NO formation in renal failure may be the cause of hypertension. 15009217: Ouabain, a sodium pump (Na+/ K+-ATPase) inhibitor, has been shown to act as a hormone and is possibly involved in the pathogenesis of hypertension. 15280798: Chronic administration of CSE inhibitor induces arterial hypertension in the rat. 16178455: As an endogenous mammalian analogue of cardiac glycosides and an inhibitor of the sodium pump, it regulates the body fluid balance, urine sodium extraction and vasoconstrictive tone, and thus plays an important role in the pathogenesis of hypertension and some other cardiovascular disorders. 18474814: Novel role for inhibitor of differentiation 2 in the genesis of angiotensin II-induced hypertension. 18638829: Potential brain protection modalities during neurosurgery include hypothermia, anaesthetic agents, specific inhibitors of peri-ischemic events, induced hypertension and haemodilution. 18728266: Experimentally increasing uric acid levels using a uricase inhibitor causes systemic hypertension in animal models. 18854744: As fructose-rich diets increase uric acid levels, hyperuricemia may also play a role in the metabolic syndrome, triggering insulin resistance and hypertension.A number of studies on rats rendered hyperuricemic by administration of uricase inhibitors have recently confirmed induction of arterial hypertension and microvascular injury, particularly in the remnant kidney or in cyclosporine-induced renal fibrosis. 20351338: Substantial evidence exists for managing hypertension as a chronic condition, but there are few prospectively collected data on managing acute hypertension caused by VSP inhibitors. 20956731: These results suggest that hypertension induced by VEGF inhibitors is mediated by suppression of NO production. 21570455: DC (Bai Bei San Qi) as in vitro inhibitors of key enzymes involved in the pathogenesis of hyperglycemia and hypertension. 21629798: With newer and often more potent antitumor agents, patients may present to their local physicians with drug-induced toxicities such as hypertension induced by vascular endothelial growth factor (VEGF) inhibitors. 21855035: In contrast, hypertension induced by VEGF inhibitors has been shown to represent an important pharmacodynamic biomarker of oncologic response. 22443474: Vascular endothelial growth factor inhibitors (VEGFi) are known to cause hypertension and renal injury that severely limits their use as an anticancer therapy. Captopril attenuates hypertension and renal injury induced by the vascular endothelial growth factor inhibitor sorafenib. 23533693: The effect of alpha-lipoic acid on mitochondrial superoxide and glucocorticoid-induced hypertension. CONCLUSION: Glucocorticoid-induced hypertension in rats is prevented by alpha-lipoic acid via mechanisms other than mitochondrial superoxide reduction. AIMS: To examine the effect of alpha-lipoic acid, an antioxidant with mitochondrial superoxide inhibitory properties, on adrenocorticotrophic hormone- (ACTH-HT) and dexamethasone-induced hypertensions (DEX-HT) in rats and if any antihypertensive effect is mediated via mitochondrial superoxide inhibition. 24646704: Anti-angiogenic drugs that target Vascular Endothelial Growth Factor (VEGF) signaling pathways caused hypertension as an adverse effect in clinical studies. To clarify whether non-clinical research using rats can appropriately estimate the clinical risk of hypertension caused by VEGF signal inhibitors, we investigated the hemodynamic effects and pharmacokinetics (PK) of the VEGF signal inhibitors cediranib (0.1, 3, and 10 mg/kg), sunitinib (5, 10, and 40 mg/kg), and sorafenib (0.1, 1, and 5 mg/kg) in telemetered rats and examined the correlation between the non-clinical and the clinical hypertensive effect. These results represent correlations between the non-clinical and the clinical hypertensive effect of VEGF signal inhibitors, suggesting that non-clinical research using telemetered rats would be an effective approach to predict the clinical risk of hypertension caused by VEGF signal inhibitors. 24867380: For example, both bevacizumab and vascular endothelial growth factor receptor (VEGFR) kinase inhibitors cause hypertension; both epidermal growth factor receptor (EGFR) antibodies and kinase inhibitors cause rash; and these toxicities correlate with response. 24890259: VEGF pathway inhibitors-induced hypertension: next step in therapy. 25218092: Vanillic acid: a potential inhibitor of cardiac and aortic wall remodeling in l-NAME induced hypertension through upregulation of endothelial nitric oxide synthase. The objective of the present study is to investigate the effects of vanillic acid on blood pressure, cardiac marker enzymes, left ventricular function and endothelial nitric oxide synthase (eNOS) expression in N(omega)-nitro-l-arginine methyl ester hydrochloride (l-NAME) induced hypertension in male albino Wistar rats. 26931476: Our aim is to provide an overview of the latest Federal Drug Administration (FDA) approved VEGF inhibitors and TKI's causing hypertension so that others managing patients on these treatments may easily recognize hypertension attributable to these agents and feel comfortable and confident in providing appropriate management and treatment of this side effect. Update of Targeted Therapy-Induced Hypertension: Basics for Non-Oncology Providers. This manuscript focuses on hypertension induced by vascular endothelial growth factor (VEGF) inhibitors and tyrosine kinase inhibitors (TKI). 2827643: These results indicates that vertebrate animals possess a regulator of Na, K-ATPase and suggests the possibility that it may be the mediator of salt-induced high blood pressure. The endogenous inhibitor of Na, K-ATPase has been implicated in the pathogenesis of salt-induced hypertension. 2834953: Endogenous inhibitors of Na, K-ATPase have been implicated in the pathogenesis of salt-induced hypertension. 2837414: From these results it is suggested that 1) DLS and ATPI might contribute to the etiology of hypertension. 29283974: OBJECTIVE: Antiangiogenic receptor tyrosine kinase inhibitors (RTKI) induce arterial hypertension which may limit their use. Renal fractional sodium excretion (FENa) is reduced in early RTKI-induced hypertension, whereas fractional lithium excretion is unaltered. 29311252: Results are compatible with a significant role of reduced renal medullary NO bioavailability in VEGF inhibitor-induced hypertension. The present study was designed to test the hypothesis that VEGF receptor inhibitor treatment leads to hypertension through decreased renal medullary formation of NO and endothelin-1. In the renal medulla, inhibition of NO formation by local L-NAME or by impaired endothelin-1 leads to hypertension. 3017854: A circulating Na+, K+-ATPase inhibitor may cause arterial hypertension in patients with suppressed plasma renin activity, either directly or by sensitizing peripheral vessels to alpha-adrenergic stimulation. 31547602: Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment. 32175644: In the last few years, secondary hypertension due to tyrosine kinase inhibitors, from the vascular endothelial growth factor class, has been recognized to be an important cause of hypertension, as well as proteinuria, and occasionally kidney dysfunction in some cases. 34862331: However, the mechanism underlying TKIs-induced hypertension remains unclear. 35811723: The mechanism of hypertension caused by tyrosine kinase inhibitors (TKIs) targeting vascular endothelial growth factors is mainly related to inhibition of the nitric oxide (NO) pathway and activation of the endothelin pathway, as well as vascular rarefaction and increased salt sensitivity; consequently, prevention and treatment differ for this type of hypertension compared with primary hypertension. 36026869: However, the mechanism underlying TKIs-induced hypertension remains unclear. 36476830: CONCLUSIONS: This study highlighted that new-onset hypertension induced by VSP inhibitors was an independent factor for favorable clinical outcomes. 36600585: BACKGROUND: Cancer treatment with vascular endothelial growth factor signalling pathway (VSP) inhibitors frequently causes hypertension. 37329221: CONCLUSION: TKI-induced hypertension was not associated with clinical benefit in metastatic CRC. There were 29 metabolites that changed with treatment and distinguished patients with and without TKI-induced hypertension. Our objective was to determine whether hypertension was associated with benefit in the context of CRC treatment, and also to gain insight on the pathogenesis of TKI-induced hypertension by monitoring associated changes in the circulating metabolome. TKI-induced hypertension is reportedly a surrogate marker for treatment benefit for some tumor types. Samples were submitted to gas chromatography-mass spectrometry to identify treatment-related metabolomic changes associated with TKI-induced hypertension, compared to pre-treatment baseline. TKI-induced hypertension was not associated with a significantly higher response rate, nor was it associated with improved progression-free or overall survival. 37699444: Widely prescribed in malignant tumor and proliferative retinal lesions, VEGF signaling pathway inhibitors may cause hypertension and renal injury in some patients, presenting with proteinuria, nephrotic syndrome, renal failure and thrombotic microangiopathy. 4374645: The study recommends: 1) women who wish oral contraceptive therapy should give careful family and personal histories and be tested for blood pressure before and during treatment (monthly, then after 6 months twice yearly); 2) careful supervision is indicated for women with high blood pressure or other cardiovascular disorders in their history, present or former kidney disorders, arterial hypertension, pregnancy toxemias, adipositas, or diabetes mellitus; 3) abnormal weight gain may be an early symptom; 4) if any rise in blood pressure is observed, ovulation inhibitor medication should be discontinued immediately; and 5) ovulation inhibitor-induced hypertension should be considered in differential diagnosis in young women with arterial hypertension. 7541779: Renal vasoconstriction and systemic hypertension induced by the inhibitor were similar in untreated and nifedipine-treated rats. 8129535: Hypertension in patients with ADPKD and normal renal function is associated with abnormalities of red cell sodium transport: an increase of Na,Li countertransport, possibly primitive, and a reduction of Na,K pump in fresh cells, possibly secondary to a circulating inhibitor. 8704112: Inhibitors of sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) have been implicated in the pathogenesis of hypertension. 8938662: Alpha-fluoromethylhistidine, an inhibitor of histamine biosynthesis, causes arterial hypertension. 12651959: This is especially important in the study of Alzheimer's disease (AD), in which spatial neuronal organization and relationships are highly disrupted because of neuronal loss. 15574357: Accumulating evidence indicates that two distinct Cdk pathways may have a role in the neuronal loss that is responsible for Alzheimer's disease. 15630088: Amyloid deposition, neuronal loss, and disturbed synaptic transmission are considered to be the main causes of Alzheimer's disease dementia. 17112517: The neurological deficits that are characteristic of Alzheimer's Disease (AD) are ultimately a result of neuronal loss in distinct anatomical regions of the brain. 20689579: BACKGROUND: A devastating aspect of Alzheimer's disease (AD) is the progressive deterioration of memory due to neuronal loss. 21447108: CONCLUSIONS: The CBF reduction in the PCC in AD was partly caused by neuronal loss in the PCC and partly supported the hypothesis that CBF reduction in the PCC was a result of functional deafferentation by neural degeneration in areas other than the PCC. 22175653: It was developed as a symptomatic treatment to compensate for the progressive loss of cholinergic signal between neurons, a consequence of neuronal cell loss in the brains of patients with Alzheimer's disease (AD). 23305945: Alzheimer's disease (AD) is a neurodegenerative disorder that causes progressive memory and cognitive decline due to the selective neuronal loss in the cortex and hippocampus of the brains. 23921129: Amyloid-beta (Abeta) induces neuronal loss and cognitive deficits and is believed to be a prominent cause of Alzheimer's disease (AD); however, the cellular pathology of the disease is not fully understood. 26440450: In Alzheimer's disease (AD), the deposition of beta-amyloid (Abeta) is hypothesized to result in a series of secondary neurodegenerative processes, leading ultimately to synaptic dysfunction and neuronal loss. 27357648: Overall, our results strongly suggest that Ras activity is required for soluble Abeta oligomer-induced aberrant neuronal cell cycle reentry and subsequent neuronal loss, which are considered important mechanisms in AD pathogenesis. 28253985: Extensive research has revealed that multiple cellular pathways involved, including amyloid beta production, mitochondrial structural and functional changes, hyperphosphorylation of Tau and NFT formation, inflammatory responses, and neuronal loss in AD pathogenesis. 28849458: Through the misfolding process of Abeta in the brain, oligomeric forms of Abeta accumulate and significantly damage the brain cells inducing neuronal loss and cognitive dysfunctions that lead to AD. 30741673: Alzheimer's disease (AD), the most common neurodegenerative dementia, leads to memory dysfunction due to widespread neuronal loss associated with aggregation of amyloidogenic proteins (APs), while schizophrenia (SCZ) represents a major psychiatric disorder characterized by delusions, hallucinations, and other cognitive abnormalities, the underlying mechanisms of which remain obscure. Conversely, the increased evolvability conditions including gene mutations of APs are supposed to be beneficial for offspring, but might lead to AD in parents. 7780790: In Alzheimer's disease, the loss of memory is likely to be due to neuronal loss in cerebral cortex and hippocampal formation, along with alterations in neurotransmitter systems (specially cholinergic, monoaminergic and aminoacidergic systems). 9202333: Activation of the classical complement pathway has been widely investigated in recent years as a potential mechanism for the neuronal loss and neuritic dystrophy characteristic of Alzheimer's disease (AD) pathogenesis. 9589388: Alzheimer's disease (AD) is associated with a reduction in cholinergic activity as a result of specific neuronal loss. 31920472: Dysfunction in neurovascular coupling that results in a mismatch between cerebral blood flow and neuronal activity has been suggested to play a key role in the pathogenesis of Alzheimer's disease (AD). 32892233: Neuronal dysfunction and loss are thought to be one of the causes of cognitive impairment in Alzheimer's disease (AD), but the specific mechanism of neuronal loss in the pathogenesis of AD remains controversial. 34080759: The relationship between neuronal loss and Abeta deposits is one of the fundamental questions in the pathogenesis of AD. 34211387: Amyloidogenicity and vascular dysfunction are the key players in the pathogenesis of Alzheimer's disease (AD), involving dysregulated cellular interactions. Overall, the current review informs about the interaction of neuronal and glial cell types in AD pathogenesis and its critical association with cerebrovascular dysfunction. 35154497: Conclusion: We found that the MeCP2-mediated dysregulation of the epigenome in the striatum is linked to the defects in cognitive behavior and neuronal activity in the AD animal model, and that this alteration is initiated even in the very early stages of AD pathogenesis. 35768560: CD36 was selected as a gene previously shown to be implicated in the etiology of AD. In silico studies suggested that the SNP's alter the expression of CD36 thus potentially affecting CD36-related neuroinflammation and other molecular and cellular mechanisms known to be involved in the neuronal loss leading to AD. 37147110: Together, our results indicate that PREPL affects neuronal function by modulating protein trafficking and synaptic function, an important mechanism of AD pathogenesis. 37207075: Neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), are caused by neuronal loss and dysfunction. 37574734: BACKGROUND: Amyloid-beta (Abeta) is a normal product of neuronal activity, including that of the aggregation-prone Abeta42 variant that is thought to cause Alzheimer's disease (AD). 38226680: Therefore, our results clarified the important role and mechanism of the Maf1-NMDAR1 signaling pathway in the stability of the synaptic structure, neuronal function, and behavior during the pathogenesis of AD, serving as a potential diagnostic and therapeutic target for the early onset of AD. 10493744: Presenilins are a highly conserved family of proteins first identified as causative genes in early onset familial Alzheimer's disease. 10984440: Presenilins were first identified as causative factors in early onset, familial Alzheimer's Disease (FAD). 11684347: A novel presenilin mutation (M233V) causing very early onset Alzheimer's disease with Lewy bodies. Presenilin 1 mutations are the major cause of autosomal dominant Alzheimer's disease: here we identify a new missense mutation causing a methionine to valine change at codon 233. 12476348: Studies of the pathogenic actions of mutations in presenilins and amyloid precursor protein that cause early-onset familial AD have established central roles for perturbed cellular calcium homeostasis and oxidative stress in the neurodegenerative process. The clinical presentation of patients with AD is dominated by cognitive deficits and emotional disturbances that result from dysfunction and degeneration of neurons in the limbic system and cerebral cortex. 12849363: Mutant genes for amyloid precursor protein (APP) or presenilin cause early-onset familial Alzheimer's disease (<1% of all cases) and have helped to elucidate APP processing and amyloid-peptide formation by alpha, beta, and gamma secretases. 12902342: Presenilins, whose mutant forms are the most common cause of early onset familial Alzheimer's disease, are involved in two very distinct processes: (i) proteolytic activity as gamma-secretase acting on amyloid precursor protein to produce amyloid peptides and (ii) storage of Ca2+ in the endoplasmic reticulum (ER). 15565529: According to the beta-amyloid cascade hypothesis, the accumulation of beta-amyloid (Abeta) deposits as amyloid plaques in the patient's brain is the primary event in the pathogenesis of Alzheimer's disease (AD). The majority of known APP and presenilin mutations responsible for familial early onset AD affect APP processing causing overproduction of Abeta, especially Abeta42. 16148264: Numerous mutations in the presenilins are known to cause early-onset familial Alzheimer's disease (FAD). 17568632: Presenilin proteins, mutated forms of which cause early onset familial Alzheimer's disease, are capable of modulating various cell signal transduction pathways, the most extensively studied of which has been intracellular calcium signalling. 17582777: The presenilins (PSs) were identified as causative genes in cases of early-onset familial Alzheimer's disease (AD) and current evidence indicates that PSs are part of the gamma-secretase complex responsible for proteolytic processing of type I membrane proteins. 20798900: Mutations in PSEN genes, which encode presenilin proteins, cause familial early-onset Alzheimer's disease (AD). 21725719: beta-amyloid precursor protein (APP) and presenilins mutations cause early-onset familial Alzheimer's disease (FAD). 22489754: This is true for HTT, the beta-amyloid precursor protein (APP) and presenilins, responsible for early onset Alzheimer's disease (AD). 24977484: By the use of mutated PS causing early onset AD in cell culture and transgenic mice we found that GCS is increased in AD, further substantiated by the use of AD post mortem brains, suffering from sporadic AD. 25814654: Of nearly 200 PRESENILIN mutations causing early onset, familial Alzheimer's disease (FAD) only the K115Efx10 mutation of PSEN2 causes truncation of the open reading frame. 30763650: Mutations in the genes encoding amyloid precursor protein (APP) or presenilin (PS) cause early onset familial Alzheimer's disease (AD), and sequential cleavages of the APP by beta-secretase and gamma-secretase/presenilin generate amyloid beta protein (Abeta), the major component of pathological hallmark, neuritic plaques, in brains of AD patients. 31625391: Dominant mutations in APP and presenilin cause early onset familial Alzheimer's disease (FAD). 8651641: Mutations in three of these, the amyloid precursor protein, presenilin I, and presenilin II, cause early-onset AD. 9106355: Various mutations in the amyloid protein precursor and presenilin genes can lead to early onset, autosomal Alzheimer's disease. 9189043: The prevalence of known mutations in presenilin genes (PS1 and PS2) causing early-onset familial Alzheimer's disease (FAD) was assessed in a population of 98 singleton early-onset AD cases, 29 early-onset FAD cases, and 15 late-onset FAD cases. 9831466: Numerous mutations in the presenilin (PS) genes cause early onset familial Alzheimer's disease (FAD). 10230703: Genetic studies on some families have shown that mutations in the genes encoding beta-amyloid precursor protein and presenilins 1 and 2 are responsible for early-onset AD. 10329743: OBJECTIVE: Presenilin-1 is a major causative gene for early onset familial Alzheimer's disease, and the apolipoprotein E epsilon4 allele is a major genetic risk factor known to influence late onset and sporadic early onset Alzheimer's disease. 10775535: We describe 21 affected individuals from a kindred with early-onset autosomal dominant familial Alzheimer's disease caused by an intronic presenilin-1 mutation (in intron 4). Alzheimer's disease due to an intronic presenilin-1 (PSEN1 intron 4) mutation: A clinicopathological study. 11906199: This findings suggest that the direct generation of Abeta from the complex may play an important role in the pathogenesis of Alzheimer's disease. Presenilin-1 (PS1) is a causative gene in early onset familial Alzheimer's disease (FAD). 15330337: Here, we show that mutations of presenilin (PS) 1 and 2, which cause familial early-onset AD (FAD), induce more severe lysosomal system neuropathology in humans than does sporadic AD (SAD). 20854432: Presenilins 1 and 2 are the major causative genes of early-onset familial AD. 21159009: Early-onset familial Alzheimer's disease (AD) caused by presenilin-1 mutation E280A (PS1-E280A) presents wide clinical and neuropathological variabilities. 22133015: The findings support the notion that a deficit in the coordination mechanism of the central executive may be a pre-clinical marker for the early detection of AD due to the E280A presenilin-1 gene mutation. This study examined dual task abilities in individuals who are at risk of early-onset familial AD due to an E280A presenilin-1 mutation. 22267728: Accumulation of Abeta could be caused by increased production, as indicated by several mutations in the amyloid precursor protein or the gamma-secretase components presenilin-1 and presenilin-2 that cause familial early-onset AD. 23123781: CONCLUSIONS: This novel presenilin-1 sequence variant cosegregated with early onset dementia in the proband and at least one other affected family member, and likely represents a mutation causing familial, early-onset Alzheimer's disease. BACKGROUND: Mutations in the gene for presenilin-1 cause familial, early-onset Alzheimer's disease. 31391004: BACKGROUND: Presenilin-1 (PSEN1) is one of the causative genes for early onset Alzheimer's disease (EOAD). 8741394: [Presenilin-1 (S182) causative gene of early-onset familial Alzheimer's disease]. 9160754: Presenilin-1 (PS1) is the major gene responsible for early-onset familial Alzheimer's disease (FAD). 10078973: Mutations in two related genes, presenilin 1 and presenilin 2 (PS1 and PS2), cause a subset of early-onset familial Alzheimer's disease (FAD). 10340748: Because distinct mutations in presenilin 1 and presenilin 2 are a major cause of early-onset familial Alzheimer's disease, we generated four monoclonal antibodies for the identification, localization, and investigation of presenilins in various cell lines and tissues from patients and controls. 11071766: In humans, many naturally occurring mutations in Presenilin 1 or 2 cause early onset Alzheimer's disease. 11405810: Autopsy-confirmed familial early-onset Alzheimer disease caused by the l153V presenilin 1 mutation. 11701593: Here, we report a family (family GB) in which early-onset Alzheimer's disease was caused by a novel presenilin 1 mutation (L282V). Nevertheless, in > 90% of cases of Alzheimer's disease amyloid is also deposited in cerebral blood vessel walls (congophilic amyloid angiopathy; CAA) but its role in Alzheimer's disease pathogenesis remains enigmatic. This was unusually severe CAA reminiscent of the Flemish amyloid precursor protein (A692G) mutation we reported previously, which causes Alzheimer's disease and/or cerebral haemorrhages. Cerebral amyloid angiopathy is a pathogenic lesion in Alzheimer's disease due to a novel presenilin 1 mutation. 11710891: This genetic change may be a prevalent cause of early-onset familial AD in the Caribbean Hispanic population. A founder mutation in presenilin 1 causing early-onset Alzheimer disease in unrelated Caribbean Hispanic families. 18479822: The P117A variant is a novel mutation in PSEN1, which causes early-onset AD in an autosomal dominant manner. Over 160 rare genetic variants in presenilin 1 (PSEN1) are known to cause Alzheimer's disease (AD). 18580586: CONCLUSIONS: This is the first description of neuropathologic findings in EOFAD owing to N135S PSEN1 mutation. OBJECTIVE: Early onset familial Alzheimer disease (EOFAD) can be caused by mutations in genes for amyloid precursor protein, presenilin 1 (PSEN1), or presenilin 2 (PSEN2). 22044463: BACKGROUND: Missense mutations in three different genes encoding amyloid-beta precursor protein, presenilin 1 and presenilin 2 are recognized to cause familial early-onset Alzheimer disease. 22702962: Mutations in genes such as those encoding amyloid precursor protein (APP), presenilin 1 and presenilin 2, are responsible for early-onset familial AD. 23142261: Mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) are responsible for early-onset autosomal dominant AD. 24838203: Mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) are responsible for early-onset autosomal dominant AD. 24906965: Clinical presentation of early-onset Alzheimer's disease as a result of mutation in exon 12 of the PSEN-1 gene. INTRODUCTION: Mutations in the gene for presenilin 1 (PSEN-1) cause familial, early-onset Alzheimer's disease (EOAD). 26141474: To date, mutations in three different genes, the Amyloid precursor protein (APP), Presenilin 1 (PS1), and Presenilin 2 (PS2), have been identified as causative in early-onset AD, making predictive testing possible. 30041064: Seizures have traditionally been related to neuronal loss in the late stages of AD as a consequence of neurodegeneration, however, recent studies indicated that seizures may contribute to the emergence of AD symptoms in early stages of the disease, mainly in familial AD. Mutations in genes encoding presenilin 1 (PSEN1), presenilin 2 (PSEN2) and amyloid precursor protein (APP) are responsible for early-onset familial AD (EOFAD). 30681848: More than 200 distinct mutations in presenilin 1 (PSEN1) cause severe early-onset familial AD (FAD) and are thus of central interest to the etiology of AD. 31440394: Presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP) mutations are responsible for autosomal dominant early-onset Alzheimer's disease (AD-EOAD). 8645246: Presenilin 1 (PSNL1) is a novel causative gene for early-onset familial Alzheimer's disease (EOFAD). 8878479: These results indicate that the presenilin mutations probably cause Alzheimer's disease through a gain of deleterious function that increases the amount of A beta42(43) in the brain. Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease. 9740395: Mutations in the gene for presenilin 1 are causative for the majority of cases of early onset familial Alzheimer's disease. Yet, the physiological function of presenilin 1 and the pathological mechanisms of the mutations leading to Alzheimer's disease are still unknown. 9834545: The second part describes the three genes, amyloid precusor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) genes, which when mutated cause early-onset autosomal dominant AD. 9886077: Presenilin 1 (PS1) has been identified as a causative gene for most early-onset familial Alzheimer's disease. 10587341: CONCLUSIONS: The disruption of the bradykinin B(2) receptor leads to hypertension, LV remodeling, and functional impairment, implying that kinins are essential for the functional and structural preservation of the heart. 11112777: This receptor is widely distributed in the central nervous system and gastrointestinal tract; target disruption leads to obesity, diabetes, and hypertension, however, its role in physiological and pathological processes remain unknown due to lack of selective ligands or identification of its natural ligand. 11557612: Disruption of D(1) or D(3) receptors in mice results in hypertension that is caused, in part, by a decreased ability to excrete an acute saline load. 11566895: Thus, complete loss of the D(2) receptor results in hypertension that is not due to impairment of sodium excretion. 12949653: Hypotensive activity of ultralow doses of antibodies to angiotensin II and its receptors was studied on adult NISAG rats with hereditary stress-induced arterial hypertension. 1297881: [Role of serotonin and its receptors in the pathogenesis of arterial hypertension]. 16014039: An impaired ETB receptor regulation of the AT(1) receptor may participate in the pathogenesis of high blood pressure in the SHR. 16450076: The results suggest that the changes of AM and its receptors in cardiovascular tissue, and the increased response of cardiovascular tissue to AM might importantly impact the pathogenesis of hypertension. 17073613: Disruption of D(1) receptor results in hypertension. 17200683: Although the effects of ET on vascular function and growth are well-recognized, the role of ET and its receptors in the regulation of blood pressure and in the pathogenesis of hypertension is not clearly established. 17875676: Accordingly, adoptive transfer of T cells lacking the angiotensin type I receptor or a functional NADPH oxidase resulted in blunted angiotensin II-dependent hypertension and decreased aortic superoxide production. Role of the T cell in the genesis of angiotensin II induced hypertension and vascular dysfunction. 19041918: These results indicate that the elevation of IMD and its receptor in the cardiovascular tissue may play an important role in the pathogenesis of spontaneous hypertension. This study was designed to explore the role of IMD and its receptor in the pathogenesis of spontaneous hypertension and cardiac hypertrophy. 19373217: CONCLUSIONS: Insulin and D(5) receptors interact to regulate renal sodium transport; an aberrant interaction between insulin and D(5) receptor may participate in the pathogenesis of hypertension. 19996062: We, therefore, examined the role of AT(1) receptors on immune cells in the pathogenesis of hypertension by generating bone marrow chimeras with wild-type donors or donors lacking AT(1A) receptors (BMKO). Activation of type 1 angiotensin (AT(1)) receptors causes hypertension, leading to progressive kidney injury. Thus, in angiotensin II-induced hypertension, bone marrow-derived AT(1) receptors limited mononuclear cell accumulation in the kidney and mitigated the chronic hypertensive response, possibly through the regulation of vasoactive cytokines. 22534490: OBJECTIVE: We examined the role of AT(1) receptors on T lymphocytes in the pathogenesis of hypertension and its complications. 23352346: Imaging AT(1) receptors with PET may provide valuable information on the role of these receptors in the pathogenesis of diseases such as hypertension, diabetic nephropathy, ventricular remodeling, and heart failure. 24979502: The mechanisms involving chemokines and their receptors in the pathogenesis of hypertension are complex and not fully understood. 26485285: Furthermore, BM transplantation (BMT) from either COX-2-deficient or mPGES-1-deficient mice into WT mice or macrophage-specific deletion of the PGE2 type 4 (EP4) receptor induced salt-sensitive hypertension and increased phosphorylation of the renal sodium chloride cotransporter (NCC). 2841255: [The role of adrenergic alpha- and beta-receptors in the pathogenesis of hypertension and heart disease]. 29897266: We previously showed that type 1A angiotensin (AT1A) receptors in vascular smooth muscle cells (VSMCs) play a critical role in BP regulation and hypertension pathogenesis, but these studies were carried out in male mice. Angiotensin II (ANG II) is a major mediator of hypertension pathogenesis. The severity of ANG II-induced hypertension was diminished (~33% reduction in BP), particularly during the last 2 wk of chronic ANG II infusion, compared with controls, but natriuresis was not altered during the first 5 days of ANG II infusion. 35430875: Here, we examined the role of AT 1 receptors on CD11c + cells in hypertension pathogenesis. 3734785: Such a receptor seems to be of the D2 type and might be involved in a sympatho-adrenal cooperative mechanism contributing to the maintenance of cardiovascular homeostasis during stressful situations as well as to the pathogenesis of hypertension. 6303177: An attempt is made to integrate our knowledge of the function and properties of intracellular Ca2+ receptor proteins with our knowledge of cellular calcium homeostasis, and relate this to the pathogenesis of hypertension. 7642168: Recent aspect of the role of peripheral dopamine and its receptors in the pathogenesis of hypertension. 8587392: These results indicate that the upregulating effect of FK 506 on the ET(A) receptor in the vasculature may contribute to the genesis of FK 506-induced hypertension. 8722444: The D1-like receptor is important in the pathogenesis of hypertension. 8781221: The further characterisation of this receptor should provide insights into the pathobiochemical events leading to heart failure in hypertension and ischemic heart disease. 11263271: These receptors play important roles in memory and cognition and participate in the pathogenesis of several brain disorders (Parkinson's and Alzheimer's diseases, Tourette's syndrome, schizophrenia, depression, attention deficit disorder). 15013213: In this context, it is interesting that LDL receptor-related protein is a receptor for MK and PTN, and this receptor has been implicated in the pathogenesis of Alzheimer's disease. 17493709: The consequences of reducing expression of the alpha7 nicotinic receptor by RNA interference and of stimulating its activity with an alpha7 agonist in SH-SY5Y cells indicate that this receptor plays a neuroprotective role in connection with the pathogenesis of Alzheimer's disease. In order to examine the neuroprotective effects of the alpha7 nicotinic receptor (nAChR) in relationship to the pathogenesis of Alzheimer's disease (AD), neuroblastoma (SH-SY5Y) cells were transfected with small interference RNAs (siRNAs) that targets specifically towards alpha7 nAChR or exposed to 20microM 3-[2,4-dimethoxybenzylidene] anabaseine (DMXB), a selective agonist of this same receptor. These findings indicate that alpha7 nAChR may play a significant neuroprotective role by enhancing cleavage of APP by alpha-secretase, regulating signal transduction, improving antioxidant defenses and inhibiting the toxicity of Abeta, which is connected with the pathogenesis of AD. 18800618: These receptors play important roles in attention, memory, and cognition and participate in the pathogenesis of several neuropsychiatric disorders (schizophrenia, depression, anxiety disorders, Parkinson's and Alzheimer's diseases, attention-deficit hyperactivity disorders, Tourette's syndrome, and autosomal dominant nocturnal frontal lobe epilepsy). 19374848: The significant decrease of IP accumulation by cholesterol depletion was also observed in cells expressing M(3) receptors and by both cholesterol depletion and enrichment in cells expressing M(1) receptors indicating relevance of reduced G(q/11) signaling for the pathogenesis of Alzheimer's disease. 19584434: Amyloid-beta protein precursor (AbetaPP) is a receptor-like, type-I membrane protein that plays a central role in the pathogenesis of Alzheimer's disease. 23098038: Targeting the imidazoline I(2) receptor emerges as a new mechanism of action to inhibit tPA-induced signaling in neurons for the treatment of AD and other neurodegenerative diseases. 23928573: This Review highlights recent insights into the structural features that determine the function of scavenger receptors and the emerging role that these receptors have in immune responses, notably in macrophage polarization and in the pathogenesis of diseases such as atherosclerosis and Alzheimer's disease. 24162852: Notably, CD36 is also a receptor for modified lipoproteins and beta-amyloid, and has been implicated in the pathogenesis of atherosclerosis and of Alzheimer's disease. 25362032: Computationally-derived clusters and modules within the networks indicated strong ties between RORA and genes involved in the AD etiology. 26738988: AGEs and receptor for AGEs (RAGE) play important roles in the pathogenesis of AD. 26837733: We also address the importance of APP function as a receptor in Alzheimer's disease etiology and discuss how this function might be potentially important for the development of novel therapeutic approaches. 28373833: Misfolding of PrPC is associated with the transmissible spongiform encephalopathies (TSEs), whereas its normal conformer serves as a receptor for oligomers of the beta-amyloid peptide, which play a major role in the pathogenesis of Alzheimer's Disease (AD). 28826177: Although a number of studies focusing on pharmacological or genetic manipulation of TNF-alpha and its receptors in AD mice have provided significant knowledge regarding the role of TNF-alpha signaling pathway in the pathogenesis of AD, the consequences of TNF-alpha genetic deletion have not been thoroughly examined. 30459541: This mini-review reinforces the rationale to consider major depressive disorder (MDD) as an important risk factor to develop AD and points the central role played by the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids (GC) and their receptors (GR) in the etiology of MDD and AD. 30916478: Surprisingly, these Abeta oligomers reportedly bind to prion protein (PrP), which acts as a receptor on the cell membrane, possibly resulting in AD. 31655116: In this review, we have summarized the different calcium channels and receptors involved in calcium dysregulation which in turn play a critical role in the pathogenesis of AD. 31702505: Dysfunction of these receptors can cause neurodegenerative diseases such as Alzheimer's disease, Parkinson Disease, X-fragile syndrome, anxiety, depression etc., hence these receptors are high profile targets for pharmaceutical industries. 34731369: In this review, we will provide a summary of recent findings regarding the role of FGFs and their receptors in the pathogenesis of AD, and discuss the possible opportunities for targeting these molecules as novel treatment strategies in AD. 36091826: Disturbed retinoic acid signaling causes inflammatory responses, mitochondrial impairment, oxidative stress, and neurodegeneration, leading to Alzheimer's disease (AD) progression. We outlined the physiology of retinoids in this review, focusing on their possible neuroprotective actions, which will aid in elucidating the critical function of such receptors in AD pathogenesis. 37843792: Orexin and its receptors are closely related to the pathogenesis of Alzheimer's disease (AD). 38007666: BACKGROUND: Emerging evidence has revealed that dysregulation of the hormone ghrelin and its receptor, growth hormone secretagogue receptor (GHSR), contributes to the pathogenesis of Alzheimer's disease (AD). 38014048: Triggering receptor expressed on myeloid cells 2 (TREM2) plays a central role in microglial biology and the pathogenesis of Alzheimer's disease (AD). 38033552: Several lipid species and their receptors have essential functions in AD pathogenesis and may be potential biomarkers. 38172904: Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer's disease (AD) pathogenesis. 38548872: Triggering receptors expressed on myeloid cells-2 (TREM2) are known to protect against AD pathogenesis. 32573587: The Morris water maze experiment showed that scopolamine-induced AD-like dementia in rats treated with PC/SHP-2-Bn/SHP-2-16 nanoparticles was significantly reduced. 33324798: Neuroprotective Effect of Spice Oleoresins on Memory and Cognitive Impairment Associated with Scopolamine-Induced Alzheimer's Disease in Rats. 34013783: We investigated the pharmacodynamics and pharmacokinetics of 2-week intranasal galantamine-bound chitosan nanoparticles (G-NP) treatment in scopolamine-induced Alzheimer's disease rat model. 34147486: Passive avoidance test showed that 1 or 5 mg/kg TFK restored memory impairment in scopolamine-induced Alzheimer's disease-like dementia in rats. 34170456: To investigate the possible neuroprotective role of Hespin an AD-like rat model induced experimentally by Scopolamine (Scop). 34173038: The method was used to study in vivo brain uptake and pharmacokinetics of galantamine from brain homogenate and plasma samples following the administration of nasal galantamine-bound chitosan nanoparticles compared to oral and nasal galantamine solutions, in scopolamine-induced Alzheimer's disease rat model. 34204787: The administration of H. erinaceus extract to zebrafish, with a pattern of AD induced by scopolamine, showed an improvement in memory evaluated by behavioral and biochemical tests on brain tissue. 34347557: This study aimed to investigate the effect of vitamin B 12 on restoration of Synaptic Plasticity on scopolamine-induced AD in rats. 35137748: Alzheimer's disease (AD) is the most prevalent form of dementia affecting people worldwide Therefore, the current research aimed to investigate potential therapeutic benefits of Salvia officinalis (SOL) cultivated in Jordan and Salvia microphylla (SML) cultivated in Egypt with regard to acetylcholinesterase activity, beta-amyloid deposition and oxidative stress associated with scopolamine-induced AD. Accordingly, the present study demonstrates the beneficial effects of Salvia species from Egypt and Jordan against scopolamine-induced AD-like disorder. 35178203: Conclusion: We revealed that curcumin provides a protective effect on scopolamine-induced cognitive impairment mimicking Alzheimer's disease. Improvement of cognitive deficit of curcumin on scopolamine-induced Alzheimer's disease models. 35411685: SCO (1 mg/kg) was administrated intraperitoneally to induce the AD in Wistar rats. Hence, this study was designed to investigate the possible therapeutic effect of betanin against SCO-induced AD on Wistar rats. Mitochondrial dysfunction and oxidative stress are identified to contribute to the mechanisms responsible for the pathogenesis of Alzheimer's disease (AD). 35559146: Clavulanic Acid: A Novel Potential Agent in Prevention and Treatment of Scopolamine-Induced Alzheimer's Disease. 35599481: OBJECTIVE: The effects of SE from Helix aspersa on learning and memory deficits in Alzheimer's type dementia (ATD) induced by scopolamine (Sco) in male Wistar rats were examined and some mechanisms of action underlying these effects were evaluated. 35718231: TMQ diminished the lipid peroxidation and cholinergic dysfunction in the scopolamine-induced AD rat model which all reflected in improving the MMN/theta response and spatial memory. 36305148: Ellagic acid prevents oxidative stress and memory deficits in a rat model of scopolamine-induced Alzheimer's disease. 36467923: The level of malondialdehyde decreased in AD animals treated with BBR-TRANS, CUR-TRANS, and BBR-CUR-TRANS, respectively, as compared to the scopolamine-induced AD animals. 36687096: Magnoflorine-Loaded Chitosan Collagen Nanocapsules Ameliorate Cognitive Deficit in Scopolamine-Induced Alzheimer's Disease-like Conditions in a Rat Model by Downregulating IL-1beta, IL-6, TNF-alpha, and Oxidative Stress and Upregulating Brain-Derived Neurotrophic Factor and DCX Expressions. 36817151: Anticholinergic effect of resveratrol with vitamin E on scopolamine-induced Alzheimer's disease in rats: Mechanistic approach to prevent inflammation. 36969860: Both Augmentin and memantine improved spatial memory in AD rats, particularly in the group that received memantine; however, the outcomes were more substantial when Augmentin was administered before scopolamine was given to induce AD. 36986277: Rosmarinus officinalis and Mentha piperita Oils Supplementation Enhances Memory in a Rat Model of Scopolamine-Induced Alzheimer's Disease-like Condition. 37261605: We, therefore, hypothesized to study the neuroprotective potential of Zinc Ortho Methyl Carbonodithioate (thereafter called ZOMEC) against Scopolamine (SCOP) induced Alzheimer's disease (AD) model using adult albino mice. 37269967: Investigation of the protective effect of long-term exercise on molecular pathways and behaviours in scopolamine induced alzheimer's disease-like condition. 37416682: Natural products have pronounced capability in treating Alzheimer disease therefore current study aimed to evaluate the neuro-protective capability of folicitin against scopolamine-induced Alzheimer disease neuropathology in mice. 37652196: CONCLUSION: This study identified numerous metabolic networks modulated by DWP that can mitigate scopolamine-induced AD neuropathology and cognitive dysfunction. Neuroprotective mechanisms of defatted walnut powder against scopolamine-induced Alzheimer's disease in mice revealed through metabolomics and proteomics analyses. 37662728: Objectives: The main objectives of proposed work are to increase the bioavailability of naringin in brain by developing Nano-suspension and preclinical evaluation of neuroprotective effect of Naringin Nano-suspension (NNS) against Scopolamine induced Alzheimer's disease in rats. 37764343: The Potential Neuroprotective Effect of Thymoquinone on Scopolamine-Induced In Vivo Alzheimer's Disease-like Condition: Mechanistic Insights. RESULTS: TQ has the potential to ameliorate cognitive deficits observed in SCOP-induced AD-like model, as evidenced by the improvement in behavioral outcomes, histopathological changes, modulation of the expression pattern of PPAR-gamma downstream targets with a significant decrease in the deposition of amyloid beta (Abeta). 37779395: Montelukast Ameliorates Scopolamine-induced Alzheimer's Disease: Role on Cholinergic Neurotransmission, Antioxidant Defence System, Neuroinflammation and Expression of BDNF. 37793605: Forst. overcome scopolamine-induced Alzheimer's type dementia in mice by activating the cholinergic system, anti-oxidant and protection of neuronal death in the brain (hippocampus region). 37832760: Experiments have demonstrated that frankincense may offer protection against scopolamine-induced Alzheimer's disease by mitigating cholinergic dysfunction and inhibiting inflammatory mediators. Preparation and characterization of brain-targeted polymeric nanocarriers (Frankincense-PMBN-lactoferrin) and in-vivo evaluation on an Alzheimer's disease-like rat model induced by scopolamine. 37924999: AIM OF THE STUDY: The study aims to assess the effects of co-treatment with WCW and donepezil on cognitive functions and serum metabolic profiles in a scopolamine-induced AD model. 38018298: Screening of the Active Substances for the Assessment of Walnut Kernel in the Treatment of Scopolamine-Induced AD Animals. 38278026: Sinomenine regulates the cholinergic anti-inflammatory pathway to inhibit TLR4/NF-kappaB pathway and protect the homeostasis in brain and gut in scopolamine-induced Alzheimer's disease mice. 38360390: Scopolamine is commonly used as a model to induce Alzheimer's disease (AD-like) symptoms. 38397604: This study used scopolamine to induce AD in rats. 22443474: Vascular endothelial growth factor inhibitors (VEGFi) are known to cause hypertension and renal injury that severely limits their use as an anticancer therapy. Captopril attenuates hypertension and renal injury induced by the vascular endothelial growth factor inhibitor sorafenib. 22687270: The cardiotoxic effects of sorafenib and sunitinib may cause hypertension, left ventricular ejection fraction (LVEF) dysfunction and/or congestive heart failure (CHF), and arterial thrombo-embolic events (ATE). 22688785: During the first month of treatment, sorafenib-induced hypertension was diagnosed in 76 patients (51.4%), and these patients had a significantly longer PFS (p < 0.00001) and a significantly lower overall mortality risk (p = 0.038). CONCLUSIONS: Sorafenib-induced hypertension is a positive predictive factor in mRCC patients treated with sorafenib, especially in patients with a history of hypertension. Patients with preexisting and sorafenib-induced hypertension had the longest PFS (p < 0.00001). Sorafenib-induced hypertension was defined as systolic BP >=140 and/or diastolic BP >=90 mm Hg during the first month of treatment. 24621095: Findings of the meta-analysis indicated a significantly high risk of sorafenib-induced hypertension. Incidence and risk of sorafenib-induced hypertension: a systematic review and meta-analysis. 26322676: There is a significantly high risk of sorafenib-induced HTN. We searched multiple databases to investigate the risk of sorafenib-induced HTN in patients with cancer. 26597814: Factors associated with OS included MSKCC risk values, bone metastasis and sorafenib-induced hypertension (all p < 0.05). 26893366: Patients with sorafenib-induced HTN had a better outcome than those without HTN (disease control rate: 63.4% vs. 28263701: After univariate and multivariate analyses, the onset of sorafenib-induced hypertension and/or dermatologic adverse events (AEs) (grade >=2) within the first month of sorafenib initiation were demonstrated as independent predictors of OS. 34775477: In the discovery set, rs444904 (G > A) in PIK3R5 was associated with an increased risk of sorafenib-induced hypertension (p = 0.006, OR = 3.88 95% CI 1.54-9.81). In the replication set, rs427554 (G > A) in PIK3R5 (in complete linkage disequilibrium with rs444904) was associated with an increased risk of bevacizumab-induced hypertension (p = 0.008, OR = 1.39, 95% CI 1.09-1.78). This study aimed to identify predictive biomarkers of hypertension induced by these drugs using a discovery-replication approach. 35718693: Sorafenib can produce arterial hypertension, thyroid disorders, abdominal pain or hyperamylasemia, among others. 38524877: It also discusses potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and highlights the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. 23789343: [Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer's disease]. 24577753: Aggregation of the microtubule associated protein tau (MAPT) within neurons of the brain is the leading cause of tauopathies such as Alzheimer's disease. 32403399: Amyloid-beta and tau proteins are triggers for AD pathogenesis, and usually used as AD candidate biomarkers in the clinical research. 32867562: miR-132 plays a critical role in regulating TAU protein levels and is important for preventing tau protein aggregation that causes Alzheimer's disease. 33065402: Tau protein is an important biomarker in the pathogenesis of Alzheimer's disease. 33093174: Clearance of intracellular tau protein from neuronal cells via VAMP8-induced secretion.In Alzheimer's disease (AD), tau - a microtubule-associated protein - becomes hyperphosphorylated, aggregates and accumulates in the somato-dendritic compartment of neurons. 33662757: Although the etiology of AD is not well understood, however, several factors such as oxidative stress, deposition of amyloid-beta (Abeta) peptides to form Abeta plaques, intraneuronal accumulation of hyperphosphorylated tau protein, and low level of acetylcholine are thought to play a major role in the pathogenesis of AD. 33843226: Abnormal expression of Tau protein can cause the development of Alzheimer's disease (AD). 34123738: Amyloid and tau protein abnormalities have been identified as the main causes of Alzheimer's disease but exact mechanisms remain to be revealed. 34308969: Misfolded, pathological tau protein propagates from cell to cell causing neuronal degeneration in Alzheimer's disease and other tauopathies. 34671002: [Beta Amyloid, Tau Protein, and Neuroinflammation: An Attempt to Integrate Different Hypotheses of Alzheimer's Disease Pathogenesis]. 34671708: According to the glymphatic hypothesis, in physiological conditions, cerebrospinal fluid flows primarily during sleep and serves to remove metabolic wastes like the amyloid-beta and tau proteins whose accumulation is believed to cause Alzheimer's disease. 34900398: Aluminum is a known neurotoxin that can induce Abeta deposition and abnormal phosphorylation of tau protein, leading to Alzheimer disease (AD)-like damages such as neuronal damage and decreased learning and memory functions. 35367762: Amyloid deposits and hyperphosphorylation of the tau protein are still believed to be the two main causes of Alzheimer's disease. 35771127: The cyclin-dependent kinase (CDK5) forms a stable complex with its activator p25, leading to the hyperphosphorylation of tau proteins and to the formation of plaques and tangles that are considered to be one of the typical causes of Alzheimer's disease (AD). 36120782: BACKGROUND: Amyloid-beta (Abeta) and tau protein accumulation in the brain is thought to be one of the causes of Alzheimer's disease (AD). 36389082: The complicated pathophysiology of AD is not well understood, although beta-amyloid (Abeta) cascade and hyperphosphorylated tau protein were regarded as the two main causes of AD. 37315665: Microtubule affinity regulating kinase 4 (MARK4) is known to hyperphosphorylate tau protein, which subsequently causes Alzheimer's disease (AD). 37386272: This flawed miRNA expression is responsible for the unusual buildup of amyloid proteins, fibrillation of tau proteins in the brain, neuronal death and other hallmarks leading to AD. 37905874: ABSTRACT: The aggregation of amyloid-beta peptide and tau protein dysregulation are implicated to play key roles in Alzheimer's disease pathogenesis and are considered the main pathological hallmarks of this devastating disease. 38559176: It is well known that Abeta and tau proteins are deposited stereotypically in brain regions to cause Alzheimer's disease. 12716059: Here we hypothesize that while short-term induction of calcipressin1 can provide stress protection, its long-term or chronic induction may cause gradual accumulation of hyperphosphorylated tau protein, eventually leading to Alzheimer's disease. 14706948: BACKGROUND: Abnormal hyperphosphorylation of the microtubule-associated protein tau and its incorporation into neurofibrillary tangles are major hallmarks of the pathogenesis of Alzheimer disease (AD). 1527090: It has been suggested that hyperphosphorylation of the tau protein in neurofibrillary tangles may be relevant to the etiology of Alzheimer's disease and that at least one of the hyperphosphorylated sites lies within a consensus sequence for the p34cdc2/cdc28 family of kinases. 16855914: It has been pointed out that hyperphosphorylation of microtubule-associated protein tau caused by stress might participate in the early stages of Alzheimer's disease pathogenesis. 17266954: Abnormal phosphorylation of tau protein represents one of the major candidate pathological mechanisms leading to Alzheimer's disease (AD) and related tauopathies. 18396294: Neuroinflammation and abnormal phosphorylation of TAU proteins have been implicated in the etiology of Alzheimer's disease (AD). 19246243: The microtubule-associated protein tau is integral to the pathogenesis of Alzheimer's disease (AD), as well as several related disorders, termed tauopathies, in which tau is deposited in affected brain regions. 21841250: Phosphorylation of tau protein is a critical event in the pathogenesis of Alzheimer's disease (AD). 21985244: Hyperphosphorylation of tau protein (tau) causes neurodegenerative diseases such as Alzheimer's disease (AD). 22222439: Specifically, we have analyzed levels of hyperphosphorylated tau proteins, bearing the AD-specific phospho-epitopes (AT-8, pT181, and PHF-1), which are implicated in the pathogenesis of AD. 22288403: The Abeta and tau proteins, two key players in the pathogenesis of Alzheimer's disease (AD), are highly homologous among primates. 24254705: Tau protein has been proposed as a trigger of Alzheimer's disease once it is hyperphosphorylated. 24497730: CDK5 and GSK3B are the two main protein kinases that have an important role in the abnormal hyperphosphorylation of MAPT which leads to Alzheimer's disease. 24618580: Hyperphosphorylation of tau protein is an important mechanism for aggregation, so many studies on the pathogenesis of AD and other tauopathies have focused on regulation of tau phosphorylation by kinases and phosphatases. 24936619: Changes in spatial learning ability and memory and induction of AD-like pathogenesis were not detected by in vivo brain imaging for amyloid-beta peptide accumulation and by immunohistochemical staining of amyloid precursor protein, amyloid-beta protein, tau, and phosphorylated tau protein. 25524708: Abnormally phosphorylated Tau protein, the major component of neurofibrillary tangles, is critical in the pathogenesis of Alzheimer's disease and related Tauopathies. 25903151: Overexpression of the amyloid precursor protein (APP) and the hyperphosphorylation of the tau protein are vital in the understanding of the cause of Alzheimer's disease (AD). 26453208: Conversion of monomeric tau protein into filamentous aggregates is a defining event in the pathogenesis of Alzheimer's disease. 27660034: Accumulation of amyloid beta (Abeta) peptide and hyperphosphorylated tau protein has been proposed to play roles in neural destruction which induce Alzheimer's disease (AD) progresses, glutamate transporter type 1 (GLT-1) and Glycogen synthase kinase3beta (GSK3beta) may be the pathological links between Abeta and tau pathology. 28179579: Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5 have been identified as being involved in the pathological hyperphosphorylation of tau proteins, which leads to the formation of neurofibrillary tangles and causes Alzheimer's disease. 28184302: In this review, we will discuss the role of exosomes in the metabolism and secretion of APP and Tau proteins and their subsequent impact on AD pathogenesis. 29065845: BACKGROUND & OBJECTIVE: Involvement of amyloid beta and tau proteins in pathogenesis of Alzheimer's disease (AD) has been studied extensively. 30062675: Clinical drug research targeting at classic pathology hallmarks, such as amyloid-beta (Abeta) and tau protein, failed to achieve effective cognitive improvement, suggesting that the pathogenesis of AD is much complicated, and there are still other unknown and undetermined important factors. 30251388: The two hexapeptide amino acid sequences 306 VQIVYK311 and 275 VQIINK280 of the tau protein are responsible for aggregation, and subsequent functional loss leading to Alzheimer's progression. 31470053: The intrinsically disordered tau protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD) and other human tauopathies. 9794144: The particular contribution of muscarinic receptors, beta-amyloid and tau proteins in the pathogenesis of Alzheimer's disease remains still unclear. Probably Alzheimer's disease could be due to a progressive degeneration in the relationship between the three components covered in this review. 10423114: Although the role of vascular factors for the pathogenesis of AD is becoming recognized, the effectiveness of antihypertensive treatment on the prevention of AD should be further clarified in the future studies. 10818514: The increased OEF with preserved vascular reserve seen in AD may implicate participation of a vascular factor in the pathogenesis of AD, possibly at the capillary level. 10867215: The increase of OEF and preserved VTT and VR seen in AD patients indicate the possible participation of vascular factors in the pathogenesis of AD perhaps at the capillary level. 12657895: Vascular factors may play a role in the etiology of Alzheimer's disease (AD) and increased serum apolipoprotein E (APOE) levels in AD could be of interest, as APOE concentration is associated with vascular disease. 15883314: The diagnosis of vascular dementia is difficult in epidemiologic studies because poststroke dementia can be due to Alzheimer disease (AD) and evidence of vascular disease can be found in the MRI of dementia cases without clinical strokes. The dementia was attributable to only vascular factors in 56 cases (probable VaD); VaD coexisted with AD in 61 cases, although the VaD component was the leading cause of dementia (probable VaD with AD); AD was the leading cause of dementia in 61 cases (possible VaD and probable AD); and in 29 cases, it was not clear that either AD or VaD was the primary diagnosis (possible AD and possible VaD). 16179827: Our finding may be another step in providing a rationale on how vascular factors could ultimately result in Alzheimer's disease. 16288900: There is already considerable evidence from epidemiological, pathological and clinical reports that vascular factors are crucial in the pathogenesis of Alzheimer's disease (AD). 18305170: Substantial evidence from epidemiological, pathological, and clinical reports suggests that vascular factors are critical in the pathogenesis of Alzheimer's disease (AD), and changes in blood flow are currently the most reliable indicators of the disease. 22377662: Some of them are related to the severity of the degenerative process itself, implying additional vascular factors in the pathogenesis of Alzheimer's dementia. 22869466: Vascular factors play a role in the etiology of Alzheimer's disease (AD), presumably due to emergence of white matter lesions. 23026534: Vascular factors and epigenetic modifications in the pathogenesis of Alzheimer's disease. 25554493: Substantial evidence from epidemiologic, pathologic, and clinical reports suggests that vascular factors are critical for the pathogenesis of AD. In Alzheimer's disease (AD), large populations of endothelial cells undergo angiogenesis due to brain hypoxia and inflammation. 33579850: BACKGROUND: Vascular factors and mitochondria dysfunction contribute to the pathogenesis of Alzheimer's disease (AD).